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(Health) Cancer: Vitamin D Needed to Cut Colon Cancer Risk
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PostPosted: Mon Apr 23, 2007 10:04 am    Post subject: Low vitamin D levels linked to poor physical performance in Reply with quote

Wake Forest University Baptist Medical Center
23 April 2007

Low vitamin D levels linked to poor physical performance in older adults

WINSTON-SALEM, N.C. -- Older adults who don't get enough vitamin D – either from their diets or exposure to the sun – may be at increased risk for poor physical performance and disability, according to new research from Wake Forest University School of Medicine and colleagues.

"With a growing older population, we need to identify better ways to reduce the risk of disability," said lead author Denise Houston, Ph.D. "Our study showed a significant relationship between low vitamin D levels in older adults and poorer physical performance."

The results are reported in the April issue of the Journal of Gerontology: Medical Sciences.

About one-fourth of people over age 60 have low vitamin D levels. Previous research has shown that vitamin D not only plays a role in bone health, but possibly also in protecting against diabetes, cancer, colds and tuberculosis.

"Recent findings showing the importance of vitamin D status on multiple health outcomes underscore the need for more research on the effects of low vitamin D levels in elderly populations," said Houston, an instructor in internal medicine - gerontology.

Vitamin D is naturally produced when skin is exposed to the sun's ultraviolet rays. Foods such as fortified milk, juice and cereals also contain vitamin D, but it is difficult to get enough through diet alone, said Houston.

Older adults are particularly prone to low vitamin D levels because they may get less exposure to sunlight and because their skin is less efficient in producing vitamin D from sun exposure compared to younger adults. Older adults also may not get enough vitamin D from dietary sources.

"There is a growing awareness that the prevalence of low vitamin D levels is common among the elderly," said Houston.

For the current study, researchers analyzed data from the InCHIANTI study, which evaluated factors contributing to the decline of mobility in late life. The study involved 976 people who were 65 years and older from two towns in the Chianti area of Italy. The mean age of participants was 74.8 years. Data were collected from Sept. 1998 through March 2000.

Participants completed a short physical performance test of their walking speed, ability to stand from a chair and ability to maintain their balance in progressively more challenging positions. In addition, handgrip strength, a predictor of future disability, was measured using a hand-held dynamometer.

The researchers found that physical performance and grip strength were about five to 10 percent lower in those who had low levels of vitamin D. After looking at other variables that could influence the results, such as body mass index, physical activity, the season of the year, mental abilities, health conditions and anemia, the results held true.

The study wasn't designed to evaluate whether low vitamin D levels actually cause poor physical performance, but the results suggest the need for additional research in this area, said Houston. She said vitamin D plays an important role in muscle function, so it is plausible that low levels of the vitamin could result in lower muscle strength and physical performance.

"But it's also possible that those with poor physical performance had less exposure to sunlight resulting in low vitamin D levels," she said.

Current recommendations call for people from age 50 to 69 to get 400 international units (IUs) of vitamin D per day and for those over age 70 to get 600 IUs. Many researchers, however, suggest that higher amounts may be needed.

"Higher amounts of vitamin D may be needed for the preservation of muscle strength and physical function as well as other conditions such as cancer prevention," said Houston. "The current recommendations are based primarily on vitamin D's effects on bone health."


###
The research is supported by the Italian Ministry of Health and in part by the National Institute on Aging. Co-researchers were Gary Schwartz, Ph.D., and Stephen Kritchevsky, Ph.D., both with Wake Forest, Matteo Cesari, M.D., Ph.D, with the University of Florida, Luigi Ferrucci, M.D., Ph.D., with the National Institute on Aging, Dario Maggio, M.D., and Antonio Cherubini, M.D., Ph.D, both with the University of Perugia in Italy, Mary Ann Johnson, Ph.D., with the University of Georgia, and Benedetta Bartali, R.D., with Cornell University.
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PostPosted: Tue Apr 24, 2007 9:59 am    Post subject: Cancer-Fighting Drug Found in Dirt Reply with quote

Cancer-Fighting Drug Found in Dirt

By Charles Q. Choi
Special to LiveScience
posted: 24 April 2007
10:10 am ET

The bark of certain yew trees can yield a medicine that fights cancer. Now scientists find the dirt that yew trees grow in can supply the drug as well, suggesting a new way to commercially harvest the medicine.

Scientists originally isolated the drug paclitaxel—now commonly known as Taxol—in 1967 from the bark of Pacific yew trees (Taxus brevifolia) in a forest near the Mount St. Helens in Washington. This yew also yields related compounds known as taxanes that can be converted to paclitaxel. Research since then has revealed other yew species generate paclitaxel and taxanes as well, as do some fungi and certain hazelnut varieties.

A decade ago, University of Portland biochemist Angela Hoffman and her colleagues were interested in growing yew in the lab from cuttings. They discovered small yew branches could secrete paclitaxel into plant food, raising the possibility that yew trees might release the drug into the soil .

For the full article:

http://www.livescience.com/hum.....drugs.html
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PostPosted: Sun Apr 29, 2007 9:54 am    Post subject: Reversing cancer cells to normal cells Reply with quote

Northwestern University
29 April 2007

Reversing cancer cells to normal cells

Tumor cells exposed to embryonic microenvironment of stem cells
In earlier work, Northwestern University scientist Mary J.C. Hendrix and colleagues discovered that aggressive melanoma cells (but not normal skin cells nor less aggressive melanoma cells) contain specific proteins similar to those found in embryonic stem cells. This groundbreaking work led to the first molecular classification of malignant melanoma and may help to explain how, by becoming more like unspecialized stem cells, the aggressive melanoma cell gained enhanced abilities to migrate, invade and metastasize while virtually undetected by the immune system.

Now, in the American Association of Anatomists’ plenary lecture and symposium, at Experimental Biology 2007 in Washington, DC, Dr. Hendrix describes new research that used an innovative experimental approach to provide unique insights into how scientists can change human metastatic melanoma cells back to normal-like skin cells - by exposing the tumor cells to the embryonic microenvironment of human embryonic stem cells, the zebra fish and the chick embryo.

Dr. Hendrix’s plenary lecture on April 29 is a highlight of the scientific program of the American Association of Anatomists. Her presentation is titled "the convergence of embryonic and cancer signaling pathways: role in tumor cell plasticity." Plasticity refers to the ability of the tumor cell, like the embryonic cell, to express or change into multiple, different types of cells.

First, a quick primer on the shared characteristics of aggressive tumor cells and embryonic stem cells: Embryonic stem cells are pluripotent, meaning they are able to differentiate into any of the more than 200 cell types in the adult body. Which type of cell they become depends on the signals they receive from their microenvironment. Similarly, during cancer progression, malignant cells receive and release signals from their own microenvironment, cues that promote tumor growth and metastasis.

In order to better understand what signals the melanoma cells are sending and receiving, Dr. Hendrix and her colleagues used the microenvironment of the zebrafish to study whether the tumor cells could communicate with the zebrafish stem cells and affect their early development. The zebrafish is a widely-used organism for genetic and developmental studies because of its prolific reproduction, rapid development, and transparent embryo that develops outside the body (making it especially easy to simply watch development), and the fact it develops organs and tissues comparable to those in humans, such as heart, kidney, pancreas, bones and cartilage.)

Using the zebrafish model, and the extraordinary technologic advances made in microscopy and molecular biology in recent years, the team was able to show that the aggressive melanoma cells secrete Nodal, a critical component underling the two-way communication between tumor cells and the embryonic microenvironment. Nodal is an embryonic factor (also called a morphogen) responsible for maintaining the pluripotency of human embryonic stem cells: their ability to develop or "morph" into one of a variety of body cells. When aggressive melanoma and other tumor cells (recent findings also report Nodal expression in breast cancer and testicular cancer) regain the ability to express a potent embryonic morphogen like Nodal, the presence of the Nodal and the signals it sends and receives appear to play a key role in tumor cell plasticity and progression.

Most noteworthy, Dr. Hendrix’s team’s also has shown that inhibition of Nodal signaling leads to a reduction in melanoma cell invasiveness and ability to create new tumors. In fact, with inhibition of Nodal, the metastatic melanoma cells are reverted to a more benign skin cell without the ability to form tumors.

Findings from the zebrafish study were further confirmed in the human embryonic stem cell model and the chick embryo model - where inhibiting Nodal signaling led to the reversal of the melanoma cells to a more normal cell type.

This is a promising area of research, says Dr. Hendrix. The discovery of a new signalizing pathway in melanoma and other tumor cell types and the ability to inhibit Nodal and thus reverse the melanoma cell back toward a normal skin cell provide a previously unknown target for regulating tumor progression and metastasis.

Dr. Hendrix’s distinguished lecture is part of a session titled the cell microenvironment in development and cancer.
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PostPosted: Sat May 12, 2007 6:36 am    Post subject: Childhood Vitamin D—A Dark Side? Reply with quote

Week of May 12, 2007; Vol. 171, No. 19

Childhood Vitamin D—A Dark Side?
Janet Raloff

Most people don't get nearly enough vitamin D, best known as the sunshine vitamin. This shortfall can be bad because the vitamin is known to fight cancer, diabetes, osteoporosis, muscle weakness, gum disease, and infections. Sadly, for some urban children there can be a downside to vitamin D: It enhances their bodies' uptakes of the toxic heavy metal lead.

A research team led by John D. Bogden of the University of Medicine and Dentistry of New Jersey–New Jersey Medical School in Newark has now quantified the effect. In the April Environmental Health Perspectives, Bogden and his team report that among urban African-American youngsters, blood concentrations of lead can rise to potentially toxic concentrations in summer, when their vitamin D concentrations also rise, presumably due to regular sun exposure.

For the full article:

http://sciencenews.org/articles/20070512/food.asp
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PostPosted: Thu May 17, 2007 12:52 pm    Post subject: Fatalistic beliefs about cancer cause many to ignore cancer Reply with quote

American Association for Cancer Research
17 May 2007

Fatalistic beliefs about cancer cause many to ignore cancer prevention advice
PHILADELPHIA -- If you feel that you are fated for cancer, your belief could turn into a self-fulfilling prophecy. According to a national survey of more than 6,000 U.S. adults published in the May issue of Cancer Epidemiology, Biomarkers & Prevention, a substantial number of American adults hold fatalistic beliefs about cancer and are correspondingly less likely to take basic steps to lower their cancer risk, such as exercising, quitting smoking and eating a healthy diet rich in fruits and vegetables.

The study, which analyzes data from the National Cancer Institute’s Health Information National Trends Survey, is the first national survey in almost 20 years to assess Americans’ knowledge about and attitudes toward cancer prevention. The findings have implications for cancer education efforts.

"Many Americans seem to feel afraid and helpless in regards to cancer, which may be exacerbated by conflicting news reports and a general lack of education on the causes and prevention of cancer," said Jeff Niederdeppe, Ph.D., professor at the University of Wisconsin, Madison. "They say ‘well, there is nothing much you can do about it’ and, as our survey shows, they indeed do nothing about it."

The survey asked respondents if they agreed with three statements about cancer. About 47 percent of those surveyed agreed with the statement that "It seems like almost everything causes cancer," while 27 percent agreed that "There’s not much people can do to lower their chances of getting cancer." Moreover, 71.5 percent of American adults agreed that "There are so many recommendations about preventing cancer, it’s hard to know which ones to follow."

People who maintained at least one of these three beliefs were less likely than others to exercise weekly and eat five daily servings of fruits and vegetables. People who believed that "it’s hard to know" what to do were more likely to smoke. All three beliefs, the researchers say, were associated with lower levels of education.

Despite the ready availability of cancer information, the researchers conclude, there has been little progress in changing the belief that "everything causes cancer" in the last 20 years. According to the researchers, it is unclear whether and to what degree media coverage of cancer influences beliefs. While this study did not specifically address the news media’s role in enforcing cancer fatalism, Niederdeppe believes that the constantly changing messages people get from the news are often confusing.

"Cancer is a difficult thing to talk about in the space of a single news story," Niederdeppe said. "Science values repetition, while the media values novelty. Those two concepts naturally butt heads, which can confuse people."

If conflicting news accounts of cancer prevention science are the cause of confusion, Niederdeppe says, educators ought to focus on developing simple, straightforward messages in teaching the general public about what they can do to prevent disease.

###
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 nearly 26,000 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 May 21, 2007 8:30 pm    Post subject: cancer risk Reply with quote

This interactive site is about cancer risk. It will help you make informed decisions about how you can lower your risk.

http://understandingrisk.cancer.gov/
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PostPosted: Wed Jun 27, 2007 12:15 pm    Post subject: Support for chromosomal theory of cancer found in cancers' d Reply with quote

University of California - Berkeley
27 June 2007

Support for chromosomal theory of cancer found in cancers' development of drug resistance

UC Berkeley's Peter Duesberg argues against mutation theory of cancer
Berkeley — Thirty-six years into the war on cancer, scientists have not only failed to come up with a cure, but most of the newer drugs suffer from the same problems as those available in the pre-war days: serious toxicity, limited effectiveness and eventual resistance.

This is no surprise to University of California, Berkeley, genetics researcher Peter Duesberg, professor of molecular and cell biology. According to his novel yet controversial "chromosomal" theory of cancer, which is receiving increased attention among cancer researchers, each cancer is unique, and there is no magic bullet.

"The mutation theory of cancer says that a limited number of genes causes cancer, so cancers should all be more or less the same," Duesberg said. The chromosomal theory, which he laid out in an article in the May 2007 issue of Scientific American, implies instead that, "even if cancers are from the same tissue, and are generated with the same carcinogen, they are never the same. There is always a cytogenetic and a biochemical individuality in every cancer."

The most that can be expected from a drug, he said, is that it is less toxic to normal cells than cancer cells, and that as a result a cancer detected early can be knocked back by chemotherapy. His chromosomal theory offers hope of early detection, however, since it ascribes cancer to chromosomal disruption, called aneuploidy, that can be seen easily through a microscope.

"By screening for aneuploidy, you could detect the cancer early and also see what possible drugs to use and whether drugs would even help," Duesberg noted. "Then, you wouldn't have to give a cocktail of drugs that includes all the best poisons, but you could leave out those you could tell wouldn't work. If you could cut chemotherapy drug toxicity in half or two-thirds, and direct it better at cancer, that is some progress. But it is not a cure."

Duesberg and colleagues discuss the major problem of drug resistance in cancer and how it supports the chromosomal theory of cancer in a paper appearing in the current issue of the journal Drug Resistance Updates (Vol. 10, issue 2).

Duesberg proposed in 2000 that the assumption underlying most cancer research today is wrong. That assumption, that cancer results from a handful of genetic mutations that drive a cell into uncontrolled growth, has failed to explain many aspects of cancer, he said, and has led researchers down the wrong path.

His alternative theory is that cancer results from aneuploidy - that is, duplication or sometimes loss of one or more of our 46 chromosomes, which throws thousands of genes out of whack. This condition, generated by a defect in the mechanism that duplicates chromosomes during cell growth, leads to more and more chromosomal disorder as the cells divide and proliferate, disrupting even more genes and providing ample opportunity for the development of resistance to drugs being used to control the cancer.

"In this new study and in one published in 2005, we have proved that only chromosomal rearrangements, rather than mutations, can explain the high rates and wide ranges of drug resistance in cancer cells," he said.

Duesberg even argues that the anti-leukemia drug imatinib (Gleevec®), the poster child for rational drug design once hailed as a therapy that would make drug resistance a thing of the past, has been rendered less useful because the aneuploid nature of leukemia has led to resistance. In fact, he said, this resistance suggests that imatinib is not a highly targeted drug, as advertised, but just another cell "poison" that happens to kill more leukemia cells than normal cells.

Development of drug resistance in cancer is one of the strongest arguments for the aneuploidy, or chromosomal, theory of cancer, Duesberg said, and is one aspect of cancer that can be studied experimentally. Normal cancers typically take decades to develop, making it hard to link cause and effect and to prove or disprove either the mutation or chromosomal theories. Drug resistance, however, often occurs quickly. Many cancer patients are initially heartened when their cancer starts to respond to a drug, only to find the cancer suddenly stop responding and begin to grow again.

In a paper responding to Duesberg's in the same issue of Drug Resistance Updates, Tito Fojo of the National Cancer Institute argues that there are many ways in which the mutation theory of cancer can explain drug resistance. A gene mutation, deletion, translocation or amplification could disrupt many cell functions, leading to resistance, or could inactivate or damage the doors through which a drug enters a cell.

Duesberg counters that aneuploidy is simpler and can explain the common development of resistance to many unrelated drugs within the same cancer. He has shown in experiments that aneuploidy causes many gene disruptions such as breakage or translocation each time a cancer cell divides, providing an opportunity for it to develop resistance to many drugs. Gene mutation rates in cancer cells, however, are no different from mutation rates in normal cells, making it difficult to understand how several simultaneous mutations can occur in cancer to make them resistant to more than one drug.

"The fundamental problem these conventional theories don't address is why it (drug resistance) doesn't happen in normal cells," he said. "Why aren't we all getting resistant to any toxic drug we are exposed to" Why does it happen only in cancer cells" Why do cancer cells become resistant and the patients don't""

In his experiments, Duesberg and his colleagues focus on the chromosomal fingerprint of a cell, its karyotype. For decades, physicians have known that cells of a particular cancer have the same set of marker chromosomes, a rogues gallery of normal chromosomes and stumps of chromosomes. Duesberg and UC Berkeley postdoctoral fellow Ruhong Li showed that the karyotype of drug-resistant cancer cells differs significantly from the karyotype of drug-sensitive cells from which they grew.

Clinicians have found, for example, that the gene expression profile of a breast cancer cell can tell them which treatments work best. This indicates, Duesberg said, that chromosomal disruption, which affects the expression of thousands of genes, is a better explanation for the cause of breast cancer than is the mutation theory.

"They see now, more and more, that aneuploidy cannot be ignored. It is a big elephant compared to their little mutations," he said.

Also, the more often a cancer changes karyotypes as it grows, he said, the more drugs it becomes resistant to.

"The inherent instability of aneuploidy thus explains the enormous adaptability of cancers against cytotoxic drugs and dims hopes for gene-specific therapies," Duesberg, Li and their co-authors wrote.

While this is bad news for cancer patients, Duesberg pointed out that the aneuploidy theory of cancer also provides a means for earlier detection of cancer. He and colleague David Rasnick have developed a cell scanner to search for aneuploid cells, such as from a Pap smear for cervical cancer or from biopsies for breast cancer. Rasnick formed a company to market the device, which recently was acquired by Modern Technology Corp. Aneuploid scanning is already employed in some European countries to screen for cancer.


###
Coauthors with Duesberg and Li on the new paper are Ruediger Hehlmann and Alice Fabarius of the Medical Clinic at the University of Heidelberg at Mannheim, Germany; Rainer Sachs, a UC Berkeley professor emeritus of mathematics and physics; and Madhvi B. Upender of the Center for Cancer Research of the National Cancer Institute in Bethesda, Md.

The work was supported by the Foundation for Advancement in Cancer Therapy, the Abraham J. and Phyllis Katz Foundation, philanthropists Herbert Bernheim and Robert Leppo, and other private sources.
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PostPosted: Tue Jul 03, 2007 9:34 am    Post subject: Researchers discover method for identifying how cancer evade Reply with quote

American Association for Cancer Research
2 July 2007

Researchers discover method for identifying how cancer evades the immune system

One of the fundamental traits of a tumor – how it avoids the immune system – might become its greatest vulnerability, according to researchers from the University of Southern California. Their findings, demonstrated in human breast and colorectal cancers, indicate that a technique for determining a tumor’s “immune signature,” could be useful for diagnosing and treating specific cancers.

In the July 1 issue of Clinical Cancer Research, a publication of the American Association for Cancer Research, the researchers describe a means for determining which genes have been altered in a tumor to allow it to evade the body’s natural defenses. In time, the researchers believe such analysis could become a standard practice in cancer diagnosis and treatment.

“The implication is that once you know the mechanism by which tumors evade the immune system, you can match that tumor to available therapies,” said senior author Alan L.Epstein, M.D., Ph.D., professor of Pathology at USC’s Keck School of Medicine. “First, we find the genetic changes that allow a tumor to defeat the immune system, then we can apply therapies that compensate for these genetic alterations.”

According to Epstein, tumors are notorious for demonstrating a broad array of genetic and biological variations. Their differences vary widely between cancer types, even between subcategories within a particular type of cancer. However, while the genetic variations that comprise an immune signature are complex, the researchers discovered that a small subset of genes is integral in explaining immunological behavior.

Using real-time PCR (rtPCR), a high-speed gene amplification technique, Epstein and his M.D./ Ph.D. student, Rebecca Sadun, screened tumors to identify 14 pro-immunity genes, which tumors downplay, and 11 key anti-immunity genes, which tumors promote. They studied the expression of these genes in five mouse tumor models for breast cancer, leukemia, colon cancer, lung cancer and renal cell carcinoma. They then compared two of these immune signatures with corresponding human tumors, eight cases of human ductal carcinoma and 11 cases of colorectal cancer.

Remarkably, the researchers found that the immune signatures of each of the human breast cancer cases nearly matched that of mice. In all cases, the researchers saw a suppression of CD83 and CD28, two genes that affect activation of immune cells, and over-production of B7-H4, a gene whose protein product inhibits immune activation. The human colorectal cancers, however, showed variations in their immune signatures, which researchers saw as an indication of the need to understand the signature for each patient’s individual cancer.

“I see it as the beginning stages of personalized medicine, where we develop tactics for treating the unique genetic make-up of a specific tumor,” Epstein said. “It becomes even more necessary when we look at all the immunotherapies that are becoming available or are beginning to emerge from research.”

In time, Epstein believes, it will be possible to study the immune signatures for most, if not all, forms of cancer. In addition, rtPCR technology allows for a relatively inexpensive and rapid analysis on equipment available at most medical centers, researchers said. “For now, we need to better understand the immune signatures for the most common human cancers in order to identify the most important targets for immunotherapy,” Epstein said.


###
The study was funded by the Philip Morris External Research program by Philip Morris USA, Inc., Philip Morris International and by support provided by Cancer Therapeutics Laboratories, Inc.
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PostPosted: Tue Jul 24, 2007 5:00 pm    Post subject: Enzyme discovery sheds light on vitamin D Reply with quote

Enzyme discovery sheds light on vitamin D
Queen's University
Tuesday July 24, 2007

Surprising findings by Queen’s researchers have shed new light on how the “sunshine vitamin” D – increasingly used to treat and prevent cancer and other diseases – is broken down by our bodies.

“The effectiveness of vitamin D therapy is partly dependent on how quickly it will be broken down,” says Biochemistry professor Glenville Jones, an expert in the field of vitamin D metabolism. “By studying the enzyme responsible for breaking down the vitamin, we hope to develop a way to prevent this from happening by blocking that response.”

First observed in Dr. Jones’s lab by undergraduate Biochemistry student Brendan O’Leary, the discovery reveals that changing a single amino acid in the hydroxylase enzyme will cause it to take a completely different pathway. Although scientists have known for 25 years that the enzyme is capable of taking two different pathways, until now they could not explain why this occurs.

The team’s findings are published on-line in the journal Proceedings of the National Academy of Sciences (PNAS). Other members include: research associate David Prosser, PhD student Martin Kaufmann, and research technician Valarie Byford.

Earlier study of the enzyme had shown that its pathway pattern is species specific. Some species, including humans and rats, favour one pathway, while others – most notably the opossum – favour the other pathway.

Using a technique called liquid chromatography mass spectrometry, the researchers studied cells from animals in both categories. They changed the human enzyme in certain key places to see if this would affect its pathway pattern.

Surprisingly, they discovered that altering a single amino acid completely changes the enzyme from a human pattern to an opossum pattern. This change can be flicked back and forth “like a light switch,” says Dr. Jones, adding: “It’s remarkable. In biochemistry you rarely see that kind of predictive work from modeling molecules and enzymes.”

The Queen’s researchers believe the hydroxylase enzyme plays an important role in human cell functions. When vitamin D drugs are used in an attempt to arrest certain types of cancer, for example, the tumour responds by making more of this enzyme. “If we can block the tumour response, we should be able to successfully treat some tumours with vitamin D compounds,” says Dr. Jones, whose research is supported by the Canadian Institutes of Health Research.

Vitamin D deficiency has also been correlated with other diseases, including multiple sclerosis, muscle weakness, and bone-related disorders, he notes.
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PostPosted: Thu Jul 26, 2007 1:23 pm    Post subject: 12 Common Cancer Myths Debunked Reply with quote

12 Common Cancer Myths Debunked
By Jeanna Bryner, LiveScience Staff Writer

posted: 26 July 2007 11:16 am ET

Numerous Americans believe a score of scientifically unproven claims about cancer, with some people thinking shampoo and underwire bras cause tumors.

A nationally representative telephone survey by the American Cancer Society of nearly 1,000 U.S. adults who had never been diagnosed with cancer revealed a surprising number agreed with inaccurate or unlikely statements about cancer risk and prevention statements.

For the full article:

http://www.livescience.com/hea.....myths.html
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PostPosted: Thu Aug 02, 2007 3:07 pm    Post subject: Electric fields have potential as a cancer treatment Reply with quote

American Institute of Physics
2 August 2007

Electric fields have potential as a cancer treatment

Experiments slow cancer cell division, brain tumor progression


Low-intensity electric fields can disrupt the division of cancer cells and slow the growth of brain tumors, suggest laboratory experiments and a small human trial, raising hopes that electric fields will become a new weapon for stalling the progression of cancer. The research, performed by an international team led by Yoram Palti of the Technion-Israel Institute of Technology in Haifa, is explained in the August issue of Physics Today, the flagship magazine of the American Institute of Physics.

For the full article:

http://www.eurekalert.org/pub_.....080207.php
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PostPosted: Wed Sep 05, 2007 1:34 pm    Post subject: Purdue researchers develop technology to detect cancer by sc Reply with quote

September 4, 2007

Purdue researchers develop technology to detect cancer by scanning surface veins

Writer: Elizabeth Gardner

A new technology for cancer detection that eliminates the need for drawing blood has been developed by Purdue University researchers.

Researchers from Purdue's Cancer Center, Department of Chemistry and Weldon School of Biomedical Engineering collaborated with cancer and biotechnology experts from the Mayo Clinic to develop technology to detect tumor cells within the human body. By shining a laser on surface veins, such as those on the wrist and inside the cheek, researchers are able to reveal and count circulating tumor cells.


In addition to being less invasive, the new detection method is able to evaluate a much larger volume of blood than what can be drawn from a patient for analysis, said Philip Low, Purdue's Ralph C. Corley Distinguished Professor of Chemistry.

"In the initial stages of cancer, there are very few circulating tumor cells - cells that indicate the spread of cancer and initiate secondary tumor formation," Low said. "By increasing the volume of blood analyzed, we improve the sensitivity of the test and allow for earlier diagnosis. If there are two cancer cells in every 50 milliliters of blood, odds are the cells would not be found in a 10-milliliter blood sample. However, the cells would be found in the 100 milliliters of blood that flow through large veins each minute."

Optical imaging provides high resolution and chemical specificity for cancer detection, but it usually suffers from limited penetration depth, making it hard to reach tumors inside the body, said Ji-Xin Cheng, an assistant professor of chemistry and biomedical engineering.


"In vivo detection of circulating tumor cells in surface veins provides an excellent way to overcome this problem," Cheng said.

"Circulating tumor cells provide a benchmark for disease progression and precise monitoring of their levels could lead to personalized treatment," Low said. "This technique allows us to quantify the amount of circulating tumor cells present, as opposed to tests that provide a 'positive' or 'negative' result.

"Through such precise monitoring, a physician could evaluate the response to chemotherapy and regularly adjust the dosage so that only the exact amount needed would be administered. This could reduce the time a patient is treated and the serious side effects that occur."

The technique could provide doctors and patients results in a matter of minutes and save the medical industry millions of dollars in testing equipment, said Wei He, a graduate student in the Department of Chemistry and the Department of Biomedical Engineering. He worked on the project with Low and Cheng.

By directly labeling tumor cells while they are in the bloodstream, some of the costs and problems associated with testing drawn blood samples can be avoided, He said.

"One sample can require five to 10 test tubes during the course of sampling, processing and analysis such as handling, labeling and washing," He said. "In addition, large hospitals can have more than 300 cancer patients in one day. Such a large influx can cause delays in sample processing and delays can affect the results of analysis."

A paper detailing the technology and detection technique was published in the July 10 Proceedings of the National Academy of Sciences. In addition to Low, He and Cheng, postdoctoral researcher Haifeng Wang and Lynn C. Hartmann, a professor of oncology and associate director for education of the Mayo Clinic Cancer Center, co-authored the paper.

The technique uses a fluorescent tumor-specific probe that labels tumor cells in circulation. When hit by a laser, which scans across the diameter of the blood vessel 1,000 times per second, the tumor cells glow and become visible. The in vivo flow detection was performed on a two-photon fluorescence microscope in Cheng's lab. The researchers compared several methods and found two-photon fluorescence provides the best signal to background ratio. The technology is able to scan every cell that is pumped through the vessel, He said.

Low's team has developed two labeling agents that attach to different forms of cancer. One label targets ovarian, non-small lung, kidney and endometrial cancer, and the other targets prostate cancer.

These labels would be administered through an injection. The first label has already been tested in humans and has no adverse side effects and could potentially be administered weekly, He said.

Computed tomography, or CT, scans and magnetic resonance imaging, or MRI, are the current methods used to track the spread of cancer. These methods have a limited resolution, and a 1 millimeter tumor could go undetected by CT or MRI. The Purdue-developed technology can achieve single-cell resolution and can detect rare cell populations.

"Our method can detect cancer cells early in disease development and the test can be conducted frequently," Low said. "Discovering the cancer early and knowing whether it has metastasized, or spread, greatly improves a patient's chance for successful treatment."

The laser penetrates to a depth of 100 microns and is able to examine shallow blood vessels near the surface of the skin. Advanced optical technology could be incorporated into the technology platform and enable the method to reach deeper vessels that handle larger volumes of blood, Cheng said.

The Purdue team continues to work with the Mayo Clinic and is planning to initiate a clinical trial to further evaluate the technique. The team also plans to develop labels for additional types of cancer and to downsize the equipment to make the technology portable.

This research was funded by an Indiana Elks Charities Grant, the Purdue Cancer Center and an Ovar'Coming Cancer Together research grant.


Writer: Elizabeth Gardner
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PostPosted: Tue Oct 16, 2007 1:44 pm    Post subject: Gold nanorods shed light on new approach to fighting cancer Reply with quote

October 15, 2007
Purdue University

Gold nanorods shed light on new approach to fighting cancer

WEST LAFAYETTE, Ind. - Researchers have shown how tiny "nanorods" of gold can be triggered by a laser beam to blast holes in the membranes of tumor cells, setting in motion a complex biochemical mechanism that leads to a tumor cell's self-destruction.
Tumor cell membranes often have an abnormally high number of receptor sites to capture molecules of folic acid, or folate, a form of vitamin B that many tumor cells crave. The Purdue researchers attached folate to the gold nanorods, enabling them to target the receptors and attach to the tumor cell membranes.


"The cells are then illuminated with light in the near-infrared range," said Ji-Xin Cheng (pronounced Gee-Shin), an assistant professor in Purdue's Weldon School of Biomedical Engineering. "This light can easily pass through tissue but is absorbed by the nanorods and converted rapidly into heat, leading to miniature explosions on the cell surface."

Scientists have recently determined that gold nanorods and other nanostructures can be used to target and destroy tumor cells, but it was generally assumed that cell death was due to the high heat produced by the light-absorbing nanoparticles. The Purdue team discovered, however, that a more complex biochemical scenario is responsible for killing the cells.

"We have found that rather than cooking the cells to death, the nanorods first punch holes in the membrane, and cell death is then chemically induced, in this case by an influx of calcium," said Alexander Wei, an associate professor of chemistry at Purdue.

Findings are detailed in a research paper appearing Oct. 19 in the journal Advanced Materials. The paper, which appeared online last week, was written by doctoral students Ling Tong, Yan Zhao, Terry B. Huff and Matthew N. Hansen, along with Wei and Cheng.

The gold rods are less than 15 nanometers wide and 50 nanometers long, or roughly 200 times smaller than a red blood cell. Their small size is critical for the technology's potential medical applications: the human immune system quickly clears away particles larger than 100 nanometers, whereas smaller nanoparticles can remain in the bloodstream far longer.

Shining light on the gold nanorods causes them to become extremely hot, ionizing the molecules around them.

"This generates a plasma bubble that lasts for about a microsecond, in a process known as cavitation," Wei said. "Every cavitation event is like a tiny bomb. Then suddenly, you have a gaping hole where the nanorod was."

The gold nanorods also are ideal for a type of optical imaging known as two-photon luminescence, used by Cheng and his research group to monitor the position of nanorods in real time during tumor-cell targeting. The imaging technique provides higher contrast and brighter images than conventional fluorescent imaging methods.

In experiments with tumor cells in laboratory cultures, the nanorods attached to the cell membranes and were eventually taken up into the cells. The researchers found that it could take far less power to injure cells by exposing the nanorods to near-infrared light while they are still on the membrane surface instead of waiting until the nanorods are internalized.

"This means that if you wait until the nanorods are inside the cell, then you really have to pump up the laser power, so localizing the nanorods on the cell membrane strongly influences their ability to inflict cell damage," Cheng said.

The findings suggest an optimal window of opportunity for applying near-infrared light to the nanorods for cancer treatment.

"We like to believe this opens the possibility of using nanorods for biomedical imaging as well as for therapeutic purposes," Cheng said.

The Purdue researchers observed that light-absorbing nanorods cause the formation of membrane "blebs, " similar to severe blistering. These blisters, however, are not produced directly by the high heat generated by the nanorods.

"The blebbing is triggered by the nanorods, but it's really caused through a complex biochemical pathway - a chemically induced process," Cheng said. "Extra calcium gets into the cell and triggers enzyme activity, which causes the infrastructure inside the cell to become loose, and that gives rise to the membrane blebs."

Researchers used a calcium-sensitive fluorescent dye to back up their argument that calcium influx caused the tumor cell death. When the nanorod-bearing tumor cells were maintained in a calcium-free nutrient medium, no blisters were formed if the nanorods were exposed to near-infrared light. But when the researchers added calcium to the medium, the blebbing took place immediately.

Although the technique offers promise for a new cancer treatment, it is too early to determine when it could be in clinical use, said Wei, who is collaborating with the National Cancer Institute to determine the suitability of the functionalized gold nanorods for future clinical studies.

The research has been supported by the National Science Foundation and the National Institutes of Health.
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PostPosted: Thu Oct 18, 2007 11:58 am    Post subject: Sidestepping cancer's chaperone Reply with quote

University of Massachusetts Medical School
18 October 2007

Sidestepping cancer's chaperone

UMass Medical School scientists target the mitochondria of tumor cells with novel anticancer agents
WORCESTER, Mass. — Cancerous tumors are wildly unfavorable environments. Struggling for oxygen and nutrients while being bombarded by the body’s defense systems, tumor cells in fact require sophisticated adaptations to survive and grow. For decades, scientists have sought ways to circumvent these adaptations to destroy cancer. Now, researchers at the University of Massachusetts Medical School (UMMS), have defined a method to target and kill cancer’s “chaperone”—a protein that promotes tumor cell stability and survival—without damaging healthy cells nearby.

In “Regulation of Tumor Cell Mitochondrial Homeostasis by an Organelle-Specific Hsp90 Chaperone Network,” published in the October 19 issue of Cell, Dario C. Altieri, MD, the Eleanor Eustis Farrington Chair in Cancer Research and professor and chair of cancer biology, and colleagues at UMMS, identify a new pathway by which cancer cells grow and survive—and provide a clear blueprint for the design and production of a novel class of anticancer agents aimed squarely at that pathway.

While previous research has demonstrated that a class of proteins known as molecular chaperones promote tumor cell survival, the specific way in which the proteins achieve this has not been well understood. And although inhibitors of a specific chaperone known as heat shock protein 90 (Hsp90) have been studied for the treatment of cancer, progress has been questionable. In this current research, Dr. Altieri and colleagues sought to both define the mechanism by which Hsp90 leads to tumor cell stability and survival, and understand why general suppression of Hsp90 has not been as successful in clinical trials.

Notably, they found a very abundant pool of Hsp90 (and its related molecule TRAP-1) in the mitochondria of tumor cells. Mitochondria are organelles that produce a cell’s energy, but also play a key role in cell death. Indeed, many current drugs and treatments work by damaging the mitochondria. Data obtained by Altieri and colleagues indicate that Hsp90 and TRAP-1 protect mitochondria in tumor cells from fulfilling their role in cell death. Significantly, the increased levels of Hsp90 and TRAP-1 were found only in the mitochondria of tumor cells—not in those of normal cells.

“We have identified this mitochondrial accumulation of Hsp90 and TRAP-1 as a critical adaptive mechanism that makes cancer cells less susceptible to the unfavorable environment of tumors, and to various anticancer agents,” Altieri explained.

This new understanding of the sub-cellular location of Hsp90 and TRAP-1 in the mitochondria also answers the question as to why the current Hsp90 inhibitors—which do not penetrate the mitochondria—are not as effective as hoped in the clinic. In this study, Altieri and colleagues synthesized a new compound, modifying an existing Hsp90 inhibitor so that it was able to reach the mitochondria. When the inhibitors were able to penetrate the mitochondria, they were able to eliminate the protective function of Hsp90, and induce massive tumor cell death. Notably, because this accumulation of Hsp90 and TRAP-1 only occurs in tumor cells, drugs conceived to target Hsp90 would largely spare normal cells, minimizing or even nullifying the dramatic side effects that plague many current cancer treatments.

“This is an important discovery that opens the door to the design of a completely new class of anticancer agents,” Altieri explained. “It really turns the tables on a field that has been explored with only partial success. We can now take a class of drugs and make them better and more efficacious by engineering them to accumulate in the mitochondria.”


###
About the University of Massachusetts Medical School

The University of Massachusetts Medical School, one of the fastest growing academic health centers in the country, has built a reputation as a world-class research institution, consistently producing noteworthy advances in clinical and basic research. The Medical School attracts more than $176 million in research funding annually, 80 percent of which comes from federal funding sources. The work of UMMS researcher Craig Mello, PhD, an investigator of the prestigious Howard Hughes Medical Institute (HHMI), and his colleague Andrew Fire, PhD, then of the Carnegie Institution of Washington, toward the discovery of RNA interference was awarded the 2006 Nobel Prize in Physiology or Medicine, hailed as the "Breakthrough of the Year" in 2002 by Science magazine and has spawned a new and promising field of research, the global impact of which may prove astounding. UMMS is the academic partner of UMass Memorial Health Care, the largest health care provider in Central Massachusetts. For more information, visit www.umassmed.edu
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PostPosted: Thu Nov 08, 2007 5:09 pm    Post subject: Could vitamin D, a key milk nutrient, affect how you age? Reply with quote

Weber Shandwick Worldwide

Could vitamin D, a key milk nutrient, affect how you age?
New study suggests boosting vitamin D may have long-term benefits for inflammation, aging

WASHINGTON, D.C. (November 8, 2007)- There is a new reason for the 76 million baby boomers to grab a glass of milk. Vitamin D, a key nutrient in milk, could have aging benefits linked to reduced inflammation, according to a new study published in the American Journal of Clinical Nutrition.

In a genetic study of more than 2,100 female twin pairs ages 19-79, British and American researchers found that higher vitamin D levels were linked to improved genetic measures of lifelong aging and chronic stress. Using a genetic marker called leukocyte telomere length (LTL), they found those with the highest vitamin D levels had longer LTL, indicating lower levels of inflammation and body stress. The telomere difference between those with the highest and lowest vitamin D levels was equivalent to 5 years of aging.

Previous research has found that shortened LTL is linked to risk for heart disease and could be an indication of chronic inflammation – a key determinant in the biology of aging. While there are several lifestyle factors that affect telomere length (obesity, smoking and lack of physical activity), the researchers noted that boosting vitamin D levels is a simple change to affect this important marker.

Studies continue to link vitamin D to an array of health benefits, securing vitamin D’s “super nutrient” status and providing even more reasons to get adequate amounts of this essential vitamin. Recent research suggests that beyond its well-established role in bone health, vitamin D also may help reduce the risk of certain cancers and autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis and multiple sclerosis.

Milk is a primary source of calcium and vitamin D in the American diet. In fact, government reports indicate that more than 70 percent of the calcium in our nation’s food supply comes from milk and milk products. Additionally, milk is one of the few food sources of vitamin D, which is fast emerging as a “super nutrient.”

The recommended three servings of low fat or fat-free milk provides 900 mg of calcium, 300 IU of vitamin D and 80 mg of magnesium daily.


###
Richards JB, Valdes AM, Gardner JP, Paximadas D, Kimura M, Nessa A, Lu X, Surdulescu GL, Swaminathan R, Spector TD, Aviv A. Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. American Journal of Clinical Nutrition 2007;86:1420-1425.
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PostPosted: Sat Dec 01, 2007 12:26 pm    Post subject: Canadians Advocate Boosting Vitamin D in Pregnancy Reply with quote

Week of Dec. 1, 2007; Vol. 172, No. 22

Canadians Advocate Boosting Vitamin D in Pregnancy
A Canadian medical society recommends pregnant women and nursing moms boost their intake of vitamin D dramatically

Janet Raloff

Canadian pediatricians certainly aren't shirking controversy when it comes to a vitamin guideline they've developed for pregnant women and nursing moms. They're asking these women to boost their intake of vitamin D dramatically—to 10 times the daily doses advocated by most health organizations in the States. This new prescription is aimed at combating rickets—leg deformations caused by soft bones—in youngsters who get too little of the sunshine vitamin.

For the full article:

http://sciencenews.org/articles/20071201/food.asp
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PostPosted: Mon Dec 17, 2007 2:50 pm    Post subject: Cancer Killed Almost 8 Million Worldwide in 2007 Reply with quote

Cancer Killed Almost 8 Million Worldwide in 2007
By Steven Reinberg, HealthDay Reporter

posted: 17 December 2007 01:01 pm ET

(HealthDay News) -- Cancer continues to cut a deadly swath across the globe, with the American Cancer Society reporting 12 million new cases of malignancy diagnosed worldwide in 2007, with 7.6 million people dying from the disease.

For the full article:

http://www.livescience.com/healthday/610938.html
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PostPosted: Mon Dec 15, 2008 12:51 pm    Post subject: Reply with quote

Raman Spectroscopy and its Role in the Detection of Cervical Dysplasia

Mahal Woldetsadik


Dysplasia is defined as the atypical growth of an organ or tissue through proliferation of abnormal cells (2). Cervical dysplasia is the development of abnormal cells on the surface of the cervix, lower portion of the uterus. A variety of factors including having multiple sexual partners, smoking cigarette and STDs are known to cause dysplasia but it is mainly caused by genital human papillomavirus (HPV), which is one of the most common sexually transmitted infections. HPVs have the ability to cause normal cells on the infected area of the skin to become abnormal and can progress to dysplasia. Dysplasia is considered to be a precancerous condition and if it remains undetected and untreated can lead to cervical cancer, which is the second most common cancer among women (4).

It can take over a decade for cervical dysplasia to develop to cancer and it is usually detected by using Papanicolaou test also known as Pap smear. During a Pap smear, sample of cells are taken from the outer opening of the cervix of the uterus and the endocervix. The cells are then observed under a microscope for pre-malignant or cancerous cells (5). Gynecologists highly recommend that women who are sexually active should have at least an annual Pap smear to check for any abnormalities. Even though the Pap smear is a simple and painless test, neither its specificity nor its sensitivity is perfect. In the case of the former, it can give false positive results by classifying a normal smear as abnormal and when it comes to its sensitivity, it can also give false negatives by not detecting abnormalities that are present (1).

In the research article, Characterization of Raman Spectra Measured in Vivo for the Detection of Cervical Dysplasia, Robichaux-Viehoever et al. evaluate the potential of near-infrared Raman spectroscopy and its ability to detect cervical dysplasia more efficiently than other methods including the Pap smear. In instances where cervical dysplasia is detected early in its evolution, treatment can prevent it from further progressing to invasive cervical carcinoma. As discussed above, Pap smears are known to give a significant amount of false positive results due to sampling and reading errors that can hinder early treatment and prevention (1). Furthermore, more accurate results can allow physicians to swiftly remove abnormal cells and keep a close watch on possible recurrences.

Raman spectroscopy is a spectroscopic technique used to study vibrational, rotational and various low-frequency modes in a system and is one of the techniques that is employed for the measurement of vibrational spectra (3). Raman spectroscopy is based on the Raman effect, inelastic scattering of photons by molecules, which was discovered by C.V Raman, an Indian Physicist, in the late 1920s. Unlike in infrared (ir) spectroscopy, transmitted light is not seen in Raman spectroscopy but rather light scattered by the sample is observed. Monochromatic light, light of a single frequency, must be used for a Raman experiment where a sample of solution is taken in a glass capillary tube and the incident light passes through the length of the capillary tube resulting in a scattered light (3).

In the study mentioned above, the authors expand on an alternate diagnostic method for women who have to undergo testing and treatment for cervical dysplasia. The standard diagnostic method for this procedure known as colposcopy directed biopsy constitutes of a physician applying 3-5% acetic acid solution to the cervix followed by an examination with a magnifying colposcope (1). Not only is this procedure difficult and incapable of providing an inclusive diagnosis, it is painful and quite uncomfortable for the patient. As a result, there is great interest to develop a noninvasive diagnostic tool that is capable of identifying dysplasia within a short period of time and causes minimal to no discomfort for the patient and that is where Raman spectroscopy comes in.

Robichaux-Viehoever et al. collected Raman spectra from the cervix of 79 patients using clinically feasible integration and multiple Raman measurements were taken from colposcopically normal and abnormal areas prior to the excision of tissue (1). The results showed that Raman spectroscopy along with statistical models has the ability to discriminate high-grade dysplasia (most extreme) and normal ectocervix (less extreme) with sensitivity of 89% and specificity of 81% compared to colposcopy by expert hands where the sensitivity and specificity was found to be 87% and 72% respectively (1). This study represents a significant milestone in developing Raman spectroscopy as a potentially enhanced tool in the screening and diagnosis of cervical dysplasia and cancer. Even though more clinical studies are needed to advance this technique, it is definitely a vital step in the right direction.




References

1. A. Robichaux-Viehoever, E. Kanter, H. Shappell, D. Billheimer, H. Jones III and
A. Mahadevan-Jansen, Applied Spect. 61, 986 (2007).

2. Encyclopedia
http://www.nationmaster.com/encyclopedia/

3. Harris, D. C., and Bertolucci, M. D. Symmetry and Spectroscopy: An Introduction to
Vibrational and Electronic Spectroscopy. New York, Dover Publications, INC.,
(1978)

4. MayoClinic.com
http://www.mayoclinic.com/heal.....ia/AN01657

5. Womens Health Channel: Your Women’s Health Community
http://www.womenshealthchannel.....ndex.shtml



Links to additional insights into this topic:


Cervical Cancer
http://www.hmc.psu.edu/healthi.....cancer.htm

Cervical Dysplasia
http://www.hopkinsmedicine.org.....ions_1.htm

Human papillomavirus (HPVs)
http://www.who.int/vaccine_res.....es/hpv/en/

HPV Test
http://www.thehpvtest.com/Abou.....-FAQs.html

High-grade dysplasia
http://www.thebody.com/content/treat/art14358.html

Infrared Spectroscopy
http://www.wag.caltech.edu/hom.....frared.htm

Monochromatic light
http://www.chemistrydaily.com/.....ectroscopy

Raman Spectroscopy
http://carbon.cudenver.edu/pub...../raman.htm

Raman Spectroscopy Video
http://www.youtube.com/watch?v.....g&NR=1

Sensitivity & Specificity
http://www.nature.com/nrc/jour.....c2287.html

Vibrational Spectra
http://hyperphysics.phy-astr.g.....ibspe.html

What is colposcopy?
http://www.mayoclinic.com/heal.....py/MY00236
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PostPosted: Mon Dec 15, 2008 12:53 pm    Post subject: Reply with quote

Jessica Urbelis
December 10, 2008
New Cancer Cell Screening:
Non-Invasive Indentification of Cancer Cells by Raman Spectroscopy

Chan, J., Taylor, D. Lane, S. Zwerdling, T., Tuscano, J., User, T. Anal Chem. 2008, 80, 2180

Although there are a variety of cancer detection techniques that have recently been at the forefront of modern technology, the screening methods currently used cannot accurately assess the malignancy of cells at the early stages of the disease's onset (1). Laser trapping Raman spectroscopy (2) has recently been developed as a technique to screen for cancer cells by characterization on a single cell-basis the identity of healthy cells versus cancerous cells (3). The benefits of using this new technique is that it is non-invasive and non-destructive meaning that it does not damage the cells and so they can therefore be used for further experiments. Additionally, the benefits of a single-cell scanning approach versus examining a bulk sample diminishes the possibility of error in which the one cancerous cell is masked by the signal of several surrounding healthy cells. It is because of this reasoning that Raman spectroscopy may be developed into methods of early detection where a single cancer cell can be analyzed.
Raman spectroscopy is an analytical technique based on the polarizability of molecular bond vibrations (4). To do so, a laser excites a photon and the inelastic scattering is measured as a function of both its wavelength and intensity. The shift between the wavelength of the incident and emitted light is done by the energy of a particular molecular vibration. Therefore, specific wavelengths (and their corresponding frequencies) are used to characterize bonds present in the sample.
In the specific case of optical-trapping and confocal Raman spectroscopy, a single tightly focused laser beam separates out and ÒtrapsÓ a single cell from a bulk sample and then subsequently excites it to generate a Raman spectrum. Each spectrum is then treated to statistical analysis to search for patterns and anomalies, mainly through principle component analysis (PDA) ad linear discriminant analysis (LDA) (5). It is from these statistical plots that the differences in the spectrum of healthy and cancer cells are obtained and identified as key ÒmarkersÓ in distinguishing the two types of cells from spectral data. It is crucial to note that the small differences in the spectra between each individual healthy cell or between leukemic cells (as same type of cells tested may have variable spectra because of their different positions in the cell cycle) are minimal compared to the variations between the bulk healthy versus bulk cancerous samples tested. It is because of this, that the results of identifying differences between healthy and cancerous cell spectra are reproducible from patient to patient and therefore can be deemed viable as a screening technique.
There are a few reasonings contributing to why there would be spectral differences between cancerous and healthy cells. Cancer cells are in different metabolic states than normal cells who spend most of their time in the resting phase of the cell cycle while cancer cells are most often in excited highly active metabolic states (6). Additionally, cancer cells have an enlarged nucleus because of their high proliferation rates and therefore a decrease in DNA density, and lower Raman intensities correspond to a decrease in local DNA concentrations in the sample (7). The markers ultimately indicate that cancer cells have a lower DNA: protein ratio than do normal cells.
The drawbacks to the technique are that only a small fraction of the entire cell can be analyzed because of the precision of the tightly focused laser. It can be assumed, however, that because of the high reproducibility of the data that it is the nucleus that is being trapped by the laser and analyzed (as the nucleus provides the most pertinent information about a cell (Cool). Additional research could be done on attempting to focus the laser elsewhere in the cell to generate more information about spectral differences and how those may contribute to the identification markers between cell types.
As means of a cancer screening process, Raman spectroscopy is unique in that it does not require an additional stain or invasive probe but instead on the intrinsic nature of the differences between healthy and cancerous cells. The nondestructive concept of the process also allows for additional experiments to be performed on the cell and opens the possibility of time related spectra as a function of the efficacy of an administered drug, allowing for the direct monitoring of elimination of cancerous cells for a given treatment.
Raman spectroscopy has previously been shown to assess the malignancy of cancer tissues during surgery, but the single-cell approach was first demonstrated on leukemia cells and hopefully can later expand to other specific types of cancer screenings. It seems reasonable for additional studies to be done to identify the spectral markers for each type of cancerous cell in comparison to its normal cell standard and compile the various markers into means of a direct cancer screening that is non-invasive, nondestructive and reliable for early detection methods.














Additional Questions

(1) What is cancer?
http://kidshealth.org/kid/heal.....ancer.html

(2) What is Raman Spectroscopy?
http://epsc.wustl.edu/haskin-group/Raman/faqs.htm
http://elchem.kaist.ac.kr/vt/c...../raman.htm

(3) How do cells become cancerous?
http://info.cancerresearchuk.o.....llsbecome/

(4) What is polarizability?
http://genchem.chem.wisc.edu/l.....Polar.html

How does one generate statistics?
http://mail.pittstate.edu/~winters/tutorial/

(6) What is cell metabolism?
http://www.biologie.uni-hambur.....e19/19.htm
http://www.ncbi.nlm.nih.gov/Ab....._cell.html
http://ghr.nlm.nih.gov/handboo.....ellsdivide

What is DNA?
http://ghr.nlm.nih.gov/handbook/basics/dna

Where is DNA located?
http://www.thetech.org/exhibit.....NA2.1.html
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PostPosted: Mon Dec 15, 2008 12:56 pm    Post subject: Reply with quote

Augusta Hofstead-Duffy
Georgetown University
Chemistry 521-Fall 2008
Dr. A. de Dios
December 15, 2008
Analysis of Photoisomerization of Sunscreen with Fourier Transform Infrared Spectroscopy

The sun is the center of our universe, supplying our planet with incalculable amounts of energy that sustains life but without precaution can be harmful to it (life) as well. The sun’s energy comes to earth in the form of radiation or light waves (1). The damaging effects of the sun’s ultraviolet (UV) radiation on skin are becoming more evident as past generation’s skin problems worsen. In fact, throughout the 70s, it was very popular and even considered healthy to have a golden tan. This trend, however, proved to be quite the opposite of healthy as the over exposure to sun slowly caused irreparable damage to skin. The damage at a cellular level can lead to various types of skin cancer (2). As new generations realize the dangers of sun damage many steps have been taken towards prevention. There are several suggestions to prevent skin damage that leads to skin cancer that range from protective attire to not going outside during the most intense radiation times of the day. Another major way to protect against UV radiation and maintain one’s current lifestyle is the application of a UV filter on the skin that is commonly known as sunscreen (3).
Sunscreen provides an invisible layer of protection on the skin’s surface by acting as a filter or screen that traps and reflects UV radiation. Sunscreen is a generic term for lotions, cosmetics, and other topical products that contain specific chemicals that have the ability to absorb the UV radiation before it reaches the skin (3). There are several different UV screening compounds used in these products, however, two important characteristics shared between them are non-toxic towards human skin and a high molar extinction coefficient (4). The molar extinction coefficient is a measure of the compound’s ability to absorb radiation of a specific wavelength. For example, a high extinction coefficient translates to a high ability to absorb (5). The colloquial measure of the absorbance efficiency for a sunscreen is referred to as the Sun Protection Factor or SPF. Similar to the molar extinction coefficient, the higher the SPF value the higher the protection from UV radiation. SPF is usually measured on a scale from 0 to 60 (3). The sunscreen label encourages reapplication after certain activities like swimming and after a spending a specific time in the sun. After swimming reapplication seems logical because water washes away the protective layer of sunscreen, leaving the skin vulnerable to harmful UV rays. The explanation for reapplication after a few hours spent in the sun is less obvious and often over looked.
First, consider the enormous amount of energy present in the sun’s radiation then imagine a single component of that radiation, a photon, striking a single molecule of the sunscreen compound that in turn absorbs the energy, what effect does absorbing that radiation have on the molecule? The significant amount of energy absorbed by the sunscreen molecule results in excitation, which describes the molecule’s increase in internal energy that pushes it into a higher energy state. From the higher energy state the molecule can release the energy that it absorbed and return to its initial energy state or it can use the extra energy to undergo a photophysical or photochemical process (6). Usually, the sunscreen undergoes a photophysical process of photoisomerization, which alters the arrangement of the compound’s components into a similar compound that has different properties from the original, i.e. the molar extinction coefficient (4). If the sunscreen is undergoing these photoisomerizations, which lead to a reduction in the absorbance efficiency of the UV radiation, then a reapplication of the product is necessary to provide the greatest amount of protection. An understanding of the extent to which these types of photophysical processes is crucial for establishing the effectiveness of the sunscreen and determining the SPF.
Most studies that investigate the photophysical processes of sunscreen compounds have been carried out in the solution phase, which seems odd because sunscreen is used in the solid phase when applied to skin.
2-Ethylhexyl-4-Methoxycinnamate (EHMC) is one common UV filter used in sunscreens that undergoes photoisomerization in the presence of UV radiation. EHMC exists as a trans (E) and a cis (Z) stereoisomers that, as previously mentioned, have different properties, namely molar extinction coefficients.
E-EHMC has about twice as high of an extinction coefficient than its Z-EHMC counterpart that has a value of 12,000 M-1cm-1 in the UV range (4). Thus, the isomerization from E to Z would result in a decrease of UV filtering efficiency and leave the skin susceptible to damaging UV radiation. All previous photoisomerization studies of EHMC have been conducted in solution. There was a study conducted in Thailand, however, that investigated the isomerization of EHMC in the solid phase using zinc selenide (ZnSe) surface and baby mouse skin.
The isomerization of EHMC was monitored by attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR). IR spectroscopy involves the analysis of the vibrational motion between atoms in a molecule that a described in images called spectra. The E and Z isomers of EHMC exhibit unique spectra, much like fingerprints, in ATR-FTIR spectroscopy (7). IR spectroscopy was used to observe the appearance of Z-EHMC that results from the isomerization of E-EHMC with UV radiation because of the difference in their IR spectra, specifically the disappearance of a peak in the spectrum at 981 cm-1 that is unique to the E isomer. The UV filtering efficiency of the sunscreen was established by determining the extent to which the E-EHMC isomerizes to Z-EHMC in the presence of UV radiation by constructing a graphical relationship between the amount of E-EHMC and the peak area at 981 cm-1. In this study, the relationship was found to be linear, which allowed for an accurate approximation of the E/Z ratio in the EHMC samples that were exposed to the UV radiation.
The study was designed to mimic the use of sunscreen in the real world, thus using solid surfaces and typical application dosages of sunscreen were crucial. The recommended application dosage for most sunscreens is about 2 mg/cm2, which represents about 0.15 mg/cm2 layer of EHMC on the skin. In the experiment, the E-EHMC applications ranged from 0.04 to 4.0 mg/cm2 and 0.2 to 4.0 mg/cm2 for the ZnSe and the baby mouse skin, respectively. The ZnSe and skin surfaces were covered with specific amounts of E-EHMC then exposed to 60 min periods of UV exposure. The study monitored the E to Z isomerization by obtaining the E/Z ratio by recording IR spectra immediately after specific intervals of UV exposure throughout the period. After abstracting the ratio of isomerization, the decrease in UV filtering efficiency could be determined using the extinction coefficients, i.e. a 50% isomerization would lead to a 25% decrease in UV protection (4).
The general analysis of ZnSe experiments indicates that more isomerization occurred at lower EHMC applications than higher. The study proposes that at higher dosages the insignificant amount of isomerization is due to the shielding of the lower layers of EHMC molecules by the uppermost layers, which implies that heavier applications would provide more protection. The skin experiments showed similar results to those of ZnSe when the EHMC dosages were the same. The researchers took the skin experiment one step further by repeating the experiments, but used natural sunlight instead of an artificial UV lamp. One hour of natural sunlight corresponds to 0.32 J/cm2 of the lamp and resulted in about 10% E to Z isomerization when 2.0 mg/cm2 of EHMC was applied, which decreased the absorption efficiency by about 5%. From the results of the experiment, the recommended application of sunscreen that contains 0.15 mg/cm2 EHMC, would undergo about 50% isomerization and lose about 25% of its UV absorbance ability within an hour of sunlight exposure (4).
The investigation supports higher application dosages of sunscreen in order to minimize isomerization that leads to decreased UV filtering efficiencies. The initial sunscreen application should be about the size of a grape if the desire is to supply the face with adequate protection. As was seen in the study, the shielding effect of sunscreen with another topical product that contains a UV filter will reduce the isomerization process. Sunscreens lose their effectiveness with UV exposure because they are undergoing these isomerizations that lead to a reduction in the absorbance abilities, so a reapplication of the product is necessary to provide the greatest amount of protection.
The discussion of the science behind how sunscreen functions and its limitations for protection is a reminder that reapplication and increased doses are important for prevention of skin damage. Hopefully, your morning routine already includes an application of sunscreen or will from now on and a bottle of sunscreen will always be kept handy for uses throughout a sunny day.

Related Links
UV Radiation:
http://www.nas.nasa.gov/About/.....ation.html

Skin Cancer:
http://www.mayoclinic.com/heal.....er/DS00190

Sunscreen:
http://www.skincancer.org/Heal.....ained.html

Prevention:
http://www.mayoclinic.com/heal.....prevention

2-Ethylhexyl-4-Methoxycinnamate:
http://www.dermacom.ch/private/alindex/ET003.htm

Stereoisomers:
http://www.cem.msu.edu/~reusch.....erisom.htm

IR Spectroscopy:
http://www.cem.msu.edu/~reusch.....frared.htm

Photochemistry:
http://www.cem.msu.edu/~reusch.....otchem.htm

References

(1) http://www.nas.nasa.gov/About/.....ation.html
(2) http://www.cancerlinksusa.com/skin/index.asp
(3) http://www.skincancer.org/Heal.....ained.html
(4) Pangnakorn, P.; Nonthabenjawan, S.; Ekgasit, C.; Thammacharoen, C.; Pattanaargson Wanichwecharungruang, S. Applied Spectroscopy, 2007, Vol. 61, pp. 193-198.
(5) McMurry, J. Organic Chemistry Sixth Edition. Pacific Grove, CA: Brooks/Cole, 2004, pp. 76, 93.
(6) http://www.cem.msu.edu/~reusch.....otchem.htm
(7) Harris, H. C.; Bertolucci, M. D. Symmetry and Spectroscopy: An Introduction to Vibrational and Electronic Spectroscopy, New York, NY: Dover, 1978, pp. 66, 93-97
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PostPosted: Mon Dec 15, 2008 12:58 pm    Post subject: Reply with quote

Victoria Harrison

Raman Spectroscopy: A Diagnostic Tool

Based off Article:

Haka, A.S.; Shafer-Peltier, K.E.; Fitzmaurice, M.; Crow, J.; Dasari, R.R.; Feld, M. Diagnosing Breast Cancer using Raman Spectoscopy. PNAS. 2005, 102, 12371-12376

Breast cancer is the most commonly diagnosed cancer in women in the United States and is directly responsible for 18% of all female cancer deaths, coming in close second to lung cancer as the leading cause of death in American women. In the United States alone, 216,000 new cases of breast cancer are diagnosed each year, and over 40,000 individuals die annually from this disease. This in effect means that more than 12% of the women born today in an industrialized nature will eventually be diagnosed with the cancer within their lifetime.

The good news, however, is that breast cancer is not a death sentence; that is, as long as the disease is detected within its initial stages. The survival rate for those whose cancer is detected while still located within the primary site is a promising 98.1%; this number decreases sharply to 27.1% for individuals whose cancer has already metastasized, i.e. has already spread from the initial site to other organs. Early detection and diagnosis of the disease is therefore important in preventing unnecessary deaths.

Over seventy percent of breast cancers are initially detected through routine self-examinations; the rest are generally detected through clinical breast examinations or mammographys. Mammography, the most common technique for detecting breast cancer, employs x-rays to probe density changes in breast tissue, however, since density changes are not always indicative of breast cancer, a biopsy is needed to confirm any diagnosis.

An estimated 500,000 breast biopsy procedures are performed each year in the United States, and approximately 70-90% of the lesions that are detected by mammogram end up being classified as benign. Tissue biopsies are invasive, incur large costs, and force a patient to wait a long time for diagnosis; for someone who does not actually have breast cancer they are a source of unnecessary trauma. These factors have motivated researchers to explore the possibility of using less invasive optical imaging and spectroscopy techniques in breast cancer detection. These methods provide immediate diagnosis and can be done using a biopsy needle consisting of optical fibers.

Raman spectroscopy has shown promise as an early cancer detection method due to the fact that there are a large number of Raman active molecules in breast tissue; molecules whose concentrations differ between healthy and malignant breast tissue. The spectral signals of these molecules are sharp and well delineated, which enables scientists to measure the concentrations of a multitude of different compounds. The ability of Raman to measure the presence of several different molecules is important because the disease often announces its presence by changing the ratio of compounds in breast tissue; measuring the concentration of just one compound would lead to a greater risk of error.

Raman Spectroscopy is a method used to analyze the vibrations of different bonds in a molecule. These bonds can be thought of as springs between atoms; springs which can bend, rotate, contract, stretch or shift in other ways. Each one of these motions occurs at a certain frequency, i.e. they occur a certain amount of times during a second. These frequencies correspond to certain energies; when a bond is hit by a photon of this specific energy, they will absorb the photon and oscillate at their set frequency. In Raman Spectroscopy, a type of electromagnetic spectroscopy, the frequency of a molecule’s vibrations is measured by first hitting it with a photon, and then measuring the energy shift of the emitted photon. The energy difference between the absorbed and emitted photon is indicative of the amount of energy that was absorbed and can thus be used to determine the frequency of the molecule’s vibrations. In general, the frequency at which a bond of a certain functional group tends to vibrate is unique and Raman spectroscopy can thus be used to determine the identity of the functional group or molecule with a low percentage of error. Not only can the peaks seen in a Raman spectrum be used to identify the compounds present, but they can also be used to measure the relative concentration of compounds in a material due to the fact that peak areas are proportional to the relative concentrations of the compounds.

It is this high degree of specificity that makes Raman spectroscopy such a good diagnostic technique for the detection of breast cancer. Normal breast tissue is composed mainly of fat and consists of both glandular and adipose tissue; there is very little collagen present. Abnormal breast tissue however has a much larger percentage of collagen, due to the fact that the formation of lesions, i.e. lumps, is often accompanied by fibrosis, a scarring process which results in higher levels of collagen. This means that the presence of stronger collagen peaks in a Raman spectra is indicative of the fact that the tissue is abnormal. However, a heightened level of collagen is not always indicative of cancer, due to the fact that several benign conditions can also result fibrosis.

Whilst tissues which have been affected by benign conditions may contain higher amounts of collagen then normal breast tissue, much like cancerous tissue, research has shown that the ratio of collagen to fat will vary between these two types of abnormal tissue. Therefore, in breast cancer detection, it is the ratio of the collagen to fat in the tissue that is used to determine whether the patient has breast cancer, not just the presence of heightened collagen levels. Raman can be used to determine the ratio of these two substances, since the two compounds’ functional groups present with peaks that are clearly delineated in the Raman Spectra. The ratio that is obtained by comparing the ratios of the functional groups can be compared to references to determine whether or not cancer is present in the tissue. At this time, Raman spectroscopy as a diagnostic tool yields an overall accuracy of 86% in cancerous cell detection.

The ultimate goal of A.S. Haka’s research group is to perfect the use of Raman spectroscopy as a diagnostic tool for breast cancer. Their paper explains that Raman spectroscopy shows promise as a noninvasive way to look at tissue composition, but also indicates that there is room for improvement in this method. The group proposes looking at how other compound concentrations in breast tissue are indicative of abnormalities and cancer since accuracy is often improved by increasing the number of data points used in a comparison. Eventually it is hoped that after this research is done and other possible improvements are made, this common vibrational spectroscopic method can replace the much more invasive diagnostic technique of tissue biopsy, leading to a decrease in patient trauma and an increase in breast cancer detection accuracy.

Questions:

What is Breast Cancer?

http://kidshealth.org/kid/grow.....ancer.html
http://www.breastcancerfund.or.....mp;b=84637

What is a Mammogram?

http://www.medic8.com/healthgu.....ogram.html

What is Biological Tissue?

http://encyclopedia.kids.net.a.....cal_tissue

How do X-Rays work?

http://www.cord.edu/faculty/ma.....ejuhl.html
http://health.howstuffworks.com/x-ray.htm

What is a Biopsy?

http://www.cancerhelp.org.uk/h.....?page=2599
http://www.everydayhealth.com/.....d=AZ_p0006

What is Spectroscopy?

http://loke.as.arizona.edu/~ck.....intro.html

What is a Spectrum?

http://csc.gallaudet.edu/soarhigh/Bspectra.html

What is Emission?

http://encyclopedia.kids.net.a.....ectroscopy

How does Raman Spectroscopy work?

http://encyclopedia.kids.net.a.....ectroscopy

http://carbon.cudenver.edu/pub...../raman.htm

http://www.harlemchildrensocie.....oscopy.ppt

What are some other applications of Raman Spectroscopy?

http://www.spectroscopynow.com.....amp;chId=6

How does Vibrational Spectroscopy work?

http://www.chem.qmul.ac.uk/surfaces/scc/

Why do Bonds Form Between Atoms?

http://www.visionlearning.com/.....php?mid=55

http://videos.howstuffworks.co.....-video.htm

How are Energy and Frequency Related?

http://science.hq.nasa.gov/kid.....aves4.html

What is a Photon?

http://www.historyforkids.org/.....photon.htm

http://membres.lycos.fr/cdadfs.....ekids.html

What are Functional Groups?
http://www.zerobio.com/videos/.....rcle1.html

http://encyclopedia.kids.net.a.....onal_group

What is Collagen?

http://www.energyinfonz.co.nz/.....asic3.html

What is the Chemical structure of fat?

http://encyclopedia.kids.net.au/page/fa/Fat
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