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April 13, 2009, 12:47 AM CT

How high-fiber diet protects you from colon cancer?

How high-fiber diet protects you from colon cancer?
Though a high-fiber diet has long been considered good for you and beneficial in staving off colon cancer, Medical College of Georgia scientists have discovered a reason why: roughage activates a receptor with cancer-killing potential.

Scientists report in the recent issue of Cancer Research that the GPR109A receptor is activated by butyrate, a metabolite produced by fiber-eating bacteria in the colon. The receptor puts a double-whammy on cancer by sending signals that trigger cell death, or apoptosis, and shutting down a protein that causes inflammation, a precursor to cancer.

"We know the receptor is silenced in cancer but it's not like the gene goes away," says Dr. Vadivel Ganapathy, corresponding author and chair of the Department of Biochemistry and Molecular Biology in the MCG School of Medicine.

Cancer shuts down the receptor by chemically modifying its gene through a process called DNA methylation. It's a typical MO for cancer to turn genes off to suit its purpose which is why DNA methylation inhibitors already are under study for a variety of cancers.

But cancer patients likely also need something to ensure the receptor gets activated by butyrate, such as eating more roughage or, more likely, getting mega doses of butyrate or a compound with similar properties, Dr. Ganapathy says.........

Posted by: Sue      Read more         Source


April 9, 2009, 4:50 AM CT

New drug for prostate cancer?

New drug for prostate cancer?
A new multi-center study shows that an experimental drug lowers prostate specific antigen (PSA) levels a marker for tumor growth in men with advanced prostate cancer for whom traditional therapy options have failed. The study, led by scientists at Memorial Sloan-Kettering Cancer Center (MSKCC), is published recently in Science Express, the online version of the journal Science

Most men with metastatic prostate cancer eventually build up resistance to the drugs that lower or block male hormones and develop a more aggressive form of the illness called castration-resistant prostate cancer (CRPC), or hormone-refractory disease. As per the study's findings, researchers studied two novel compounds, RD162 and MDV3100, and not only gained an understanding of their novel mechanism of action, but observed that these agents showed activity in CRPC cells in culture and in mice.

The study also reports on a Phase 1/2 trial of MDV3100 in 30 patients with advanced CRPC and observed that 22 out of 30 men showed declining PSA levels, and 13 out of 30 men (43 percent) had PSA levels fall by more than half.

Several years ago, the senior author of the study, Charles Sawyers, MD, and colleagues at the University of California, Los Angeles (UCLA), uncovered a potential reason why metastatic patients with prostate cancer eventually relapse with CRPC. This insight was used to discover RD162 and MDV3100.........

Posted by: Mark      Read more         Source


April 8, 2009, 5:06 AM CT

Treating drug-resistant prostate cancer

Treating drug-resistant prostate cancer
A new treatment for metastatic prostate cancer has shown considerable promise in early clinical trials involving patients whose disease has become resistant to current drugs.

Of 30 men who received low doses of one the drugs in a multisite phase I/II trial designed to evaluate safety, 22 showed a sustained decline in the level of prostate specific antigen (PSA) in their blood. Phase III clinical trials are planned to evaluate the drug's effect on survival in a large group of patients with metastatic prostate cancer.

The drugs are second-generation antiandrogen therapies that prevent male hormones from stimulating growth of prostate cancer cells. The new compounds manufactured by the pharmaceutical company Medivation and known as MDV3100 and RD162 appear to work well even in prostate cells that have a heightened sensitivity to hormones. That heightened sensitivity makes prostate cancer cells resistant to existing antiandrogen therapies.

The drugs were discovered in the laboratory of Howard Hughes Medical Institute investigator Charles Sawyers at Memorial Sloan-Kettering Cancer Center in collaboration with chemist Michael Jung at UCLA. He and colleagues described the development of the drugs and initial testing in an article posted online April 9, 2009, in Science Express, which provides electronic publication of selected Science articles in advance of print. Sawyers's team collaborated on the studies with scientists from the University of California Los Angeles, Oregon Health and Science University, University of Washington and Medivation.........

Posted by: Mark      Read more         Source


April 6, 2009, 9:42 PM CT

Avastin for brain cancer

Avastin for brain cancer
The use of Avastin alone to treat a subgroup of recurrent Grade 3 brain tumors showed it was safe and effective at delaying tumor progression, as per a retrospective study of 22 patients conducted by a researcher at the Seattle Cancer Care Alliance.

The patients all had a recurrent cancerous glioma known as alkylator-refractory anaplastic oligodendroglioma (AO), for which there is no existing standard treatment. Oligodendrogliomas begin in brain cells called oligodendrocytes, which provide support around nerves by building a sheath of myelin and facilitating electrical nerve impulses. The relatively uncommon tumor affects about 2,000 persons annually in the U.S. Most are under age 50.

Avastin, known generically as bevacizumab, is the first approved treatment designed to inhibit angiogenesis, the process by which new blood vessels develop and carry vital nutrients to a tumor. It is approved so far to treat certain metastatic colon cancers and non-small cell lung cancer.

"Bevacizumab is an important drug for us," said Marc Chamberlain, M.D., author of the study reported in the April 15 edition of the journal Cancer "Of all of the targeted therapies for gliomas, this has been the most promising. And this is practice changing."

Therapy for treating recurrent high-grade gliomas is palliative. All patients with these high-grade tumors eventually die of their cancer. However, bevacizumab has the potential to be the best palliative therapy, as per Chamberlain, who is director of the Neuro-oncology Program at the SCCA and a professor of neurology and neurological surgery at the University of Washington School of Medicine.........

Posted by: Janet      Read more         Source


April 6, 2009, 9:25 PM CT

Finding pancreatic cancer early

Finding pancreatic cancer early
A cancer scientist from Johns Hopkins has convinced an international group of colleagues to delay their race to find new cancer biomarkers and instead begin a 7,000-hour slog through a compendium of 50,000 scientific articles already published to assemble, decode and analyze the molecules that might herald the furtive presence of pancreas cancer.

With limited resources available for the exhaustive and expensive testing that needs to be done before any candidate can be considered a bona fide biomarker of clinical value, it's important to take stock of the big picture and strategize, says Akhilesh Pandey, M.D., Ph.D., an associate professor in the McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, and founder and director of the Institute of Bioinformatics in Bangalore, India.

Having mined the literature to amass 2,516 potential biomarkers of pancreas cancer, Pandey and his team are publishing their compendium on April 6 in PLoS Medicine They systematically cataloged the genes and proteins that are overexpressed in pancreas cancer patients, then characterized and compared these biomarker candidates in terms of how worthy each is of further study.

More than 200 genes are shortlisted because they were reported in four or more published studies to be overexpressed meaning that the proteins they make are in higher abundance in people with pancreas cancer than in people without the disease. This qualifies them as "excellent candidates" for the further studies that are needed to validate them as sensitive and specific biomarkers, note the authors.........

Posted by: Sue      Read more         Source


April 2, 2009, 10:07 PM CT

More efficient production of paclitaxel

More efficient production of paclitaxel
Shown is the broad specificity of the enzyme from yew plants that make the potent cancer drug paclitaxel (Taxol). Each acyl CoA shown can 'funnel' to the reactive site 'conveyor' of the enzyme and transfer to a prodrug skeleton. Graphic conceived by Kevin D. Walker, drafted by Thomas P. Carter.

Research by Michigan State University chemist Kevin Walker is paving the way for potentially cleaner, more efficient production of cancer-fighting paclitaxel - better known as the blockbuster drug Taxol.

First isolated from the bark of the Pacific yew in 1967, paclitaxel has since been made by synthetically modifying an intermediate substance isolated from yew needles using toxic solvents or by fermenting cell cultures.

Walker's method employs natural enzymes instead. "Pharmaceutical companies could reduce the steps involved in making Taxol," he said, "while cutting chemical byproducts".

Walker, an assistant professor of chemistry, biochemistry and molecular biology, studies enzymes that assemble the Taxol molecule in Taxus plants. "This process is like painting from a palette," Walker said. "We can add select colors to the palette from which the enzyme chooses, so the molecule can be crafted in a variety of ways. The enzyme does all the work.

"A plant enzyme can do in one step what traditional synthetic construction does in multiples steps," Walker said. "Under our process, the construction of Taxol uses a biological assembly line where each enzyme does its job to create the final product. Particular enzymes on the assembly line can attach slightly different components on the molecular frame to create new-generation Taxol molecules. This can lead to more effective drug variants and eventually better health care therapy".........

Posted by: Janet      Read more         Source


April 2, 2009, 5:09 AM CT

Radiation therapy and impairment of fertility

Radiation therapy and  impairment of fertility
In female cancer patients of reproductive age, radiation therapy directly to the ovaries should be avoided because there is a direct relationship between certain types of radiation treatment and fertility problems, as per a review in the April 1 issue of the International Journal of Radiation Oncology*Biology*Physics, the official journal of the American Society for Radiation Oncology (ASTRO).

Radiation treatment to the pelvic region can cause ovarian failure or result in damage that makes the uterus unable to accommodate the growth of a fetus. These effects are not a great concern to cancer patients past their reproductive years, but due to the growing number of pediatric and young-adult cancer survivors, these effects are increasingly relevant.

Scientists at the Harvard Radiation Oncology Program and the Department of Radiation Oncology at Brigham and Women's Hospital and Dana-Farber Cancer Institute, both in Boston, sought to review the impact of radiation treatment on fertility, pregnancy and neonatal outcomes among female patients and the effectiveness of ovarian transposition, or moving the ovaries out of the field of radiation, as a means of preserving fertility.

The study authors evaluated the outcomes of past studies that reported fertility, pregnancy and neonatal outcomes as a result of cranio-spinal, abdominal and pelvic radiation and determined that cranio-spinal irradiation caused hormonal changes that affected a woman's ability to become pregnant during the later part of life. Women who received abdominal or pelvic radiation had an increased risk of uterine dysfunction that lead to miscarriage, preterm labor, low birth weight and placental abnormalities. The study also determined that women who received low doses of ovarian radiation can suffer early menopause.........

Posted by: Janet      Read more         Source


April 2, 2009, 5:00 AM CT

Ovarian cancer screening

Ovarian cancer screening
The only available screening tests for ovary cancer fail to catch early signs of the disease and often result in unnecessary surgery, said scientists at the University of Alabama at Birmingham (UAB) Comprehensive Cancer Center.

The newly released study looked at a screening regimen that combines ultrasound and a blood test for CA-125, a marker for women's cancer.

Results showed the combo screening caught 70 percent of the ovary cancers in their late stages, when effective therapy options are limited.

Knowing this screening limitation means the search has intensified for a better way to detect ovary cancer, often called the "silent killer," said Edward Partridge, M.D., director of the UAB Comprehensive Cancer Center and the lead study author.

"We still have some comparison data to review, but right now it looks like the positive predictive value of these tests is pretty low," Partridge said.

The study puts the positivity value for both tests at around 1.6 percent per 100 positive screening results, a remarkably low positivity rate that led to a number of false positives, he said. False positives are erroneous signals of cancer where there is none.

The UAB results are published April 1 in the journal Obstetrics & Genecology.........

Posted by: Emily      Read more         Source


March 30, 2009, 5:14 AM CT

Getting down to cancer basics

Getting down to cancer basics
Scientists have identified a new cancer gene - one that is common to a number of cancers and affects the most basic regulation of our genes. The new example - a gene on the X chromosome called UTX - is found in 10% of cases of multiple myeloma and 8% of esophageal cancers.

UTX plays a role in overall regulation of the activity of a number of genes and it is possible that other genes with similar roles will also be found to be involved in different tumor types. This is the first example of mutations in a gene of this functional class. The finding arose from a study of mutations in 4000 genes in kidney cancer.

"UTX is an important component of the transcriptional control machinery - it influences some of the most fundamental mechanisms controlling gene activity in our cells," explains Dr Andy Futreal, co-leader of the Cancer Genome Project at the Wellcome Trust Sanger Institute. "Unlike a number of cancer genes, UTX does not appear to be directly involved in cell division or cell death but in basic gene regulation and shows the depths to which cancers will plumb in order to get themselves ready to go".

The normal UTX protein modifies part of the structure holding DNA together in our cells. The composite DNAprotein structure, called chromatin, is not simply a scaffold, but plays an active role in controlling gene activity. The UTX protein alters a key organising subunit component of chromatin, called a histone. The protein is likely to be involved in both turning genes on and off, making it a key regulator of the yin-yang of gene control.........

Posted by: Janet      Read more         Source


March 30, 2009, 5:07 AM CT

Molecular interplay that moves cancer cells

Molecular interplay that moves cancer cells
Based on research that reveals new insight into mechanisms that allow invasive tumor cells to move, scientists at the Mayo Clinic campus in Florida have a new understanding about how to stop cancer from spreading. A cancer that spreads elsewhere in the body, known as metastasis, is the process that most often leads to death from the disease.

In the March 29 online issue of Nature Cell Biology, scientists say that a molecule known as protein kinase D1 (PKD1) is key to the ability of a tumor cell to "remodel" its structure, enabling it to migrate and invade. The scientists observed that if PKD1 is active, tumor cells cannot move, a finding they say explains why PKD1 is silenced in some invasive cancers.

During metastasis, invasive cancer cells respond to biological signals to move away from a primary tumor. Multiple research groups at Mayo Clinic in Florida are particularly interested in this process. One team, led by cancer biologist Peter Storz, Ph.D., has been investigating a process known as actin remodeling at the leading edge - the most forward point - of these migrating tumor cells.

"The events that reorganize the actin cytoskeleton at the leading edge are complex a multitude of molecules act in concert," Dr. Storz says. "But it appears that PKD1 must be turned off if cancer cells are to migrate".........

Posted by: Janet      Read more         Source



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Cancer
Cancer is a very common disease, approximately one out of every two American men and one out of every three American women will have some type of cancer at some point during the course of their life. Cancer is more common in the elderly and 77 percent of cancers occur in people above age 55 or older. Cancer is also common in children. Cancer incidence is said to have two peaks once during early childhood and then during late years in life. No age period is completely exempted from development of cancers. Some cancers occur predominantly in the elderly, other types occur in children, Cancer occurs in all ethnic races, however the cancer rates and rates of specific cancer types may vary from group to group. Late stages of cancer may be incurable in most cases, but with the advancement of medicine, more and more cancers are becoming curable.

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