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October 9, 2006, 8:47 PM CT

Genome ID Method To Curb Cancer

Genome ID Method To Curb Cancer
A mathematical discovery has extended the reach of a novel genome mapping method to humans, potentially giving cancer biology a faster and more cost-effective tool than traditional DNA sequencing.

A student-led group from the laboratory of Michael Waterman, USC University Professor in molecular and computational biology, has developed an algorithm to handle the massive amounts of data created by a restriction mapping technology known as "optical mapping." Restriction maps provide coordinates on chromosomes analogous to mile markers on freeways.

Lead author Anton Valouev, a recent graduate of Waterman's lab and now a postdoctoral fellow at Stanford University, said the algorithm makes it possible to optically map the human genome.

"It carries tremendous benefits for medical applications, specifically for finding genomic abnormalities," he said.

The algorithm appears in this week's PNAS Early Edition.

Optical mapping was developed at New York University in the late 1990s by David Schwartz, now a professor of chemistry and genetics at the University of Wisconsin-Madison. Schwartz and a collaborator at Wisconsin, Shiguo Zhou, co-authored the PNAS paper.

The power of optical mapping lies in its ability to reveal the size and large-scale structure of a genome. The method uses fluorescence microscopy to image individual DNA molecules that have been divided into orderly fragments by so-called restriction enzymes.........

Posted by: Janet      Permalink         Source


October 9, 2006, 8:29 PM CT

New Way To Treat Colon Cancer?

New Way To Treat Colon Cancer?
Scientists at University of Utah's Huntsman Cancer Institute have discovered a new target for possible future colon cancer therapys a molecule that is implicated in 85 percent of colon cancer cases.

These findings were published online Oct. 6, 2006, in the Journal of Biological Chemistry.

By knocking out that is, genetically disabling a molecule called C-Terminal Binding Protein (CTBP) scientists were able to rescue zebrafish from the effects of a mutation in the adenomatous polyposis coli (APC) gene.

In humans, mutations in this gene long have been known to initiate a series of events that cause colon polyps, which eventually become malignant. APC mutations play a role in 85 percent of colon cancers. The new findings mean CTBP also is involved in that proportion of colon cancers.

In zebrafish, APC mutations keep the intestine from developing properly. "In essence, knocking out CTPB promotes normal development of the intestine in zebrafish carrying an APC mutation," says David A. Jones, a University of Utah associate professor of oncological sciences and leader of the study.

In normal cells of both humans and zebrafish, the APC gene controls the amount of CTBP present by marking it for destruction. In tumor cells with mutated APC, CTPB is not destroyed; instead it accumulates in the cell.........

Posted by: Sue      Permalink         Source


October 9, 2006, 8:24 PM CT

Mechanism Of Cancer-drug Resistance

Mechanism Of Cancer-drug Resistance Dr. Michael Roth, professor of biochemistry, and assistant Iryna Zubovych
Using the worm Caenorhabditis elegans, scientists at UT Southwestern Medical Center have discovered a mechanism by which cancer cells become resistant to a specific class of drugs.

They observed that a mutation in a single protein in the worm renders a potential new cancer drug ineffective. The drug is a derivative of a compound called hemiasterlin. Because hemiasterlin compounds are being tested as a way to fight multi-drug resistance, this newly discovered resistance effect is problematic, the scientists said.

"A major problem for cancer treatment is that if cancer cells can survive long enough, they have a chance to undergo mutations that make them resistant to anticancer drugs," said Dr. Michael Roth, professor of biochemistry and senior author of a paper published this week in the online edition of the Proceedings of the National Academy of Sciences

One way that cancer cells resist multiple drugs is through the action of the multi-drug resistance protein, which pumps most drugs out of the cell before they can have any effect.

However, hemiasterlin bypasses this pump altogether and kills cancer cells by preventing them from dividing.

Derivatives of hemiasterlin are being tested as anti-cancer therapies, with one already in clinical study. The drug works by interfering with tubulin, which forms the structure that separates chromosomes as cells divide.........

Posted by: Janet      Permalink         Source


October 8, 2006, 6:17 PM CT

Breast Reconstruction Not Very Safe For Obese

Breast Reconstruction Not Very Safe For Obese
Significantly obese women may wish to consider delaying breast reconstruction following mastectomy until they achieve a healthier body weight. As per findings presented today at the American Society of Plastic Surgeons (ASPS) Plastic Surgery 2006 conference in San Francisco, women who are significantly obese are at higher risk for complications and have a lower satisfaction rate than do normal and overweight patients.

"Just because someone is overweight doesn't mean they should not be entitled to undergo breast reconstruction after mastectomy," said Elisabeth Beahm, MD, ASPS Member Surgeon, author of the study, and associate professor at M. D. Anderson Cancer Center. "Feeling 'whole' can be an integral part of recovery from cancer, yet significant concerns have been raised about the wisdom of doing breast reconstruction in very obese patients due to a high complication rate.

The current retrospective study observed that patients with a BMI greater than 35 demonstrated significantly increased complication rates for all types of breast reconstruction, from implants to flaps. The complication rate approached 100 percent for morbidly obese patients with a BMI over 40.

"We investigated whether plastic surgeons can safely perform breast reconstruction for these patients or if we would be depriving them reconstruction simply because of empiric concerns for their weight," said Dr. Beahm. "We observed that significantly obese patients, those having a BMI of 35 or higher, had a higher risk for complications. Our experience suggests that in a number of cases it may be more prudent to delay breast reconstruction until the patient has lost weight".........

Posted by: Janet      Permalink         Source


October 5, 2006, 9:57 PM CT

Tumor Suppressor Promoteing Cancer Cell Growth?

Tumor Suppressor Promoteing Cancer Cell Growth?
Scientists have shown that the tumor suppressor gene H-REV107-1 may actually stimulate tumor progression in some non-small cell lung carcinomas. The related report by Nazarenko et al., "H-REV107-1 stimulates growth in non-small cell lung carcinomas via the activation of mitogenic signaling," appears in the recent issue of The American Journal of Pathology.

Tumor suppressor genes function by regulating normal cell growth and proliferation. When a tumor suppressor gene is turned off, by mutation, deletion, or blocked expression, cell growth can proceed without safeguards, contributing to cancer cell proliferation. However, this appears not to be the case in some non-small cell lung carcinomas (NSCLC), in which a tumor suppressor (H-REV107-1) actually promotes cancer cell growth.

Nazarenko et al. found H-REV107-1 expression in a portion of human NSCLC samples examined. When they further characterized this expression in relation to normal lung tissue, H-REV107-1 was found in nonproliferating and proliferating cells in normal lung tissue, localized mainly to the nucleus. In cultured NSCLC cells, however, H-REV107-1 was found in either the cytoplasm or both the cytoplasm and nucleus.

The group then examined whether cellular localization of H-REV107-1 in NSCLC tumor samples is linked with tumor behavior. Strikingly, cytoplasmic localization correlated with decreased patient survival (24 months versus 41 months for nuclear localization). These data suggested that cytoplasmic H-REV107-1 stimulates cell growth. This was then confirmed by suppression of H-REV107-1 RNA, which inhibited cell proliferation, and overexpression of H-REV107-1 protein, which stimulated cell growth pathways and increased proliferation.........

Posted by: Janet      Permalink         Source


October 3, 2006, 10:22 PM CT

New Fodder For The Next Clean Air Fight

New Fodder For The Next Clean Air Fight
New research from researchers at Harvard University measured secondhand tobacco smoke in cars and found pollution levels that are likely hazardous to children.

"The levels were above the threshold for what's considered unhealthy for sensitive groups -- people like children and the elderly -- as determined by the Environmental Protection Agency," said lead study author Vaughan Rees, Ph.D., a research associate at the Harvard School of Public Health.

During 45 driving trials, the scientists strapped a pollution monitor into a child-safety seat, and then asked a smoker-volunteer to light up at different times along the near hour-long route. The road tests were conducted under two different ventilation conditions: all car windows rolled down, then with just the driver's side window cracked about two inches.

"Common sense tells you if you smoke in a pretty confined space, such as a car, without ventilation, there's going to be a lot of secondhand smoke which is potentially dangerous," said Rees.

He added, "Before this study we had no idea what sorts of levels of secondhand smoke were generated. And we had no way of comparing that with other studies that have looked at secondhand smoke levels in other indoor environments like bars and restaurants".........

Posted by: Janet      Permalink         Source


October 3, 2006, 9:54 PM CT

Three Molecular Targets For Leukemia

Three Molecular Targets For Leukemia
he road to better therapy for the most common form of adult leukemia will require blocking multiple molecular pathways that fuel the disease, scientists at The University of Texas M. D. Anderson Cancer Center report in the Oct. 1 edition of the journal Blood.

The research team examined blood and bone marrow samples of 188 adults with acute myelogenous leukemia (AML) and then followed the patients' progress to gauge the cumulative impact of a trio of cell-signaling chain reactions on the disease.

"We observed that the more of these pathways that are active in a patient, the worse their prognosis," says first author Steve Kornblau, M.D., associate professor in the Department of Blood and Marrow Transplantation.

Patients who had none of the three molecular cascades active had a median survival time of 78.6 weeks. For those with one highly active pathway, median survival was 57.9 weeks. With two, it was 42.3 weeks. Patients with high activation of all three pathways had a median survival time of just 23.4 weeks.

"Targeting just one of these pathways won't be effective because we also observed that they cross-activate each other, they essentially cover for each other," Kornblau said. "New therapies will have to target multiple pathways to be effective".........

Posted by: Janet      Permalink         Source


October 3, 2006, 9:46 PM CT

Target For Skin Cancer Treatment

Target For Skin Cancer Treatment
When normal skin cells become a melanoma tumor, they sometimes turn on genes not commonly found in the skin. As per scientists at the University of Virginia Health System, some of these genes are normally active in the male testis at the time sperm are formed.

The genes, called cancer-testis antigens, could be useful targets for drugs that could selectively kill a melanoma tumor, while sparing the rest of the body's tissues. The antigens could also help scientists develop a vaccine to stimulate the immune system to attack and suppress melanoma tumors.

"Researchers are beginning to see patterns in the profile of genes expressed in individual tumor cells," said John C. Herr, Ph.D., professor of cell biology at UVa and a scientist at the UVa Cancer Center. " Patients who express a given cancer-testis antigen may eventually be helped by such selective therapies. This scenario represents one aspect of the growing opportunities envisioned for personalized medicine".

Researchers at the UVa Cancer Center have studied melanoma tumors from patients at various stages of the disease over the last few years. They discovered that more than half of these tumors made the cancer-testis antigens, called SPANX proteins. As per a research findings reported in the Sept. 29, 2006 online edition of the Journal Molecular Human Reproduction, Herr and his UVa research team showed that the SPANX proteins play a role in the formation of the nuclear envelope of the developing human spermatid. The paper can be found online at this link: http://molehr.oxfordjournals.org/cgi/content/abstract/gal079........

Posted by: George      Permalink         Source


October 3, 2006, 5:07 AM CT

Progress In Pancreatic Cancer Research

Progress In Pancreatic Cancer Research
Scientists at SUNY Downstate Medical Center and the Brooklyn VA Hospital have observed that when a human protein, PNC-28, is administered to pancreatic tumor cells in animals, the tumors are destroyed. The research was published in the October 1st edition of the International Journal of Cancer.

Matthew R. Pincus, MD, PhD, professor of pathology at SUNY Downstate and chairman of pathology and laboratory medicine at the Brooklyn VA, said, "The results are very encouraging. PNC-28 may be an effective agent in treating cancers, particularly if delivered directly to the tumor".

PNC-28 is a p53 peptide, a naturally occurring human protein known to suppress tumor growth. The scientists previously observed that PNC-28 induces death of a variety of human tumor cell lines, including a pancreas cancer cell line, while not harming healthy cells.

The research team has now given PNC-28 to laboratory animals to test its ability to block the growth of pancreas cancer cells. When administered over a two-week period in the peritoneal cavities of mice containing simultaneously transplanted tumors, PNC-28 caused complete destruction of these tumors.

When delivered concurrently with tumor implantation, PNC-28 completely blocked tumor growth during the two-week period of administration and two weeks post-treatment, followed by weak tumor growth that leveled off at low tumor sizes.........

Posted by: Sue      Permalink         Source


October 3, 2006, 5:02 AM CT

Obese smokers at higher risk of death

Obese smokers at higher risk of death
People who are both very obese and who smoke increase their risk of death by 3.5 to 5 times that of people of normal weight who never smoke, finds a study in the recent issue of the American Journal of Preventive Medicine.

As per the study, 20 percent of obese adults in the United States smoke, which puts them at a higher risk of death caused by cancer and circulatory disease. The authors further observed that, in general, being a current smoker was a far stronger risk factor for cancer death than being obese.

"Smoking has been known as a very strong risk factor for a number of cancers, especially lung cancer, which is the most common site of cancer death," said lead author D. Michal Freedman, Ph.D., of the Division of Cancer Epidemiology and Genetics at the National Cancer Institute.

The study surveyed more than 80,000 current and former radiologic technologists between the ages of 22 and 92 who completed a self-administered questionnaire in the period from 1983 to 1989. They all were followed through December 2002 and the number of deaths was reported.

The questionnaire collected information such as birth date, height, weight and smoking behavior. Participants' body mass indexes were calculated from their weight and height A BMI of 30 to 34.9 was considered obese, and more than 35 was very obese.........

Posted by: Janet      Permalink         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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