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(Health) Cancer: Vitamin D Needed to Cut Colon Cancer Risk
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PostPosted: Wed Dec 28, 2005 10:25 am    Post subject: (Health) Cancer: Vitamin D Needed to Cut Colon Cancer Risk Reply with quote






Cancer Researchers Determine Specific Amount
of Vitamin D Needed to Cut Colon Cancer Risk in Half



Press Release
University of California, San Diego
By Nancy Stringer
December 20, 2005

Taking 1,000 international units (IU) of vitamin D 3 daily appears to lower an individual’s risk of developing colorectal cancer by 50 percent, according to an extensive literature review led by cancer prevention specialists at the Moores Cancer Center at the University of California, San Diego (UCSD) Medical Center. The researchers call for prompt public health action to increase intake of vitamin D 3 as an inexpensive, non-toxic prevention for a disease that claims 56,000 U.S. lives each year.

“Studies over the last 25 years have shown that vitamin D is associated with preventing colon cancer, but we haven’t known how much is needed to produce a benefit,” said Edward D. Gorham, assistant adjunct professor of Family and Preventive Medicine at UCSD School of Medicine and a cancer epidemiologist affiliated with the Moores UCSD Cancer Center. “This paper establishes the target level of vitamin D that could reduce the incidence of colorectal cancer by half.”

Gorham added that this review, an invited publication in the current issue of the peer-reviewed Journal of Steroid Biochemistry and Molecular Biology, does not prove a causal relationship and further studies need to be done.

“Interventional studies, or clinical trials, are needed to further define the relationship between vitamin D and colon cancer,” he said, “but such studies could take more than 20 years to complete. Since the safety of daily intake of vitamin D 3 in the recommended range has been thoroughly assessed and confirmed by the National Academy of Sciences, and the benefits found so far in observational studies are considerable, expanded use of vitamin D as a public health measure should not be delayed.”

In the paper, the authors conclude: “Intake of 1,000 IU/day of vitamin D, half the safe upper intake established by the National Academy of Sciences, was associated with 50 percent lower risk (of colorectal cancer).” They further write that individuals with vitamin D blood levels of 33 nanograms per milliliter, generated through modest sunlight exposure, also had a 50 percent lower incidence of colorectal cancer.

Approximately 145,000 new cases of colorectal cancer are diagnosed each year in the U.S. Results of this paper suggest that approximately 72,500 new cases and 28,000 deaths could be prevented with appropriate intake of vitamin D .

The findings are based upon an extensive systematic review of scientific papers on the relationship of blood serum levels or oral intake of vitamin D with risk of colorectal cancer published worldwide between January 1966 and December 2004. Forty four articles were identified; 18 articles met the study’s criteria for inclusion. A majority (10) of the studies found that inadequate vitamin D status was significantly associated with higher risk of colorectal cancer. The other eight studies ranged from a borderline association to no association.

This complex analysis of virtually every scientific paper written on the subject, called a systematic review, paints a clearer picture than any single study and is recognized by scientists as an important tool for establishing a consensus of findings. For example, some studies, particularly those conducted in Scandinavian countries, did not find an effect.

“When we looked at the Scandinavian studies in the context of all of the studies, we realized there may be reasons specific to those countries that can explain the anomaly,” Gorham said. “In Scandinavian countries, vitamin D comes largely from fish. Most of their fish is smoked, salted or preserved. These are carcinogenic, so the carcinogens could offset the benefit.”

Gorham said that while this study looked at all forms of vitamin D – intake through diet or supplements, and photosynthesis through modest sun exposure – as a practical matter, the majority of people will most easily achieve the target levels by taking supplements.

“Many people are deficient in vitamin D. A glass of milk, for example, has only 100 IU. Other foods, such as orange juice, yogurt and cheese, are now beginning to be fortified, but you have to work fairly hard to reach 1,000 IU a day,” he explained. “Sun exposure has its own concerns and limitations. We recommend no more than 15 minutes of exposure daily over 40 percent of the body, other than the face, which should be protected from the sun. Dark-skinned people, however, may need more exposure to produce adequate amounts of vitamin D, and some fair-skinned people shouldn’t get any vitamin D from the sun. The easiest and most reliable way of getting the appropriate amount is from a daily supplement.”

As an appendix to the research paper, the authors make nine recommendations for action, including that the federal government officially recommend intake of 1,000 IU per day of vitamin D for cancer prevention; that it establish a national research program to further explore the beneficial effects of vitamin D on a variety of cancers; and that it standardize vitamin D measurements and make that standard available to scientists throughout the world to streamline future research.

The researchers conducted a cost/benefit analysis of their recommendations and conclude with the following: “Preventing approximately half of colorectal cancer incidence by a program that would ensure vitamin D adequacy could save an estimated $20 billion per year. Annual supplementation of all Americans with 1,000 IU per day of vitamin D 3 would cost approximately $5 billion. Although further economic investigation would be desirable, a gross estimate of the annual return on investment, considering the cost of supplementation, would be $15 billion per year, amounting to a nearly 40 percent per annum return on investment.”

Media Contacts: Nancy Stringer, 619-543-6163.

*************************************************************

Questions to explore further this topic:

What is vitamin D?

http://ods.od.nih.gov/factsheets/vitamind.asp
http://www.wholehealthmd.com/r.....05,00.html
http://healthlink.mcw.edu/article/982088787.html

Detailed Structure and Synthesis of Vitamin D

http://arbl.cvmbs.colostate.ed.....amind.html

Vitamin has also been found to reduce the risk of Diabetes I

http://news.bbc.co.uk/1/hi/health/1632649.stm

What is Vitamin D deficiency?

http://health.enotes.com/child.....deficiency

What is cancer

http://kidshealth.org/parent/m.....ancer.html
http://www.insidecancer.org/

What are the different types of cancer

http://cancernet.nci.nih.gov/c.....moncancers

Brain Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

Breast Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

Colon Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

Leukemia
http://www.nlm.nih.gov/medline.....0_no_0.htm

Lung Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

Melanoma
http://www.nlm.nih.gov/medline.....0_no_0.htm

Ovarian Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

Prostate Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

Skin Cancer
http://www.nlm.nih.gov/medline.....0_no_0.htm

What is the digestive system

http://kidshealth.org/parent/g.....stive.html

What is colon cancer and what is the colon?

http://en.wikipedia.org/wiki/Colon_(anatomy)
http://en.wikipedia.org/wiki/Colon_cancer
http://www.cancer.org/docroot/.....&dt=10
http://www.cancer.gov/cancerto.....and-rectal

GAMES

http://www.nichd.nih.gov/milk/kids/kidsteens.cfm
http://www.aahom.org/movie/Brain_On_Problems.mov
http://www.aahom.org/movie/Dots_Dabs.swf


Last edited by adedios on Sat Jan 27, 2007 4:46 pm; edited 5 times in total
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PostPosted: Tue Jan 03, 2006 6:22 pm    Post subject: Studies: Statins Don't Lower Cancer Risk Reply with quote

Studies: Statins Don't Lower Cancer Risk
By CARLA K. JOHNSON, Associated Press Writer
3 January 2006

Two new studies deal a double blow to hopes that cholesterol-lowering statin drugs could help prevent cancer as well as heart disease.

In one report, researchers analyzed 26 rigorous, randomized studies involving more than 73,000 patients and concluded that drugs such as top-selling Lipitor and Zocor had no effect on the risk of developing or dying from any form of cancer.

The findings appear in Wednesday's Journal of the American Medical Association.

The other study, published in the Journal of the National Cancer Institute, found that cholesterol-lowering drugs, including statins, were of no benefit for preventing colorectal cancer.

"We were very hopeful that we would verify there was an anti-cancer effect," said C. Michael White of the University of Connecticut School of Pharmacy, who led the analysis appearing in JAMA. "We ended up showing no change in cancer or cancer death."

White said the new findings — as well as the rare but potential side effects of statins, which can include liver damage and muscle pain — should discourage doctors from prescribing them solely to prevent cancer.

People should continue taking them to lower cholesterol and prevent heart attacks, he said. "It really is a great drug for heart disease," White said.

Hope for statins as cancer fighters was sharpened by the fact that so many people already take them to lower cholesterol and the drugs are widely considered safe. Previous research, including animal studies and observational studies of people, had suggested statins might prevent various types of cancer.

For example, researchers looked at medical records for 1.4 million patients treated at 10 Veterans Affairs centers and found that those taking statins had lower rates of breast, prostate and lung cancer than those who hadn't taken such drugs.

And a study of Israeli patients published last year showed a 47 percent lower risk of colorectal cancer in people who used statins for at least five years.

However, these were not randomized studies — meaning patients were not randomly picked to receive statins and then studied to see what effects the drugs had. Researchers consider randomized studies to yield the best evidence.

The colorectal cancer study was observational — the weakest sort of evidence — but very large. Researchers found no link between statin use and colorectal cancer when they looked at data on more than 132,000 people enrolled in the cancer prevention study.

In an accompanying editorial, John McLaughlin of the Prosserman Centre for Health Research in Toronto, wrote "... it remains premature to conclude that a large chemoprevention trial with statins that is aimed at reducing colorectal cancer risk is warranted."

White also believes it is time to stop spending money on more studies of cancer and statins.

However, Dr. Stephen Gruber of the University of Michigan, who led the Israeli study, said the new analysis is valuable but suggests that more research is needed.

"When you see contrasting conclusions like this, it's often an opportunity to learn more," Gruber said.
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PostPosted: Sat Jan 07, 2006 7:10 pm    Post subject: Soda-Cancer Link Revealed as Myth Reply with quote

Soda-Cancer Link Revealed as Myth
By LiveScience Staff
posted: 05 January 2006
09:32 am ET

Despite what many may have heard, drinking soda does not increase the risk of developing esophageal cancer. In fact it might protect against it, a new study finds.

Cases of cancer affecting the esophagus, the muscular tube linking the mouth and stomach, in the United States have more than tripled since the 1970s. And in the past 50 years, Americans have increased their annual consumption of carbonated soft drinks nearly five-fold, from 10.8 gallons in 1946 to a whopping 42.2 gallons in 2000.

The two trends are strongly correlated and in 2004, Indian researchers suggested they might be linked. But as any scientist will tell you, apparent correlations do not necessarily mean connections.

The idea of a link between drinking too much soda and developing cancer is rooted on biological logic, however. Carbonated soft drinks are known to cause gastric distension that might affect the lower part of the esophagus. They have also been associated with nighttime heartburn, a known risk factor for a type of esophageal cancer known as esophageal carcinoma.

The new study is the first to actually test the hypothesis.

Susan Mayne, a cancer epidemiologist at the Yale University School of medicine, and colleagues studied 1,095 cancer patients and compared them to 687 healthy control subjects. They conducted full dietary interviews and compiled data on how much regular and diet soda each subject drank.

The researchers found that soda drinkers were actually less likely to develop esophageal carcinoma. Furthermore, when the researchers separated subjects who drank mostly regular soda versus diet soda, they found that the latter group had a 53 percent lower risk of developing the cancer.

The researchers warned against chugging diet soda as a ward against cancer, however, since it carries its own health risks, such as damaging tooth enamel.

The study was detailed in the Jan. 4 issue of the Journal of the National Cancer Institute.
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PostPosted: Wed Jan 25, 2006 3:49 pm    Post subject: Lunasin natin ang cancer! Lunasin – anti cancer Reply with quote

Lunasin natin ang cancer! Lunasin – a novel cancer preventive substance from seeds
STAR SCIENCE By Ben O. De Lumen, Ph.D.
The Philippine STAR 01/26/2006

Lunasin (from Pilipino word lunas for cure) is a novel cancer preventive peptide (a small protein) that was first discovered in soy and now found in other seeds. Strictly speaking, lunas is not the proper word because lunasin has so far been found to be preventive not curative – but it sounds good anyway! Would iwasanin (from iwasan) be more appropriate? The serendipitous discovery of lunasin in our laboratory provides another explanation for the known anti-cancer properties of soy and other seed crops and opens up the opportunity to develop nutraceuticals and pharmaceuticals based on lunasin technology. It is not unusual that many profound discoveries were made serendipitously – without the intention of making the discoveries. Lunasin is such an example.

Many years ago, my laboratory initiated a project on enhancing the nutritional of soy protein and other legumes through bioengineering. This requires increasing the level of methionine, the essential amino acid, which is most limiting in soy and other legumes, including mung bean. The strategy is quite straightforward: clone a gene coding for methionine-rich protein (MRP) and over-express the gene in soy or any target legume. We were faced with two choices for the source of the MRP gene – obtain it from other plants or from soy itself. I made the fateful decision to clone the MRP gene from soy itself, which eventually led to the discovery of lunasin as a cancer preventive agent. Had I not made this decision, I would not be writing about lunasin now – but who knows? At that time, there were two other groups that made the other choice – one group (Pioneer Hybrid International Inc.) cloned the MRP gene from Brazil nut which has a high methionine content and over-expressed it in soy, and the other (Dr. T.J. Higgins at Division of Plant Industry, Canberra, Australia) chose to clone the MRP gene from sunflower seed and over-express it in lupine, a cover crop used to feed sheep in Australia. The Brazil nut MRP in transgenic soy turned out to be allergenic to humans and led to the termination of the project. The Australian project is successful, in fact resulting in increased yield of wool for sheep fed on the transgenic lupines.

The choice to clone the MRP gene from soy is based on the hypothesis that there must be non-abundant MRPs in soy because most of the proteins in soy seed are notoriously low in methionine and therefore, there must be other MRPs that contribute to the overall methionine content of soy protein but they are non-abundant. The process of cloning the MRP gene turned out to be not easy, taking about four years, two graduate students and a postdoctoral scientist. One of the graduate students is a Filipina (now Dr. Jamie Revilleza from UPLB), and the postdoctoral scientist is another Filipino from UPLB (Dr. Alfredo Galvez). Dr. Revilleza contributed to the purification of the MRP from soy that eventually led to the cloning of the gene, and Dr. Galvez took over the project and discovered the anti-mitotic effect of the lunasin gene when transfected into mammalian cells and the cancer preventive effect of the lunasin peptide. While it was not by design that the major contributors to lunasin discovery were both Filipinos, it is a source of pride to point this out.

Since its discovery in 1999, lunasin has been shown to be effective in preventing the transformation of normal cells to cancer cells caused by chemical carcinogens as well as cancer-causing agents from viruses such as the one known to cause cervical cancer in women. This is relevant to the Philippines, other Asian countries and other developing countries all over the world where cervical cancer is the most prevalent cancer among women. Indeed, there is a plan to conduct clinical trials on cervical cancer in the Philippines when the proper time comes.

In the first animal model, lunasin was found to prevent skin cancer in mice when applied topically. It is likely then that the first commercial application of lunasin would be in skin cancer or at least in the formulation of over-the-counter "cosmeceuticals" to maintain a healthy skin. Topical application to prevent cervical cancer is also a likely application in the immediate future.

Since lunasin is a small protein, it is expected to be digested when we eat soy. We now have evidence that lunasin is protected from digestion by naturally present protease inhibitors in soy and other seeds.

The way lunasin works still needs to be elucidated further. However, accumulated evidence points to a unique and novel "epigenetic" mechanism – lunasin selectively kills cells that are being attacked by carcinogenic agents while leaving other cells unharmed by interfering with the unfolding of the chromosome that is necessary for cell proliferation. This unique epigenetic mechanism lends scientific legitimacy to lunasin and makes it different from currently studied soy chemopreventive agents such as phenolics and isoflavones that function as antioxidants and phystoestrogens.

Lunasin may play a key and fascinating role during seed development. Seed development in angiosperm is characterized by three major stages. First, there is rapid cell division and differentiation; secondly, cell division stops and the cells enlarge, accompanied by synthesis of DNA, lipids, proteins and carbohydrates; and finally, the seed dries up. We believe that lunasin could be an effector molecule that allows the arrest of cell division to initiate the second stage. The hypothesis remains to be tested and proven.

Lunasin technology, because of its promise, is protected by numerous patents owned by the University of California at Berkeley, a necessary first step in its commercial development. Patents have been filed and granted in the US, Canada, Japan, European Union and other countries. A start-up biotech company, FilGen BioSciences Inc., has been formed and granted a license to commercialize lunasin. It is noteworthy that the initial investors in the company are Filipino-Americans.

Lunasin’s story is a fascinating one and continues to be so. Its discovery is serendipitous, its applications myriad, and its mechanism of action novel. * * *
Ben O. de Lumen, Ph.D., is a professor at the Department of Nutritional Sciences and Toxicology, University of California at Berkeley, CA. He is a member of the Philippine Academy of Science and Engineering. E-mail him at nitto@nature.berkeley.edu.
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PostPosted: Thu Feb 16, 2006 8:08 am    Post subject: Antioxidant Supplementation and Prostate Cancer Reply with quote

Source: Journal of the National Cancer Institute

Posted: February 15, 2006

Antioxidant Supplementation Not Associated With Decreased Risk Of Prostate Cancer

Intakes of dietary or supplemental antioxidants were not associated with a decreased risk of prostate cancer among men in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, according to a study in the February 15 issue of the Journal of the National Cancer Institute . The study did find that vitamin E and beta-carotene supplementation may be associated with reduced prostate cancer risk in certain population subgroups.

Research suggests that micronutrients such as vitamin E, vitamin C, and carotenoids may play a role in preventing cancer development because of their ability to combat free radicals, agents that can damage cellular DNA, lipid membranes, and proteins. In many studies, vitamin E has been associated with a reduced risk of prostate cancer, and beta-carotene has been associated with increased lung cancer risk in previous studies. However, no studies have examined associations between intakes of these three antioxidant micronutrients and the risk of prostate cancer.

Richard B. Hayes, Ph.D., at the National Cancer Institute, and colleagues assessed the risk of prostate cancer for 29,361 men ages 55 to 74 enrolled in the PLCO Cancer Screening Trial, based on their daily intake of beta-carotene, vitamin E, and vitamin C. The researchers looked at intake of antioxidants from both dietary sources and from supplements.

The authors found that, overall, dietary or supplemental intake of vitamin E, vitamin C, or beta-carotene was not associated with prostate cancer incidence in this group of PLCO trial participants. However, certain micronutrients were associated with prostate cancer risk in specific subgroups of men. For current or recent smokers, high-dose, long-duration vitamin E supplementation was associated with a reduced risk of advanced prostate cancer. For men with a low dietary intake of beta-carotene, high-dose supplements of beta-carotene were associated with a reduced risk of prostate cancer.

"Our cohort findings, although based on relatively short follow-up, do not provide strong support for population-wide implementation of high-dose antioxidant supplementation for the prevention of prostate cancer," the authors write. "They do suggest, however, that in certain population subgroups there was an association between supplement intake and reduced risks of prostate cancer."

In an accompanying editorial, I-Min Lee, Sc.D., of Brigham and Women's Hospital in Boston, Mass., and colleagues discuss the implications of Hayes and colleagues' study in the context of earlier studies of vitamin E supplementation and cancer risk. The editorialists agree that the study results do not provide strong support for the implementation of antioxidant supplementation for the prevention of prostate cancer. They note that the data remain unclear about the benefits of vitamin E supplementation for prostate cancer prevention in the general population; however, there are strong data supporting smoking cessation to reduce cancer incidence. The authors write, "Now and in the future, regardless of the eventual findings on vitamin E supplementation and prostate cancer risk, an important course of action for overall cancer prevention is to continue efforts to prevent the initiation of smoking and to promote the cessation of smoking among those who do smoke."

###
Citations:
Article: Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, et al. Supplemental and Dietary Vitamin E, Beta-Carotene, and Vitamin C Intakes and Prostate Cancer Risk. J Natl Cancer Inst 2006;98:245-254.
Editorial: Lee I-M, Gaziano JM, Buring JE. Vitamin E in the Prevention of Prostate Cancer: Where Are We Today? J Natl Cancer Inst 2006;98:225-227

Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oxfordjournals.org/
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PostPosted: Wed Mar 15, 2006 6:29 am    Post subject: Pepper component hot enough to kill prostate cancer cells Reply with quote

American Association for Cancer Research
15 March 2006

Pepper component hot enough to trigger suicide in prostate cancer cells

Capsaicin, the stuff that turns up the heat in jalapeños, not only causes the tongue to burn, it also drives prostate cancer cells to kill themselves, according to studies published in the March 15 issue of Cancer Research.
According to a team of researchers from the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center, in collaboration with colleagues from UCLA, the pepper component caused human prostate cancer cells to undergo programmed cell death or apoptosis.

Capsaicin induced approximately 80 percent of prostate cancer cells growing in mice to follow the molecular pathways leading to apoptosis. Prostate cancer tumors treated with capsaicin were about one-fifth the size of tumors in non-treated mice.

"Capsaicin had a profound anti-proliferative effect on human prostate cancer cells in culture," said Sören Lehmann, M.D., Ph.D., visiting scientist at the Cedars-Sinai Medical Center and the UCLA School of Medicine. "It also dramatically slowed the development of prostate tumors formed by those human cell lines grown in mouse models."

Lehmann estimated that the dose of pepper extract fed orally to the mice was equivalent to giving 400 milligrams of capsaicin three times a week to a 200 pound man, roughly equivalent to between three and eight fresh habañera peppers – depending on the pepper's capsaicin content. Habañeras are the highest rated pepper for capsaicin content according to the Scoville heat index. Habañero peppers, which are native to the Yucatan, typically contain up to 300,000 Scoville units. The more popular Jalapeño variety from Oaxaca, Mexico, and the southwest United States, contains 2,500 to 5,000 Scoville units.

As described in their study, the scientists observed that capsaicin inhibited the activity of NF-kappa Beta, a molecular mechanism that participates in the pathways leading to apoptosis in many cell types.

Apoptosis is a normal cellular event in many tissues that maintains a balance between newer replacement cells and aged or worn cells. In contrast, cancer cells seek to be immortal and often dodge apoptosis by mutating or deregulating the genes that participate in programmed cell death.

"When we noticed that capsaicin affected NF-kappa Beta, that was an indication that we might expect some of the apoptotic proteins to be affected," said the study's senior author, Phillip Koeffler, M.D., director of Hematology and Oncology, Cedars-Sinai Medical Center, and professor at UCLA.

The pepper extract also curbed the growth of prostate cancer cells through regulation of androgen receptors, the steroid activated proteins that control expression of specific growth relating genes.

In prostate cancer cells whose growth is dependent on testosterone, the predominant male sex steroid, capsaicin reduced cell proliferation in a dose-dependent manner. Increased concentrations of capsaicin caused more prostate cancer cells to freeze in a non-proliferative state, called G0/G1.

Prostate cancer cells that are androgen independent reacted to capsaicin in a similar manner. Capsaicin reduced the amount of androgen receptor that the tumor cells produced, but did not interfere with normal movement of androgen receptor into the nucleus of the cancer cells where the steroid receptor acts to regulate androgen target genes such as prostate specific antigen (PSA). Capsaicin also interfered with the action of androgen receptors even in cells that were modified to produce excess numbers of androgen receptors.

The hot pepper component also reduced cancer cell production of PSA, a protein that often is produced in high quantities by prostate tumors and can signal the presence of prostate cancer in men. PSA content in the blood of men is used as a diagnostic prostate cancer screening measure. PSA is regulated by androgens, and capsaicin limited androgen-induced increases of PSA in the cancer cell lines.

More men in the United States develop prostate cancer than any other type of malignancy. Every year, more than 232,000 new cases of prostate cancer are diagnosed in the U.S., and more than 680,000 develop the disease worldwide. Approximately 30,000 men die from prostate cancer in the U.S. each year, which is about 13 percent of all new cases. Worldwide, there are 221,000 deaths – approximately 31 per cent – among men with prostate cancer.


###
Lehman conducted the studies in Koeffler's laboratory in collaboration with UCLA cancer researchers Akio Mori, James O'Kelly, Takishi Kumagai, Julian Desmond, Milena Pervan, and William McBride. Mosahiro Kizaki, a former post-doctoral fellow in Koeffler's laboratory who initiated the capsaicin studies, is currently at the Keio University School of Medicine, Tokyo, Japan.

Founded in 1907, the American Association for Cancer Research is a professional society of more than 24,000 laboratory, translational, and clinical scientists engaged in all areas of cancer research in the United States and in more than 60 other countries. AACR's mission is to accelerate the prevention and cure of cancer through research, education, communication, and advocacy. Its principal activities include the publication of five major peer-reviewed scientific journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. AACR's Annual Meetings attract nearly 16,000 participants who share new and significant discoveries in the cancer field. Specialty meetings, held throughout the year, focus on the latest developments in all areas of cancer research.
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PostPosted: Sat Mar 18, 2006 2:57 pm    Post subject: Anticancer Properties Of Vitamin D Reply with quote

Source: Georgetown University Medical Center

Posted: March 18, 2006

Researchers Reveal Possibility Of Separating Anticancer Properties Of Vitamin D

At the right dose, vitamin D is important for bone development and may help protect against the development of several cancers, particularly colorectal cancer. However, large quantities designed to exploit the vitamin’s anticancer properties can lead to a toxic overdose of calcium in the blood. Now, research done at Georgetown University’s Lombardi Comprehensive Cancer Center indicates that it may be possible to separate the anticancer properties of vitamin D from its other functions.

Their study, reported in the journal Molecular Cell, found that mutant forms of the protein that binds to vitamin D in the cell do not allow vitamin D to promote bone development and calcium transport but do permit it to regulate an oncogenic protein known as beta catenin. Some modified forms of vitamin D itself, which do not alter bone and calcium, were also found to regulate beta-catenin.

“We found that we might be able to separate the two functions at the molecular level, and this raises the possibility that vitamin D can be chemically modified into a drug that will only have anticancer effects,” said Professor Stephen Byers, Ph.D. He and Salimuddin Shah, Ph.D., led an international group of investigators in this study.

The human body produces a lot of vitamin D from a brief exposure of the sun. The vitamin is made in the skin when a cholesterol-like molecule interacts with ultraviolet light. It has long been known that a lack of vitamin D can lead to the bone deformities associated with rickets, and the vitamin helps maintain calcium and phosphorous levels in bone and blood. Too much vitamin D, however, can spill calcium into the blood and lead to heart disease and death.

Population studies have also uncovered an interesting fact — that the risk of developing colon cancer is lower in people who live in sunny climates. Epidemiology studies have indicated that vitamin D is responsible for the protective effect of sunlight exposure on the incidence of several other cancers besides colon, including breast and prostate.

Byers and the research team suspected that beta catenin may interact with vitamin D in some fashion because of another known fact — activation of beta catenin causes most colon cancers.

To help them understand what vitamin D is doing in the cell, the researchers studied findings by other scientists who had looked at families who develop rickets due to an inherited mutation in their vitamin D receptor. Most of these patients had both rickets and alopecia (baldness). However a small number of families had mutations in the receptor which only led to rickets. “We know beta catenin is also involved in regulation of hair growth and we wondered if these particular mutations might also allow the receptor to regulate beta catenin,” Byers said.

“We found a mutation which caused rickets but not alopecia but which still allowed beta catenin to bind to the vitamin D receptor,” he said. This suggested to the researchers that it may be possible to separate the anti-cancer role of vitamin D from its effects on bone and calcium.

If a drug mimic of vitamin D can be developed, it could prove useful in preventing some cancers at their earliest stages, but would probably not offer any therapeutic benefit for later stage cancers, Byers said. “That’s because we know that by the time colon cancer is well advanced it fails to respond to vitamin D.”

About Georgetown University Medical Center
Georgetown University Medical Center is an internationally recognized academic medical center with a three-part mission of research, teaching and patient care (through our partnership with MedStar Health). Our mission is carried out with a strong emphasis on public service and a dedication to the Catholic, Jesuit principle of cura personalis—or “care of the whole person.” The Medical Center includes the School of Medicine and the School of Nursing and Health Studies, both nationally ranked, and the world renowned Lombardi Comprehensive Cancer Center.
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PostPosted: Mon Mar 27, 2006 7:01 am    Post subject: Evolutionary biology research techniques predict cancer Reply with quote

The Wistar Institute
26 March 2006

Evolutionary biology research techniques predict cancer

In diverse ecosystems, packed with wildly different species, evolution whizzes along. As different species accumulate mutations, some adapt particularly well to their environment and prosper. It happens in marine sediments, mountain forests – and, as a new study illustrates, in precancerous tumors, too.
In a study published online today in Nature Genetics, Carlo Maley, Ph.D., a researcher at The Wistar Institute, and his colleagues report that precancerous tumors containing a population of highly diverse cells were more likely to evolve into cancer than those containing genetically similar cells. The finding suggests that, in at least some forms of cancer, the more genetically diverse a precancerous tumor is, the more likely that tumor is to progress to full-blown cancer. If so, genetic diversity might act as a biomarker for cancer risk among patients with precancerous tissues.

"Although researchers first defined cancer in evolutionary terms in the 1970s, few researchers have actually studied the disease this way," says Maley, lead author on the study and an assistant professor in the molecular and cellular oncogenesis program at Wistar. "We wanted to know: If we measured a precancerous tumor's genetic diversity at baseline, could we predict who would go on to get cancer?"

To find out, the scientists decided to analyze data on a precancerous condition called Barrett's esophagus, in which cells lining the lower esophagus change due to repeated exposure to stomach acid from reflux, a condition often referred to as heartburn. Doctors typically adopt a "wait and watch" approach to treating patients with Barrett's esophagus because the condition only rarely leads to cancer and is difficult to treat surgically.

In the study, Maley and colleagues analyzed precancerous tumor data from 268 patients, including multiple biopsies within each tumor. On average, these patients were followed for 4.4 years, during which time 37 developed cancerous tumors. Overall, the database used in the study represents more than 32,000 distinct genotypes of different cells within the tumors.

Using computational techniques to analyze the data, the researchers calculated measures of diversity inside the tumors. Essentially, they counted cell varieties and measured the genetic difference, or divergence, between those varieties. "Simply put, we took ecology measures of species diversity and translated them into measures of cell diversity within tumors," Maley says. The found a striking correlation between increased diversity of tumor cells and progression to cancer. For every additional cell variety detected in a tumor, the patient was twice as likely to progress to cancer.

Maley suggests that genetically diverse tumors have a high probability of generating mutant cells that will flourish and spread, allowing the tumor to transform and grow. In the future, in addition to serving as a biomarker for cancer risk, he adds, measures of genetic diversity might help doctors assess the success of cancer prevention therapies.

In fact, he speculates, genetic diversity among tumor cells might help explain why therapy sometimes fails. If a tumor contains a diverse population of cells, some of those cells are more likely to resist treatment, Maley says. Adapting to and surviving chemotherapy, these resistant cells could breed, leading to a cancer relapse. He hopes to pursue this hypothesis in the future. "More immediately," he adds, "we intend to validate the new study with other cohorts and other types of tumors."


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Maley is lead author on the study, which was initiated when he was a staff scientist at Fred Hutchinson Cancer Research Center in Seattle, prior to his arrival at Wistar. The additional coauthors are Patricia C. Galipeau, Xiaohong Li, Carissa A. Sanchez, Thomas G. Paulson, Patricia L. Blount, Peter S. Rabinovitch and Brian J. Reid, all at Fred Hutchinson Cancer Research Center, and Jennifer C. Finley, V. Jon Wongsurawat, and Rosa-Ana Risques at the University of Washington. Blount, Rabinovitch, and Reid also have appointments at the University of Washington.

Support for the research was provided by the National Institutes of Health and the Commonwealth Universal Research Enhancement Program of the Pennsylvania Department of Health. Support for Maley's ongoing research is also being provided by the McLean Contributionship.

The Wistar Institute is an independent nonprofit biomedical research institution dedicated to discovering the causes and cures for major diseases, including cancer, cardiovascular disease, autoimmune disorders, and infectious diseases, including AIDS and influenza. Founded in 1892 as the first institution of its kind in the nation, The Wistar Institute today is a National Cancer Institute-designated Cancer Center focused on basic and translational research. Discoveries at Wistar have led to the creation of vaccines for such diseases as rabies, rubella, and rotavirus; significant insights into the mechanisms of skin, brain, breast, lung, and prostate cancers; and the development of monoclonal antibodies and other significant research technologies and tools. News releases from The Wistar Institute are available to reporters by direct e-mail upon request.
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PostPosted: Mon Mar 27, 2006 7:02 am    Post subject: 'Custom' nanoparticles could improve cancer diagnosis and tr Reply with quote

American Chemical Society
26 March 2006

'Custom' nanoparticles could improve cancer diagnosis and treatment
ATLANTA, March 26 — Researchers have developed "custom" nanoparticles that show promise of providing a more targeted and effective delivery of anticancer drugs than conventional medications or any of the earlier attempts to fight cancer with nanoparticles. Designed at the molecular level to attack specific types of cancer without affecting healthy cells, the nanoparticles also have the potential to reduce side effects associated with chemotherapy, the researchers say. Their study was described today at the 231st national meeting of the American Chemical Society, the world’s largest scientific society.

The particles, considered the next generation of cancer therapeutics, are the most uniform, shape-specific drug delivery particles developed to date, according to researchers at the University of North Carolina (UNC) in Chapel Hill. Other potential benefits of the tiny uniform particles include enhanced imaging of cancer cells for improved diagnosis and use as delivery vehicles for gene therapy agents, they say.

To date, the UNC researchers have produced a variety of custom nanoparticles from biocompatible organic materials using techniques they adapted from processes used by the electronics industry to make transistors. In cell studies, they have shown that the uniform nanoparticles can attach to specific cell targets, release important chemotherapy drugs inside cells, and hold MRI contrast agents. Animal studies began recently and human studies are anticipated, the researchers say.

"I think this will transform the way one detects and treats disease," says study leader Joseph DeSimone, Ph.D., a chemistry professor at UNC and director of the school’s Institute for Advanced Materials, Nanoscience and Technology. He has co-founded a company, Liquidia Technologies, to develop and produce the nanoparticles.

Researchers have been experimenting with nanoparticles as drug delivery vehicles for years but have had only limited success in cell and animal studies, DeSimone says. Each carrier has drawbacks with regard to stability in the bloodstream or ability to be directed toward a specific cancer site. In addition, there has been no general method available that allows precise control of the particle’s size, shape and composition, which are considered key features for the success of targeted drug delivery, he says.

Now, DeSimone and his associates at UNC have developed a new fabrication technique that allows, for the first time, unprecedented control over the structure and function of drug delivery nanoparticles. Called PRINT (Particle Replication In Non-wetting Templates), the technique is similar to injection molding and uses principles borrowed from the electronics industry for transistor fabrication, they say. The technique was first detailed last June in the online version of the Journal of the American Chemical Society.

The manufacturing process starts with a silicon wafer that is etched with the shape and size of the desired nanoparticle, resulting in a template. Next, nonstick liquid fluoropolymers are poured into the template and cured to form a fixed mold. The finished mold is then injected with organic materials that can contain imaging agents, anticancer drugs, DNA (for gene therapy) and other materials, depending on the intended function, DeSimone says. The new manufacturing technique uses gentler processing methods that are less likely to harm important organic components than traditional nanoparticle manufacturing techniques, he adds.

The resulting nanoparticles can be as small as 20 nanometers, or thousands of times smaller than the width of a single human hair. The shapes of the particles can also be made to mimic the shapes of objects found in nature like red blood cells or virus particles, DeSimone says.

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Funding for the current study is provided by the National Science Foundation and the National Institutes of Health.

The American Chemical Society — the world’s largest scientific society — is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

The paper on this research, COLL 9, will be presented at 11:35 a.m., Sunday, March 26, OMNI at CNN Center, International Ballroom E, during the symposium "Biomolecular and Polymeric Nanostructures and Interfaces: Fabrication, Characterization, Function, and Applications."

Joseph M DeSimone, Ph.D., is the William R. Kenan, Jr., Distinguished Professor of Chemistry and Chemical Engineering at the University of North Carolina, Chapel Hill.
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PostPosted: Fri Apr 07, 2006 10:59 am    Post subject: Cancerous vs. healthy cells Reply with quote

American Association for Cancer Research 97th Annual Meeting
7 April 2006

Cancerous vs. healthy cells: Researchers identify the road to success
Studies determine best route for targeted therapies


WASHINGTON, D.C. − Conventional cancer treatments are generally effective in wiping out tumor cells, but in the process they also may kill healthy cells. Researchers are focusing their efforts now on treatments that can target just the cancerous cells, without harming healthy tissue in their midst. These new types of drugs are known as targeted therapies, and physicians are studying their effectiveness and possible side effects in a variety of different types of cancer.
Several targeted therapies are being studied alone and in combination to treat a variety of cancer types. In particular, cancerous brain tumors can be more difficult to treat than other cancers, and oncologists are developing therapies that target these cells to improve patients' survival. Researchers also are gaining a better understanding of the molecular differences between cancerous and healthy cells, improving current treatment and survival rates, according to studies presented today at the 97th Annual Meeting of the American Association for Cancer Research.

NF-kB as a Therapeutic Target in Malignant Gliomas: Abstract No. 1506

Researchers from the National Cancer Institute in Bethesda, Md., have found they may be able to successfully treat brain tumor cells with a new targeted therapy that inhibits the activity of a cell protein called nuclear factor-Kappa B (NF-kB).

The drug, called bortezomib or (Velcade®) – when used alone or in combination with other cancer treatments – represents a potential new way to treat malignant glioma, a particularly stubborn and aggressive brain tumor.

"Targeting the NF-kB pathway either alone or in combination with other chemotherapy agents, is an effective anti-glioma treatment," said Ai-Min Hui, M.D., Ph.D., research fellow at the NCI and the lead investigator of the study.

In their study, the NCI researchers set out to determine the role of NF-kB in reversing the apoptotic (or programmed cell death) effect of selective estrogen receptor modulators (SERMs) in brain cancer, as well as potential therapies that can be used either alone or in combination to block the protein. High levels of NF-kB are activated and present in transplanted glioma cells and glioma tumor samples, but not in normal brain tissue cells.

SERMs have shown some value in inducing cell death in brain cancers by a previously unknown method. They are designed to deliver the benefits of estrogen without its negative side effects, although gliomas do not generally express the estrogen receptor. However, previous studies have shown that NF-kB protects glioma cells from breaking down, therefore reversing the effect of SERM therapies.

Researchers looked at 203 glioma samples and determined that NF-B was activated. They also noticed that the level of activation was related to the grade of the tumor, suggesting that NF-B is related to tumor progression. Treatment with bortezomib suppressed both unregulated and signal-oriented activation in NF-kB by inhibiting the breakdown of IkB-alpha. IkB-alpha is one of a series of inhibitory proteins that controls the activation of NF-kB, preventing it from binding to DNA in the nucleus. Bortezomib not only stops the degradation of IkB-alpha, it also suppresses the activation of NF-kB, thus stopping cell growth.

"By interfering with the function of IkB-alpha proteins, bortezomib was shown to induce glioma cell degradation and enhance anti-cancer effects of SERMs," said Ai-Min Hui, M.D., Ph.D., research fellow at the National Cancer Institute and lead investigator on this trial.

"New studies looking at the combined use of bortezomib and high-dose tamoxifen may provide a viable treatment option for patients with recurrent, high grade malignant gliomas," he said.

Malignant gliomas are one of the most common brain tumors, accounting for more than half of the 18,000 primary cancerous brain tumors diagnosed annually in the United States, and are the fourth most common cause of cancer death in patients aged 15 to 44.

Standard treatment for patients diagnosed with brain cancer is surgery followed by radiation, sometimes with added chemotherapy. However, current therapies are considered inadequate to fight this deadly disease and researchers have been trying to identify new targets and develop new agents with different mechanisms of action to help increase patients' survival.

PTEN-Loss Mediated Herceptin (trastuzumab) Resistance and Targeting the PI3K Pathway as a Counteracting Strategy: Abstract No. IS-445

Researchers from The University of Texas M. D. Anderson Cancer Center, Houston, have identified why some women with Her-2 positive breast cancer, an aggressive form of the disease, do not respond to the drug trastuzumab (Herceptin®) or may actually develop a resistance to the treatment.

The investigators discovered that a combination of trastuzumab and a new kinase inhibitor, PI3K, may work together to increase these patients' chances of survival.

Trastuzumab treats women with metastatic breast cancer whose tumors overproduce the ErbB2 gene. The overproduction of the ErbB2 gene, also called Her-2/neu, leads to aggressive breast cancer and poorer patient survival. ErbB2 is part of a family of genes called epidermal growth factor receptors (EGFR) that stimulate cell growth and division. Trastuzumab has shown outstanding efficacy for patients with high levels of the ErbB2 gene.

Approximately one-third of patients who possess the ErbB2 gene will respond to trastuzumab therapy, but the treatment is sometimes combined with other chemotherapy agents to make it more effective.

Still other patients develop resistance to the therapy over time.

In this study, researchers found that loss of PTEN can lead to resistance of trastuzumab. The PTEN gene (phosphatase and tensin homolog deleted on chromosome ten) acts as a tumor suppressor gene, helping to regulate the cycle of cell division by keeping cells from growing and dividing uncontrollably or too rapidly, and ultimately forming tumors. Normally, the PTEN enzyme acts as part of a chemical pathway that signals cells to stop dividing and causes cells to undergo apoptosis.

However, reduced levels of PTEN contribute to trastuzumab resistance, both in vivo (humans and mice) and in vitro (culture). Patients with PTEN-deficient breast cancer have poorer outcomes and response to trastuzumab therapy when compared to those with normal PTEN levels.

The researchers then examined the role played by phosphoinositide 3-kinase (PI3K) pathway inhibitors to reverse PTEN-reduction-mediated trastuzumab resistance. PI3K regulates several key signals that initiate cell processes frequently disrupted by carcinogenesis, a process by which normal cells are transformed into cancer cells.

Seven PI3K pathway inhibitors, either currently in use or under development in clinical trials, were examined. One inhibitor used in combination with trastuzumab successfully inhibited cell growth, and a second, when used with trastuzumab, sensitized the therapeutic effects of the drug. Researchers said the next step is to conduct a phase I/II study looking at these combinations in patients who did not respond to traztuzumab as a first-line therapy.

"PTEN seems to be a very sensitive and specific predictor to trastuzumab-based therapy and data suggest that activation of PTEN is a novel mechanism underlying the anti-tumor activity of trastuzumab.

Combination therapy may provide more effective therapeutic regimens, allowing more patients to benefit from trastuzumab," said Dihua Yu, M.D., Ph.D., professor in the department of surgical oncology and director of research in the Surgery Division, The University of Texas M. D. Anderson Cancer Center.

A Novel, Potent and Selective IGF-1R Small Molecule Inhibitor Blocks Activation of IGF-1R Signaling in Vitro and Inhibits IGF-1R Dependent Tumor Growth in Vivo: Abstract No. LB-281

Researchers from OSI
Pharmaceuticals have identified a new small molecule inhibitor that may stop the growth of colon cancer. In this study, investigators discovered and tested an IGF-1R inhibitor, referred to as Compound 1.*

Compound 1 was shown to hinder the signaling response of IGF-1R -- specifically blocking the activation of two downstream pathways, stopping tumor cell growth and survival. The study also showed that the colon cancer tumors respond to the drug because they produce and are dependent on the growth-promoting effects of IGF-II.

"We are very encouraged by the results seen in our pre-clinical IGF-1R inhibitor program. The most important finding of our study was that, when administered orally, our IGF-1R inhibitor prevented the growth of human colon cancer tumors in mice," said Jonathan A. Pachter, Ph.D., senior director of cancer biology, OSI Pharmaceuticals, Long Island, N.Y. Insulin-like growth factor 1 receptor (IGF-1R) is a cellular protein with a molecular structure similar to that of the receptor for insulin, a hormone that regulates the amount of glucose sugar in the blood. The IGF-1R has been shown to play roles in tumor cell growth and the inhibition of cell death. There are two circulating proteins (or ligands) that activate the IGF-1R (IGF-I and IGF-II). The excess production of IGF-II is thought to encourage tumor growth.

Certain tumors, including colorectal, non-small cell lung, ovarian and some cancers in children, drive their own growth and survival through the overproduction of IGF-II. This IGF-II activates the IGF-1R on the surface of cancer cells to stimulate tumor growth, making IGF-1R an important treatment target for many human cancers.

"This small molecule represents a potent and selective IGF-1R kinase inhibitor that could be effective in the treatment of IGF-II driven human cancers," said Dr. Pachter.

A variety of approaches to block IGF-1R signaling have been used to cause cell death in a broad range of cancers, both in cell cultures and live models. Through the use of structure-based design, OSI Pharmaceuticals has been able to identify small molecules that selectively block the ability of IGF-1R to increase cell growth.

Another major challenge in the development of IGF-1R inhibitors is to avoid blocking the closely related insulin receptor that regulates glucose levels in the blood. Results from the study showed that in addition to diminishing or halting tumor growth in human cancer cells transferred to live test animals, OSI's IGF-1R inhibitor showed no substantial rise in blood sugar.


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* Compound 1's formal name is: cis-3-[3-(4-methyl-piperazin-1-yl)-cyclobutyl]-1-(2-phenyl-quinolin-7-yl)-imidazo[1,5-a]pyrazin-8-ylamine.

The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes more than 24,000 basic, translational, and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 60 other countries. AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants. The AACR Annual Meeting attracts over 16,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment, and patient care. AACR publishes five major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. Its most recent publication, CR, is a magazine for cancer survivors, patient advocates, their families, physicians, and scientists. It provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship, and advocacy.
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PostPosted: Sun Apr 09, 2006 10:43 am    Post subject: Vitamin D And Flavonoids Examined For Impact On Breast And O Reply with quote

Source: American Association for Cancer Research

Posted: April 7, 2006

Vitamin D And Flavonoids Examined For Impact On Breast And Ovarian Cancers
While risk factors for breast and ovarian cancers include menopause, obesity, family history and specific genetic mutations, researchers also are looking at the role of diet in the development, as well as the treatment and prevention of these tumors. At the 97th Annual Meeting of the American Association for Cancer Research, two groups of scientists using sophisticated statistical techniques report their findings of possible preventive properties of Vitamin D against breast cancer. Two other groups of scientists present their work analyzing the possibility that natural antioxidants found in plants, substances called flavonoids, could play a powerful role in preventing both breast and ovarian cancer.

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Potential Reduction in Breast Cancer Risk Associated with Vitamin D: Abstract No. 4009

Though scientists have suspected that Vitamin D helps to prevent and possibly even treat breast cancer, population-based studies on the possible link have been few and of limited scope.

Now, new studies by researchers at the Samuel Lunenfeld Research Institute at Mount Sinai Hospital in Toronto suggest the "sunshine" vitamin may play a significant role in reducing breast cancer risk. The results, based on population data, found the reduction was most apparent among subjects exposed to the highest levels of vitamin D when they were young.

By interviewing about 576 patients who had been diagnosed with breast cancer and 1,135 people who had no cancer, the scientists discovered that significant reductions in breast cancer were found in those who had either worked in an outdoor job, had taken part in outdoor activities when young, or consumed cod liver oil or milk.

Working an outdoor job between ages 10 to19 resulted in an estimated 40 percent reduced risk of breast cancer, while frequent outdoor activities between ages 10 to 29 lowered breast cancer risk by an estimated 35 percent.

"These outdoor activities included those that didn't involve physical activity," said Julie Knight, who headed the Mount Sinai research team. "And so we believe that this is evidence of a reduction of breast cancer risk, associated with earlier exposure to the sun."

For dietary influences on cancer development, taking cod liver oil between ages 10 to 19 reduced breast cancer risk by about 25 percent, and consuming at least nine glasses of milk every week between the ages of 10 to 29 reduced the risk by 35 percent. The dietary and lifestyle reductions were significant, even when adjusted for other risk factors for breast cancer such as age, ethnicity, close relatives with breast cancer, age at menarche and age at a woman's first birth.

"What you are exposed to during breast development may be particularly important in determining future breast cancer risk," Knight said. "Current thinking is that exposures during adolescence or before a full-term pregnancy may have a greater effect, as that is when breast tissue is going through the most rapid development."

Knight emphasizes that these findings are preliminary estimates of the risk reduction of breast cancer brought about by Vitamin D. The researchers are now looking to solidify these findings, and determine whether physical exercise while outdoors is in any way associated with breast cancer.

Evidence of Need for Increased Vitamin D Fortification of Food Based on Pooled Analysis of Studies of Serum 25-hydroxyvitamin D and Breast cancer: Abstract No. 4008

Increasing doses of dietary Vitamin D may help prevent breast cancer, with the optimal level of intake of Vitamin D more that three times the current average for Americans, according to a study conducted at the University of California, San Diego.

Previous studies have suggested a link between Vitamin D deficiency and higher incidence of breast cancer. Cedric Garland, Dr. P.H., and Edward Gorham, Ph.D., of UCSD, and their colleagues examined existing cancer studies to determine if higher Vitamin D levels in the blood could reduce the risk of cancer.

"There is a strong inverse dose-response relationship between the serum concentration of 25-hydroxyvitamin D and the risk of breast cancer," Garland said. "It's a close fit to a linear model," meaning that higher amounts of 25-hydroxyvitamin D in the serum resulted in decreased risk of breast cancer. The evidence further pointed to a level of Vitamin D measured in blood that correlated with a 50 percent reduction in the incidence of breast cancer.

Garland, Gorham and their colleagues studied a serum Vitamin D metabolite known as 25 hydroxyvitamin D and its association with breast cancer occurrence in a pooled study that included 1,760 women. The studies that provided the data for the pooled analysis were conducted by Elizabeth R. Bertone-Johnson and colleagues at Harvard, and L.C. Lowe and associates at Saint George's Hospital Medical School in London.

According to the pooled analysis, Vitamin D in blood serum equal to 52 nanograms per milliliter was associated with a 50 percent reduced risk of breast cancer. To move closer to a serum concentration of 52 nanograms/milliliter, a typical individual would have to consume no less than 1,000 International Units (IU) of Vitamin D every day, through supplements or vitamin D-fortified foods. Currently, a typical American consumes only 320 International Units of Vitamin D a day. The upper limit for vitamin D intake established by the National Academy of Sciences is 2,400 IU/day, but no toxic effects of vitamin D intake have been reported for intakes below 3,800 IU per day.

"There is no substantial downside to a serum level of 52 nanograms per milliliter of Vitamin D," said Gorham. "Such levels are common in sunny climates. There is no known adverse effect of serum levels below 160 nanograms per milliliter."

However, since many people use sunscreens and are involved in indoor occupations or shift work, dietary supplements and vitamin D fortified foods are necessary to maintain optimal levels of Vitamin D, the scientists noted.

High intakes of calcium, which could occur with intake of Vitamin D supplements containing calcium, could increase the risk of kidney stones, they warn. However, the dosage level of vitamin D associated with kidney stones in patients far exceeded 3,800 IU/day. Until more studies are completed, the scientists recommended that everyone consume at least 1,000 IU/day of vitamin D3.

Dietary Flavonoid Intake and Breast Cancer Risk among Women in the Long Island Breast Cancer Study Project: Abstract No. 4014

Flavonoids, a class of antioxidants found in plants, is associated with a reduced risk of breast cancer among post-menopausal women, according to results of the Long Island breast cancer study project. The results are one of the first epidemiologic studies to suggest that these compounds could have a chemoprotective effect among women.

Brian Fink, Susan Steck and Marilie Gammon of the University of North Carolina, Chapel Hill, and other colleagues studied data from a large study of breast cancer incidence and risk factors conducted among women living during the mid-1990s on Long Island, N.Y.

Breast cancer risk was reduced for the highest percentages of total flavonoid intake, compared to the lowest intake of the plant antioxidants. The decreased risk was about 45 percent among post-menopausal women. Risk decreases were not seen in pre-menopausal women. Specific flavonoids -- including flavones, flavan-3-ols and lignans -- were associated with reduced cancer risks ranging from 26 to 39 percent; other flavonoids, such as flavanones, isoflavones and anthocyanidins, showed no relationship with reduced cancer risk.

"These results are consistent with other studies conducted among Mediterranean women," said Fink. "Few epidemiologic studies have examined whether there is a relationship between breast cancer and dietary flavonoids. Our study proposes that dietary flavonoids can help American post-menopausal women reduce their risk of breast cancer."

The researchers examined data from the Long Island study, which was conducted by Dr. Gammon and colleagues between August 1996 and July 1997. The team compared data from 1,434 women with breast cancer to data from 1,440 women who were not diagnosed with the disease.

Flavonols, flavones, lignans and anthocyanidins are all flavonoids, molecules that give plants protection from oxidative damage due to disease and environmental stresses. Flavonoids are classified according to chemical structure, and have been studied for their varying degrees of effectiveness against human diseases, both in treatment and prevention. They are found in green tea, red wine, soybeans, fruit and vegetables.

"There are no recommended dietary standards for ingestion of flavonoids, and we do not know exactly how these chemicals may work on a cellular level," said Fink, whose work was supported with funding from the National Institutes of Health and the Lance Armstrong Foundation. "Minute differences in chemical structure could determine how a certain natural antioxidant may work to prevent disease, including cancer. More study is needed to determine why certain flavonoids appear to be effective at reducing cancer risk, and others do not appear to have these properties."

A Prospective Analysis of Dietary Flavonoid Intake and Epithelial Ovarian Cancer Incidence: Abstract No. 4013

The incidence of ovarian cancer may be reduced with increased consumption of dietary flavonoids, plant chemicals that are found in tea, red wine, fruits and vegetables, according to researchers from Brigham and Women's Hospital and the Harvard School of Public Health.

The study, conducted by Margaret Gates, a doctoral candidate at the Harvard School of Public Health, looked at food intake surveys and ovarian cancer data from 66,384 participants in the Harvard Nurses' Health Study, which collected health data from 121,700 women over a period of 30 years. "This is the first prospective analysis of flavonoid intake and ovarian cancer incidence," Gates said.

Gates studied the association between flavonoid intake from food frequency questionnaires completed by the women in 1984, 1990, 1994 and 1998; and 344 confirmed cases of ovarian cancer diagnosed between 1984 and 2002. While there was a significant trend toward decreasing incidence of ovarian cancer with increasing total flavonoid intake, Gates warned that "because this is one of the first studies of the topic, this association needs to be evaluated in another prospective study population before conclusions can be made."

Gates also analyzed individual flavonoids to evaluate their impact on ovarian cancer incidence. The flavonoid kaempferol, which the nurses consumed primarily from caffeinated tea, broccoli and kale, was associated with decreased ovarian cancer risk. Women with the highest levels of kaempferol intake had a significant 38 percent decrease in ovarian cancer incidence, compared to women with the lowest levels of intake. Two other flavonoids, myricetin and quercetin, showed a possible inverse association with ovarian cancer risk, although the results were largely non-significant.

"The associations were stronger when exposure was defined as cumulative average flavonoid intake over a period of 14 years, which suggests that long-term intake of flavonoids may be important," Gates said.

But she cautioned that "these findings need to be confirmed by others before any public health recommendations can be made. However, if confirmed, consumption of flavonoids would provide another means for women to decrease their risk of ovarian cancer."
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PostPosted: Sat May 13, 2006 7:06 am    Post subject: why exercise can protect against skin and bowel cancers Reply with quote

Oxford University Press
12 May 2006

Studies shed new light on why exercise can protect against skin and bowel cancers

Two studies published today (Saturday 13 May) have shown that exercise can protect against skin and bowel cancer, and they have identified new mechanisms that could be responsible for this effect.*
Published in the journal "Carcinogenesis", one study found that female mice that had 24-hour access to running wheels and were exposed to ultraviolet B light (UVB) took longer to develop skin tumours, developed fewer and smaller tumours, and had decreased amounts of body fat compared to mice that did not have access to running wheels. The second study looked at the development of pre-cancerous polyps in the intestines of male mice and discovered that voluntary exercise and a restricted diet reduced the number and size of polyps and improved survival.

Dr Allan Conney, Garbe Professor of Cancer and Leukemia Research and Director of the Susan Lehman Cullman Laboratory for Cancer Research at Rutgers University, New Jersey, USA, is one of the authors of the skin cancer study. He said that programmed cell death (apoptosis), triggered by exercise, might explain why the running wheel mice did better.

"Preliminary indications from follow-up work in the laboratory suggest that voluntary exercise enhances UVB-induced apoptosis in the skin, and that it also enhances apoptosis in UVB-induced tumours. So, although UVB is triggering the development of tumours, exercise is counteracting the effect by stimulating the death of the developing cancer cells.

"Our studies may be the first to suggest an apoptotic mechanism for the effect of voluntary exercise in the development of cancer. In addition, we found that voluntary exercise decreased body fat and that the number of tumours decreased with decreasing amounts of fat. This effect may also play an important role in the mechanism and warrants further investigation, bearing in mind the growing rates of obesity in the Western world, particularly in the USA and UK," he said.

Dr Lisa Colbert, Assistant Professor at the University of Wisconsin-Madison, USA, lead author of the bowel cancer study, said that her study was the first to suggest that a negative energy balance, produced by increasing the mice's energy output (by use of a running wheel) while maintaining a restricted calorie intake, appeared to be the important factor in inhibiting the growth of polyps (the fore-runners of bowel tumours).

"Negative energy balance was indicated by a lower body weight among the exercising mice, although they retained more body fat at the end of the study than the non-exercising mice – an observation that might be due to the fact that the exercising mice were healthier, while the health of the non-exercising mice was beginning to decline due to higher numbers of polyps. There were higher levels of hormones known to be associated with the onset of cancer – insulin-like growth factor-1 (IGF-1) and corticosterone – amongst the exercising mice, but this did not correlate with higher total polyp numbers. These data suggest that voluntary exercise that induces a negative energy balance protects against the onset of cancer in these mice, but that the mechanism is unlikely to be related to body composition, IGF-1 or corticosterone."

Dr Conney emphasised that it was not known yet whether exercise decreased the risk of sunlight-induced skin cancer in humans, and clinical trials were needed to investigate this further. However, in bowel cancer, evidence from population studies already suggests that physically active people have a reduced risk of developing the disease, but the mechanisms remain unclear.

The skin cancer study involved two experiments. In a "high risk" model, mice were exposed to UVB three times a week for 16 weeks, and then for the subsequent 14 weeks, in the absence of further UVB treatment, half the mice had access to running wheels in their cages while the other half did not. In a second, "complete carcinogenesis" model, mice were exposed to UVB twice a week for 33 weeks and, from the beginning, half had access to a running wheel and half did not. Mice not exposed to UVB acted as controls for the study. In both models, the exercising mice increased their food intake and maintained their normal body weight.

The exercising mice in the high risk model had an average of seven weeks without tumours after the UVB exposure ceased, while the non-exercising mice only had an average of 3.5 tumour-free weeks.

Dr Conney said: "In both the no running wheel and running wheel groups, the number of tumours per mouse increased with time, but throughout the 14 weeks of tumour development, animals with access to running wheels had a decreased number of tumours per mouse compared to animals with no running wheels. At all times, the tumour size in the no running wheel group was greater than in the running wheel group; on average, the tumour size per mouse for the no wheel group was just over three times more than for the exercise group."

In the complete carcinogenesis model, mice with no running wheel started to develop tumours 20 weeks after the start of UVB exposure, while tumours in the running wheel group started after 23 weeks. The average tumour-free time was 25 weeks for the no running wheel group and 27 weeks for the running wheel group.

Dr Conney said: "The rate of increase in tumour numbers per mouse for the no running wheel group was significantly greater than that for the running wheel group. On average, the tumour size per mouse for the no running wheel group was about 3.5 times more than in the exercise group.

"In both models, voluntary running decreased the number of non-malignant tumours per mouse by 34%. Exercise substantially decreased the size of non-malignant tumours and malignant tumours: in the high risk model, the non-malignant tumour size per mouse was decreased by 54% and the malignant tumour size per mouse by 73%, and in the complete carcinogenesis model, tumour size per mouse was decreased by 75% and 69% respectively."

For the bowel cancer study, Dr Colbert and her co-authors used mice (APC Min mice) that had a genetic mutation that predisposed them to develop intestinal polyps. "Our studies are relevant for humans in that these Min mice have a mutation in one of the same genes, APC, that is also mutated in human colon cancer," she explained. "The protective effect of exercise and lower body weight in our mice is consistent with epidemiological evidence in humans that suggests higher levels of activity and lower body weight reduces the risk of colon cancer."

Mutations in the APC gene in humans are responsible for an inherited condition called familial adenomatous polyposis (FAP). FAP affects about one in 10,000-15,000 people worldwide, 95% of whom will develop numerous polyps in the bowel which eventually develop into colon cancer, usually before the age of 40. The gene is mutated in sporadic forms of colon cancer as well.

The researchers randomly assigned seven-week-old male mice to either voluntary wheel running or to no exercise for 10 weeks. For the first three weeks both groups had the same amount of food and water, but after that the exercising mice were fed the amount that the non-exercising mice had eaten the week before so that their food consumption was unable to rise with their increased activity, thereby producing a negative energy balance.

By the end of the ten weeks, six of the 23 control mice had died due to the number of polyps that had grown and the resulting anaemia, while all the 24 exercising mice were still alive.

"The exercising mice ran an average of 3.8 km a day, and the further they ran the fewer polyps they had. Exercise significantly reduced total polyp number and polyp size, as well as prolonging survival," said Dr Colbert. "On average there were 16 polyps per mouse in the exercising mice compared to 22 polyps in the control mice – a decrease of 25%."
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PostPosted: Fri Aug 11, 2006 7:28 am    Post subject: Contagious Cancer Reply with quote

Cell Press
10 August 2006

Contagious cancer in dogs confirmed; origins traced to wolves centuries ago

This press release is also available in German.

--------------------------------------------------------------------------------

See article by Murgia et al. in the August 11, 2006, issue of the journal Cell
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A new study in the August 11, 2006 issue of the journal Cell provides evidence that a form of cancer afflicting dogs has spread from one individual to another by the transmission of the tumor cells themselves. The disease demonstrates how a cancer cell can become a successful parasite with a worldwide distribution, according to the researchers.

The findings may have broad implications for conservation biology and for scientists' understanding of cancer progression, the researchers said.

Robin Weiss of University College London and his colleagues traced the origin of so-called canine transmissible venereal tumor (CTVT) to a single clone. They estimated that the parasitic cancer arose at least 200 years ago in either a wolf or a closely related ancient dog breed. That makes the tumors the oldest cancer known to science, and possibly the longest continually propagated mammalian cell lineage in the world.

"Our results, based on several independent genetic markers in tumor-bearing dogs living on five continents, show that CTVT arose from a common ancestral cancer cell," Weiss said. "The cancer escaped its original body and became a parasite transmitted from dog to bitch and bitch to dog until it had colonized all over the world." Early in its evolution, the clone diverged into two separate lineages, each of which now has a broad geographic range, he added.

CTVT, also known as Sticker's sarcoma, is apparently transmitted among dogs through sexual contact but may also spread through licking, biting, and sniffing tumor-affected areas, the researchers said. Earlier studies found that the cancer could be transmitted only by experimental transplantation of living tumor cells, not by killed cells or cell filtrates. Scientists had also noticed similar chromosomal abnormalities in tumor samples collected in different geographic regions. However, several reports of virus-like particles in CTVT had led some to suspect that a cancer-causing virus might play a role.

"The idea that this cancer in dogs might be caused by the transmission of tumor cells themselves has been around for some time--30 years or more," said Weiss. "But the actual truth wasn't there."

The idea that cancer may be spread by cell transfer has attracted renewed interest due to the recent emergence of a facial tumor apparently transmitted by the bite of the Tasmanian devil, an endangered marsupial species, he added.

In the current study, the researchers applied forensic science to the study of CTVT, systematically examining tumor and blood samples from 16 unrelated dogs in Italy, India, and Kenya. They also examined tumor samples taken from animals in Brazil, the U.S., Turkey, Spain, and Italy.

They quickly found that DNA isolated from the tumor and blood samples were not a match.

"We saw that the tumor cells didn't belong to the dogs," Claudio Murgia, the veterinarian who is first author on the study said. Rather the tumors collected from dogs around the world were closely related to one another, stemming from a single cancer clone.

The researchers traced the origin of the CTVT cancer by comparing the sequences of tumor genes to the related genes of gray wolves and dogs. They found that CTVT clustered most closely with gray wolves, suggesting that the disease originated in wolves or a closely related East Asian breed of dog. Based on genetic variation among the very similar CTVT samples, the researchers estimated that the disease has been transmitted among dogs for two centuries or more.

The team further found evidence that CTVT has adapted to evade dogs' immune responses. Otherwise, the unrelated tumor tissue "ought to be rejected," Murgia said.

Interestingly, he added, most dogs infected with CTVT develop a tumor that then regresses several months later and disappears.

"It looks like there is an aggressive phase of growth as the foreign tumor initially isn't recognized by the immune system," Murgia said. "In the long run, the immune system gets the better of it."

"As a sexually transmitted cell, CTVT would not have been able to colonize dogs worldwide if it killed them too quickly; the host must survive in a fit state long enough to transmit the tumor, which in the case of females probably entails an estrous cycle."

The findings in CTVT might lead to new insights for cancer more generally, they said.

"It's a curiosity of nature, but apart from that, it might also raise important new ideas about the instability of cancer," Weiss said.

It has become dogma that as cancer develops, it tends toward greater genomic instability and becomes "more and more aggressive," he added. After the gross chromosomal rearrangements soon after its emergence, however, CTVT--the longest lived of all known tumor clones--bears "no evidence of genome loss or progressive instability."

The findings challenge the idea that there is "an inevitable progression of cancer towards more instability," Weiss said.

The study also raises important issues for conservation biology, said Elaine Ostrander in an accompanying preview of the article.

"At present, CTVT can enter the wild canid population through physical contact between individuals (licking and biting) or mating between closely related species," she said. "For highly endangered canids, exposure to CTVT could theoretically create an immediate threat to the population's survival."

It's also possible that the small population sizes of endangered species like the Tasmanian devil might leave them generally more prone to developing other forms of transmissible cancer.

"It has not yet been checked thoroughly, but the Tasmanian devil tumor looks as if it might be the same phenomenon," Weiss said.

"The low numbers of these animals has led to inbreeding. Therefore, the tumor probably isn't recognized as foreign," he speculated.

Although difficult to study, Weiss said that the possibility of sexually transmitted tumors--for example, prostate or cervical cancer--may have merit in humans, particularly among people with compromised immune systems such as organ transplant recipients and those with AIDS. In humans, occult tumors in donor organs have been known to emerge on rare occasions in immunosuppressed transplant recipients, Weiss noted.


###

The researchers include Claudio Murgia of University College London in London, UK and University of Glasgow Veterinary School in Glasow, UK; Jonathan K. Pritchard and Su Yeon Kim of the University of Chicago in Chicago, IL; Ariberto Fassati and Robin A. Weiss of University College London in London, UK.

C.M. was a Wellcome Trust Clinical Veterinary Research Training Fellow, and A.F. is a Wellcome Trust University Research Fellow. R.A.W. was supported by grants from the Special Trustees of the Middlesex Hospital and the Medical Research Council.

Murgia et al.: "Clonal Origin and Evolution of a Transmissible Cancer." Publishing in Cell 126, 477–487, August 11, 2006. DOI 10.1016/j.cell.2006.05.051

Related Preview by vonHoldt et al.: "The Singular History of a Canine Transmissible Tumor."
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PostPosted: Sun Aug 27, 2006 6:13 pm    Post subject: Synthetic molecule causes cancer cells to self-destruct Reply with quote

University of Illinois at Urbana-Champaign
27 August 2006


Synthetic molecule causes cancer cells to self-destruct

CHAMPAIGN, Ill. -- Scientists have found a way to trick cancer cells into committing suicide. The novel technique potentially offers an effective method of providing personalized anti-cancer therapy. Most living cells contain a protein called procaspase-3, which, when activated, changes into the executioner enzyme caspase-3 and initiates programmed cell death, called apoptosis. In cancer cells, however, the signaling pathway to procaspase-3 is broken. As a result, cancer cells escape destruction and grow into tumors.

"We have identified a small, synthetic compound that directly activates procaspase-3 and induces apoptosis," said Paul J. Hergenrother, a professor of chemistry at the University of Illinois at Urbana-Champaign and corresponding author of a paper to be posted online this week ahead of regular publication by the journal Nature Chemical Biology. "By bypassing the broken pathway, we can use the cells' own machinery to destroy themselves."

To find the compound, called procaspase activating compound one (PAC-1), Hergenrother, with colleagues at the U. of I., Seoul National University, and the National Center for Toxicological Research, screened more than 20,000 structurally diverse compounds for the ability to change procaspase-3 into caspase-3.

The researchers tested the compound's efficacy in cell cultures and in three mouse models of cancer. The testing was performed in collaboration with William Helferich, a professor of food science and human nutrition at the U. of I., and Myung-Haing Cho at Seoul National University. The researchers also showed that PAC-1 killed cancer cells in 23 tumors obtained from a local hospital.

Cell death was correlated with the level of procaspase-3 present in the cells, with more procaspase-3 resulting in cell death at lower concentrations of PAC-1.

"This is the first in what could be a host of organic compounds with the ability to directly activate executioner enzymes," said Hergenrother, who is also an affiliate of the Institute for Genomic Biology at the U. of I. "The potential effectiveness of compounds such as PAC-1 could be predicted in advance, and patients could be selected for treatment based on the amount of procaspase-3 found in their tumor cells."

Such personalized medicine strategies are preferential to therapies that rely on general cytotoxins, the researchers say, and could be the future of anti-cancer therapy.


###
The work was funded by the National Science Foundation, the National Institutes of Health, and the University of Illinois.
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PostPosted: Thu Aug 31, 2006 6:46 pm    Post subject: Transforming immune cells into tumor fighters Reply with quote

American Association for the Advancement of Science
August 31, 2006

Science researchers genetically transform immune cells into tumor fighters
Engineered cells can persist in the body and shrink large tumors in humans
This press release is also available in French, Spanish and Japanese.


A team of researchers has genetically engineered normal immune cells to become specialized tumor fighters, demonstrating for the first time that these engineered cells can persist in the body and shrink large tumors in humans.

Two of the 17 people with advanced melanoma who received the experimental treatment saw their tumors shrink and were declared clinically free of disease more than a year and half after the therapy began, Steven A. Rosenberg of the National Cancer Institute and his colleagues report in a study published online by the journal Science at the Science Express website on 31 August. Science and Science Express are published by AAAS, the nonprofit science society.

So far, the therapy has only been used in this small group of melanoma patients, but Rosenberg says his team has demonstrated ways to engineer similar immune cells in the laboratory that would attack more common tumors such as breast, lung and liver cancers.

The technique developed by the Science researchers "represents the first time that gene manipulations have been shown to cause tumor regression in humans," Rosenberg says.

"This work marks an important next step in harnessing the power of our immune systems to fight cancer. The publication of this paper should help highlight the significant work to a broad spectrum of people, including patients, clinicians and those involved in basic research," said Stephen Simpson, Science's senior editor, immunology.

Rosenberg and colleagues have a long history of looking for ways to boost the body's natural immune defenses against cancer, focusing specifically on T cells, a special type of immune cell that can recognize and attack "foreign" cells such as those found in tumors. In their earlier experiments, the researchers removed tumor-fighting T cells from melanoma patients and multiplied these cells in the laboratory. After using chemotherapy to clear out a patient's old T cells, the researchers repopulated the patients' immune systems with these new fighters.

But some people with melanoma don't have these tumor-fighting T cells, and in other types of cancer it's difficult to identify T cells that attack tumors, Rosenberg says, so the researchers had to come up with a way to create these types of T cells from scratch.

T cells carry a receptor protein on their surface that recognizes specific molecules called antigens on tumor cells. The receptor's genetic makeup determines the antigen types that the T cell can recognize, so that some cells contain genes that make a T cell receptor that homes in on melanoma cells, while other cells contain genes that make a T cell receptor that recognizes breast or lung cancer cells.

With this in mind, Rosenberg and colleagues created tumor fighters by removing normal T cells from people with advanced metastatic melanoma, genetically engineering these normal cells to carry the receptor that recognizes melanoma cells and returning these "re-armed" cells to rebuild the patients' immune systems.

"We can take normal lymphocytes from patients and convert them to tumor-reactive cells," Rosenberg says, adding that the engineered cells could be tailored to fight tumors other than melanoma. "We've identified T cell receptors that will now recognize common cancers," he notes.

The newly engineered T cells showed signs of persistence in 15 of the patients in the study, making up at least 10 percent of their circulating T cells for at least two months after treatment. New T cell levels were higher in the two people whose tumors shrunk noticeably with the treatment.

Rosenberg and colleagues are now searching for ways to fine-tune the treatment so that greater numbers of the engineered T cells will survive and continue expressing their new receptor genes, since their expression does seem to wane over time, the Science researchers found.

Devising new ways to insert the receptor genes in the T cells, usually encoded in a retrovirus, has been one of the most challenging aspects of the treatment, Rosenberg says. "It's a lot of sophisticated molecular biology and most of our work is going into designing retroviruses, putting genes into cells efficiently and getting them expressed."


###
"Cancer Regression In Patients Mediated by Transfer of Genetically Engineered Lymphocytes" by R.A. Morgan et al.

Rosenberg's co-authors are Richard A. Morgan, Mark E. Dudley, John R. Wunderlich, Marybeth S. Hughes, James C. Yang, Richard M. Sherry, Richard E. Royal, Suzanne L. Topalian, Udai S. Kammula, Nicholas P. Restifo, Zhili Zheng, Azam Nahvi, Christiaan R. de Vries, Linda J. Rogers-Freezer and Sharon A. Mavroukakis of the National Cancer Institute.

The study was supported by the National Cancer Institute.

The American Association for the Advancement of Science (AAAS) is the world's largest general scientific society, and publisher of the journal, Science (www.sciencemag.org). AAAS was founded in 1848, and serves some 262 affiliated societies and academies of science, serving 10 million individuals. Science has the largest paid circulation of any peer-reviewed general science journal in the world, with an estimated total readership of one million. The non-profit AAAS (www.aaas.org) is open to all and fulfills its mission to "advance science and serve society" through initiatives in science policy; international programs; science education; and more. For the latest research news, log onto EurekAlert!, www.eurekalert.org, the premier science-news Web site, a service of AAAS.
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PostPosted: Tue Sep 19, 2006 9:36 pm    Post subject: A spicy solution for colon cancer? Reply with quote

University of Texas Medical Branch at Galveston
19 September 2006

A spicy solution for colon cancer?
GALVESTON, Texas -- Looking for a cancer cure? Try the spice rack.

In the last few years, that tactic has proved productive for researchers investigating turmeric, a curry spice used for centuries in Indian traditional medicine.

They've found that turmeric's active ingredient, curcumin, works in the lab to fight skin, breast and other tumor cells. In fact, human clinical trials employing curcumin have already been launched.

Now, working with cell cultures in a laboratory, scientists at the University of Texas Medical Branch at Galveston (UTMB) have discovered that curcumin blocks the activity of a gastrointestinal hormone implicated in the development of colorectal cancer, the country's second leading cancer killer with nearly 60,000 deaths annually. In a paper published in the current issue of Clinical Cancer Research, the UTMB researchers link the gastrointestinal hormone neurotensin, which is generated in response to fat consumption, to the production of IL-8, a potent inflammatory protein that accelerates the growth and spread of a variety of human cancer cells, including colorectal and pancreatic tumor cells.

"We found that in colon cancer cells, neurotensin increases not just the rate of growth but also other critical things, including cell migration and metastasis," said UTMB surgery professor B. Mark Evers, senior author of the article and director of UTMB's Sealy Center for Cancer Cell Biology. "The fact that all that can be turned off by this natural product, curcumin, was really remarkable."

Evers' group, including lead author and UTMB research associate Xiaofu Wang, probed curcumin's effect on the process by which neurotensin stimulates colon cancer cells to generate IL-8 in detail.

Neurotensin's influence, they found, depends on biochemical signaling pathways inside the cell. Their experiments showed that curcumin damped down those signals, reducing the production of IL-8. Experiments also showed that neurotensin increased the migration of colorectal cancer cells, and that curcumin could suppress this migration -- possibly reducing the ability of colorectal cancer to spread to other locations in the body.

"Our findings suggest that curcumin may be useful for colon cancer treatment, as well as potential colon cancer suppression, in cells that respond to this gastrointestinal hormone, neurotensin," Evers said. "About a third of all colorectal cancer cells have the receptor for neurotensin. Thus, the concept would be sort of like what we do for breast and prostate cancer, where the main therapy involves blocking hormones. We hope to do similar things with gastrointestinal cancers that respond to this hormone."
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PostPosted: Tue Sep 19, 2006 9:51 pm    Post subject: Exciting New Cancer Treatments Emerge Amid Persistent Myths Reply with quote

Exciting New Cancer Treatments Emerge Amid Persistent Myths

By Christopher Wanjek
LiveScience’s Bad Medicine Columnist
posted: 19 September 2006
09:40 am ET

The last couple of weeks have brought much needed good news about cancer. Of course, this is cold comfort for millions of people, including myself, who has lost an old friend, a friend's son and a family member to cancer within the span of just two months.

Nevertheless, as reported in the journal Science on Aug. 31, scientists at the National Cancer Institute used gene therapy for the first time to completely cure two patients with an advanced and deadly skin cancer called melanoma.

In the journal Nature on Sept. 6, three science teams reported a major link between tumor suppression and stem cell division. And on the same day in the journal Cancer, doctors announced the continued, dramatic decline in cancer deaths, which began in the early 1990s.


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http://www.livescience.com/hum.....ancer.html
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PostPosted: Sun Oct 15, 2006 8:08 pm    Post subject: Warming Up to Hyperthermia Reply with quote

Week of Oct. 14, 2006; Vol. 170, No. 16 , p. 250

Warming Up to Hyperthermia
Heat therapy could improve existing cancer treatments
Christen Brownlee

In March 1999, Jason Foster was unpleasantly surprised by a BB-size lump that he found in one of his testicles. He ignored it for a week, hoping that it would go away. But instead, the lump swelled to the size of a pea. "I had alarm bells going off in my brain," recalls Foster. A trip to the urologist confirmed his fears—Foster had testicular cancer. The news set him on a grueling, 4-month path of surgery and multiple chemotherapy drugs. Foster lost his hair, spent hours throwing up, and was exhausted. To stay upbeat, he tried to keep the disease in perspective.

For the full article:

http://sciencenews.org/articles/20061014/bob10.asp
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PostPosted: Tue Oct 31, 2006 8:14 am    Post subject: Microwave pre-cooking of French fries reduces cancer chemica Reply with quote

John Wiley & Sons, Inc.
31 October 2006

Microwave pre-cooking of French fries reduces cancer chemicals

Research news from the Journal of the Science of Food and Agriculture
Microwaving your French fries before you fry them reduces the levels of a cancer-causing substance, reveals findings published today in the SCI's Journal of the Science of Food and Agriculture.

The discovery of acrylamide - a possible carcinogenic in humans – has led to much research being done to investigate the benefits of alternative cooking methods. Acrylamide forms during processes such as frying, baking and roasting where high-temperature and low-moisture conditions exist.

Although numerous studies have been conducted to explore the possibilities of reducing acrylamide levels in French fries, a team of researchers from Turkey has shown that by reducing the frying time and hence the acrylamide formation by microwave pre-cooking of potato strips prior to frying.

Publishing their work in the Journal of the Science of Food and Agriculture, the researches showed that microwave application prior to frying resulted in a marked reduction of the acrylamide level in the surface region. When the potato strips were subjected to frying after a microwave pre-cooking step, acrylamide content in the whole potato strip was reduced by 36%, 41% and 60% for frying at 150, 170 and 190oC respectively.

"Microwaving French fries before cooking takes little time and in fact, microwave pre-cooked samples fried to the same degree of cooking appeared to have a more acceptable colour, probably due to the more gentle heat treatment they experienced during frying," says lead author Koray Palazoglu, of the University of Mersin, Turkey.
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PostPosted: Fri Nov 10, 2006 8:27 pm    Post subject: The Antibiotic Vitamin Reply with quote

The Antibiotic Vitamin
Deficiency in vitamin D may predispose people to infection

Janet Raloff
10 November 2006

In April 2005, a virulent strain of influenza hit a maximum-security forensic psychiatric hospital for men that's midway between San Francisco and Los Angeles. John J. Cannell, a psychiatrist there, observed with increasing curiosity as one infected ward after another was quarantined to limit the outbreak. Although 10 percent of the facility's 1,200 patients ultimately developed the flu's fever and debilitating muscle aches, none did in the ward that he supervised.


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http://sciencenews.org/articles/20061111/bob9.asp
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PostPosted: Tue Feb 06, 2007 8:32 am    Post subject: 2 new studies back vitamin D for cancer prevention Reply with quote

University of California - San Diego
6 February 2007

2 new studies back vitamin D for cancer prevention

Two new vitamin D studies using a sophisticated form of analysis called meta-analysis, in which data from multiple reports is combined, have revealed new prescriptions for possibly preventing up to half of the cases of breast cancer and two-thirds of the cases of colorectal cancer in the United States. The work was conducted by a core team of cancer prevention specialists at the Moores Cancer Center at University of California, San Diego (UCSD), and colleagues from both coasts.

The breast cancer study, published online in the current issue of the Journal of Steroid Biochemistry and Molecular Biology, pooled dose-response data from two earlier studies - the Harvard Nurses Health Study and the St. George's Hospital Study - and found that individuals with the highest blood levels of 25-hydroxyvitamin D, or 25(OH)D, had the lowest risk of breast cancer.

The researchers divided the 1,760 records of individuals in the two studies into five equal groups, from the lowest blood levels of 25(OH)D (less than 13 nanograms per milliliter, or 13 ng/ml) to the highest (approximately 52 ng/ml). The data also included whether or not the individual had developed cancer.

"The data were very clear, showing that individuals in the group with the lowest blood levels had the highest rates of breast cancer, and the breast cancer rates dropped as the blood levels of 25-hydroxyvitamin D increased," said study co-author Cedric Garland, Dr.P.H. "The serum level associated with a 50 percent reduction in risk could be maintained by taking 2,000 international units of vitamin D3 daily plus, when the weather permits, spending 10 to 15 minutes a day in the sun."

The colorectal cancer study, published online February 6 in the American Journal of Preventive Medicine, is a meta-analysis of five studies that explored the association of blood levels of 25(OH)D with risk of colon cancer. All of the studies involved blood collected and tested for 25 (OH)D levels from healthy volunteer donors who were then followed for up to 25 years for development of colorectal cancer.

As with the breast cancer study, the dose-response data on a total of 1,448 individuals were put into order by serum 25(OH)D level and then divided into five equal groups, from the lowest blood levels to the highest.

"Through this meta-analysis we found that raising the serum level of 25-hydroxyvitamin D to 34 ng/ml would reduce the incidence rates of colorectal cancer by half," said co-author Edward D. Gorham, Ph.D. "We project a two-thirds reduction in incidence with serum levels of 46ng/ml, which corresponds to a daily intake of 2,000 IU of vitamin D3. This would be best achieved with a combination of diet, supplements and 10 to 15 minutes per day in the sun."

Vitamin D3 is available through diet, supplements and exposure of the skin to sunlight, or ultraviolet B (UVB). In the paper, the researchers underscored the importance of limiting sun exposure such that the skin does not change color (tan) or burn. For a typical fair-skinned Caucasian individual, adequate vitamin D could be photosynthesized safely by spending 10 to 15 minutes in the noontime sun on a clear day with 50 percent of skin area exposed to the sun. Darker skinned individuals may require more time in the sun, such as 25 minutes. For people with photosensitivity disorders, or anyone with a personal or family history of nonmelanoma skin cancer, any amount of extra sun exposure would be inadvisable.

The meta-analysis on colorectal cancer includes data from the Women's Health Initiative, which had shown in 2006 that a low dose of vitamin D did not protect against colorectal cancer within seven years of follow-up. However, the researchers wrote, the meta-analysis indicates that a higher dose may reduce its incidence.

"Meta-analysis is an important tool for revealing trends that may not be apparent in a single study," said co-author Sharif B. Mohr, M.P.H. "Pooling of independent but similar studies increases precision, and therefore the confidence level of the findings."


###
The authors recommend further research to study individuals for the effect of vitamin D from sunlight, diet and supplements on the risk of cancer.

Co-authors on both the breast cancer and colorectal meta-analysis papers are Edward D. Gorham, MPH, Ph.D., Cedric F. Garland, Dr.P.H.; Frank C. Garland, Ph.D.; Sharif B. Mohr, MPH; William B. Grant, Ph.D; Martin Lipkin, M.D.; Harold L. Newmark, ScD; Edward Giovannucci, M.D., ScD; and Michael F. Holick, M.D., Ph.D. Co-author on the colorectal meta-analysis paper only was Melissa Wei, B.S. Authors' institutional affiliations are UCSD Department of Family and Preventive Medicine and Moores UCSD Cancer Center (Gorham, Garland, Garland); Naval Health Research Center, San Diego (Gorham, F.C. Garland, Mohr); SUNARC-Sunlight, Nutrition and Health Research Center, San Francisco (Grant); Strang Cancer Prevention Center of Rockefeller University, New York, NY (Lipkin); Rutgers--The State University of New Jersey and Cancer Institute of New Jersey (Newmark); Harvard Schools of Public Health and Medicine (Giovannucci, Wei); and Boston University School of Medicine (Holick). Funding for this research was provided by a Congressional allocation to the Hollings Cancer Center of the Medical University of South Carolina through the Department of the Navy.
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PostPosted: Fri Feb 16, 2007 8:02 am    Post subject: HIV protein enlisted to help kill cancer cells Reply with quote

Washington University School of Medicine
15 February 2007

HIV protein enlisted to help kill cancer cells

Cancer cells are sick, but they keep growing because they don't react to internal signals urging them to die. Now researchers at Washington University School of Medicine in St. Louis have found an efficient way to get a messenger into cancer cells that forces them to respond to death signals. And they did it using one of the most sinister pathogens around — HIV.

"HIV knows how to insert itself into many different types of cells," says senior author William G. Hawkins, M.D., assistant professor of surgery and a member of the Siteman Cancer Center at the School of Medicine and Barnes-Jewish Hospital. "A portion of the HIV protein called TAT can transport biologically active compounds into cells. TAT is small, but it can move massive molecules. You could almost hook TAT up to a train, and TAT would drag it inside a cell. So we've taken advantage of this ability."

In an article published online in January 2007 in the Annals of Surgical Oncology, the researchers describe using TAT to pull a protein called Bim into cancer cells. TAT alone cannot cause AIDS and has no adverse health effects. Bim acts as a tumor suppressor and causes cancer cells to die through apoptosis, a process by which cells "commit suicide."

The research team found that the TAT-Bim compound activated apoptosis mechanisms in cancer cells and augmented the cell-killing effect of radiation. When mice with malignant tumors were treated with TAT-Bim, their tumors shrank, and they survived longer than mice that didn't get the treatment. After 40 days, 80 percent of mice receiving TAT-Bim were alive compared to 20 percent of mice that didn't get the treatment.

Hawkins asserts that this success marks the beginning of a very promising new approach to cancer therapy. "This is the tip of the iceberg," he says. "Now that we've proven we can do this, we've started creating a battery of proteins that can push cancer cells to die."

Hawkins says he thinks treatments that activate apoptosis mechanisms could provide new options for patients with the deadliest cancers — such as pancreatic cancer — which have very low rates of survival. He says he believes that clinical trials of these compounds could be just a few years away.

Hawkins began researching TAT-Bim after discussions with co-author Richard S. Hotchkiss, M.D., professor of anesthesiology, medicine and surgery and associate professor of molecular biology and pharmacology. Hotchkiss was seeking proteins that inhibit apoptosis in patients with life-threatening infections and found that TAT-Bim had the unwanted effect of increasing cell death. Hawkins wondered if TAT-Bim could be effective against cancer, and a productive scientific collaboration began between their labs to exploit the anticancer potential of TAT-Bim.

"Unlike most healthy cells, cancer cells grow very fast. So they are always on the verge of running out of natural ingredients like sugars, and mistakes are accumulating in their DNA," Hawkins says. "This results in signals telling cancer cells to die, but the cells don't quite have the permission they need to do it. Proteins like TAT-Bim can tip the balance in favor of death."

To further enhance the cancer-killing power of TAT-Bim and similar proteins under development, Hawkins and his colleagues are working on a technique that will concentrate them within tumors while sparing healthy cells. In collaboration with Robert H. Mach, Ph.D. professor of radiology, they are linking the anticancer proteins to tracer molecules that selectively bind to cancer cells.

"Dr. Mach designed tracers to visualize cancer in PET (positron emission tomography) scans," Hawkins says. "By binding our molecules to the tracers, we can deliver them to cancer cells. We've seen phenomenal results in the lab."

Next Hawkins plans to combine pro-apoptotic proteins such as TAT-Bim with chemotherapy, radiation therapy and other anticancer therapeutics in hopes of further increasing cell-suicide signals within cancer cells.

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Kashiwagi H, McDunn JE, Goedegebuure PS, Gaffney MC, Chang K, Trinkhaus K, Piwnica-Worms D, Hotchkiss RS, Hawkins WG. TAT-Bim induces extensive apoptosis in cancer cells. Annals of Surgical Oncology Jan 6, 2007 (advance online publication).

Funding from the Barnes-Jewish Hospital Foundation supported this research.

Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.

Siteman Cancer Center is the only NCI-designated Comprehensive Cancer Center within a 240-mile radius of St. Louis. Siteman Cancer Center is composed of the combined cancer research and treatment programs of Barnes-Jewish Hospital and Washington University School of Medicine.
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PostPosted: Mon Feb 19, 2007 9:54 am    Post subject: Cancer that colonizes our bodies Reply with quote

Natural Sciences and Engineering Research Council
18 February 2007

Cancer that colonizes our bodies

To Robert C. von Borstel, cancer is a metaphorical example of the perfect invasion by a founder species. Like the first pregnant finch that landed on a deserted island in the Galapagos Archipelago, the first cancer cell in the human body has to undergo many mutations through many generations to establish itself as an invader of different organs in the body. But once it is there, like any newly stabilized species in different ecological niches, cancer is tough to get rid of.

The former University of Alberta biologist has been working with DNA – the molecule that carries our cells’ genetic information – ever since 1947, six years before its structure was described by Watson and Crick. His fundamental Natural Sciences and Engineering Research Council (NSERC) work on how radiation can kill cells, how the DNA molecule itself can control mutation, and other research has earned him a fellowship in the American Association for the Advancement for Science (AAAS).

Now, von Borstel, at the AAAS conference in San Francisco, to be held between Feb. 15 and 19, will deliver a talk about how cancer cell mutation and selection are metaphorically similar to how a new species begins its evolution.

"Of course, the difference with cancer is that it destroys itself when it kills you off, whereas many new species stabilize," von Borstel says. "Obviously, no metaphor is the be-all of reality. But I’m hoping this symposium I am hosting will help people look at cancer in a new light."

After growing up on a wheat and cattle ranch in Oregon, von Borstel was drafted into the U.S. Navy as a seaman first-class in 1944. Following the Second World War, he pursued his university education in the United States and joined Tennessee’s Oak Ridge National Laboratory in 1953, where he studied the effects of radiation on insects, and described the mechanisms by which control of insect pests by X-irradiation is achieved.

From there, he accepted a position as chair of the University of Alberta’s Genetics Department. While there, he received NSERC grants over a 25-year period after the Council was formed. Von Borstel’s principal research efforts were on the causes of spontaneous mutations and how genes repair themselves.

He remained at the university past his mandatory retirement in 1992, continuing research for another 10 years. It was during his "retirement" years that he discovered how DNA and their components, the nucleosides, can repair chromosomes damaged by radiation. This suggests there are many natural ways for animals and humans to heal themselves. Also, he and his colleague Oksana Iavorovska discovered that human ovarian endometriosis is induced in sun-lovers by the ultraviolet radiation in sunlight.

"It’s been a privilege for me to do my work for so long and, as a matter of fact, I wish I was able to continue doing it today," the 82-year-old professor emeritus says. "Just before my laboratory was closed, my team of researchers was studying the number of genes responsible for spontaneous mutation rates in yeast, and in our first random sample we discovered that one-third of them control the mutation rate, and we had expected that only about 4 per cent might affect the rate. This shows that no matter how long you carry out research, there’s always something surprising around the corner."

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PostPosted: Thu Mar 01, 2007 8:25 am    Post subject: Green tea and COX-2 inhibitors combine to slow growth of pro Reply with quote

American Association for Cancer Research
1 March 2007

Green tea and COX-2 inhibitors combine to slow growth of prostate cancer

PHILADELPHIA -- Drinking a nice warm cup of green tea has long been touted for its healthful benefits, both real and anecdotal. But now researchers have found that a component of green tea, combined with low doses of a COX-2 inhibitor, could slow the spread of human prostate cancer.

In the March 1 issue of Clinical Cancer Research, researchers from University of Wisconsin-Madison demonstrate that low doses of the COX-2 inhibitor celecoxib, administered with a green tea polyphenol called pigallocatechin-3-gallate (EGCG), can slow the growth of human prostate cancer. Their experiments were performed in cell cultures and in a mouse model for the disease.

“Celecoxib and green tea have a synergistic effect -- each triggering cellular pathways that, combined, are more powerful than either agent alone,” said Hasan Mukhtar, Ph.D., professor of dermatology at the University of Wisconsin and member of Wisconsin’s Paul Carbone Comprehensive Cancer Center. “We hope that a clinical trial could lead to a preventative treatment as simple as tea time.”

Previous research has linked the cyclooxygenase-2 enzyme, commonly known as COX-2, to many cancer types, including prostate cancer, said Mukhtar. Mukhtar and his colleagues have previously shown COX-2 inhibitors like celecoxib (known under the brand name Celebrex™) suppress prostate cancer in animal models. COX-2 inhibitors also have been shown to cause adverse cardiovascular effects when administered at high doses over long durations.

In 2004, Mukhtar and his colleagues demonstrated that green tea polyphenol EGCG has cancer-fighting abilities of its own. Their study, published in Cancer Research, showed that EGCG can modulate the insulin-like growth factor-1 (IGF-1)-driven molecular pathway in a mouse model for human prostate cancer, pushing the cells toward programmed cell death (apoptosis).

“We believed that COX-2 inhibitors may still prove beneficial if used in combination with complementary agents,” Mukhtar said. “Our studies showed that the additive effect of green tea enables us to utilize the cancer-fighting abilities of COX-2 inhibitors, but at lower, safer doses.”

In this latest research, Mukhtar and his colleagues looked at the effects of the two substances on cultured human prostate cancer cells. Alone, both EGCG and NS-398, a COX-2 inhibitor similar to celecoxib, demonstrated the ability to slow cancer cell growth and limit the presence of known cancer-promoting proteins within the cell samples. Together, EGCG and NS-398 suppressed cell growth by an additional 15 to 28 percent.

The researchers repeated the experiment in mouse models of prostate cancer, using celecoxib and an oral suspension of the decaffeinated green tea polyphenol. By using pharmacy-grade celecoxib and actual tea, they had hoped to replicate real-life conditions. “The idea is that it would be easier to get people to drink green tea than it would be to take an additional dietary supplement,” Mukhtar said.

In mice that were not treated with either substance, the tumor volume averaged 1,300 cubic millimeters, whereas mice given either the tea or celecoxib had tumors averaging 835 cubic millimeters and 650 cubic millimeters, respectively. Tumors taken from mice given both agents, however, measured on average a volume of 350 cubic millimeters.

In parallel to tumor growth inhibition, mice that received a combination of green tea and celecoxib registered a greater decrease in prostate specific antigen (PSA) levels compared to that in celecoxib alone or green tea alone treated animals. PSA is a protein produced by the cells of the prostate and is used as a marker for detection and progression of prostate cancer. These results, combined with a marked decrease in the presence of cancer-promoting proteins, offered clear indications that green tea and celecoxib, combined, could be useful in slowing prostate cancer growth, Mukhtar said.

“Prostate cancer typically arises from more than one defect in the cellular mechanics, which means that a single therapeutic might not work fighting a particular cancer long-term,” Mukhtar said. “If tests in human trials replicate these results, we could see a powerful combined therapy that is both simple to administer and relatively cost effective.”


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The study was funded by the National Cancer Institute.

The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes more than 24,000 basic, translational, and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 70 other countries. AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants. The AACR Annual Meeting attracts more than 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment, and patient care. AACR publishes five major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. Its most recent publication, CR, is a magazine for cancer survivors, patient advocates, their families, physicians, and scientists. It provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship, and advocacy
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PostPosted: Mon Mar 26, 2007 9:52 am    Post subject: Cancer-fighting foods, supplements explored in day-long symp Reply with quote

American Chemical Society

Cancer-fighting foods, supplements explored in day-long symposium

March 25, 2007

CHICAGO, March 25 — Researchers worldwide are discovering a cornucopia of compounds in foods and dietary supplements that show promise for preventing cancer. More than a dozen research papers on this topic will be presented during a one-day symposium, “Natural Products, Diets and Cancer Prevention,” on Sunday, March 25, at the 233rd national meeting of the American Chemical Society.

All papers in this symposium are embargoed for 8:00 a.m. (Central Time), March 25. The symposium will be held at McCormick Place Lakeside, Room E264, Level 2.

Selected highlights are shown below:

Black raspberries show promise for preventing cancer of the esophagus, colon — Using animal models (rodents) of cancer development, researchers at Ohio State University showed that animals whose diets were supplemented with black raspberries had a 60 percent reduction in tumors of the esophagus and up to an 80 percent reduction in colon tumors. Clinical trials are now underway to determine whether the berries will prevent the development of esophageal and colon cancer in humans, says study leader Gary D. Stoner, Ph.D., a researcher and professor of internal medicine at the university. (AGFD 008, Sunday, March 25, 8:45 a.m.)

Blueberries contain chemical that may help prevent colon cancer — A compound found in blueberries shows promise in animal studies of preventing colon cancer, according to a joint study by scientists at Rutgers University and the U.S. Department of Agriculture. The compound, pterostilbene, is a potent antioxidant that could be developed into a pill with the potential for fewer side effects than some commercial drugs that are currently used to prevent the disease, according to study leader Bandaru Reddy, Ph.D., a professor in the Department of Chemical Biology at the university. (AGFD 009, Sunday, March 25, 9:15 a.m.) FULL NEWS RELEASE AVAILABLE.

Grape seed compounds may prevent skin cancer by boosting immune system — Chemicals obtained from grape seed extract show promise in animal studies as a way to prevent sunlight-induced skin cancer when used as a dietary supplement, according to researchers at the University of Alabama in Birmingham. In studies using mouse models of ultraviolet-light-induced (non-melanoma) skin cancer, mice that were fed diets supplemented with the grape seed compounds, a group of antioxidants called proanthocyanidins, showed a reduction in tumor number (up to 65 percent fewer) and size (up to 78 percent smaller) in comparison to control animals that did not receive the compounds, the researchers say. The compounds appear to work by inhibiting suppression of the immune system caused by ultraviolet light exposure, says Santosh Katiyar, Ph.D., an associate professor in the university’s department of dermatology. (AGFD 011, Sunday, March 25, 10:25 a.m.)

Compound found in high-fiber foods shows promise against prostate cancer — A dietary component found in most whole grain foods, beans, nuts and other high-fiber items shows promise in animal studies as a potent weapon for preventing prostate cancer. The compound, inositol hexaphosphate (IP6), was fed to animal models of prostate cancer and resulted in up to a 66 percent reduction in tumor size in comparison to control animals that were given water instead, the researchers say. The compound, which is sold in stores as a dietary supplement, adds to a growing number of products — including lycopene, milk thistle extract, vitamin E and selenium — that also have shown promise against prostate cancer, says Rajesh Agarwal, Ph.D., a professor in the Department of Pharmaceutical Sciences at the University of Colorado Health Sciences Center in Denver. (AGFD 013, Sunday, March 25, 11:25 a.m.)

Drinking cloudy apple juice daily may help prevent colon cancer — Researchers in Germany say that drinking two to three glasses of cloudy apple juice (unfiltered) per day may help keep colon cancer at bay. In a ten-week study using a mouse model for colon cancer, animals that were fed either cloudy apple juice or a potent extract of the juice showed a 38 percent and 40 percent reduction (respectively) in benign tumors of the small intestine, an indicator of its potential to fight colon cancer, in comparison to control animals that were given water instead of juice, according to Clarissa Gerhäuser, Ph.D., a researcher with the German Cancer Research Center in Heidelberg. The anticancer effect is likely due to a potent class of antioxidants called procyanidins, the researcher says. A widely publicized recent study by a group of researchers in Poland found that cloudy apple juice also is richer in antioxidants — up to four times higher — than clear apple juice. (AGFD 023, Sunday, March 25, 1:05 p.m.)


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The American Chemical Society — the world’s largest scientific society — is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
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