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December 16, 2008, 9:34 PM CT

Pre-existing diabetes for persons diagnosed with cancer

Pre-existing diabetes for persons diagnosed with cancer
Patients with diabetes at the time of a cancer diagnosis have an increased risk of death in comparison to patients without diabetes, as per a meta-analysis of studies published in the December 17 issue of JAMA

Approximately 20 million Americans have diabetes mellitus, which is about 7 percent of the U.S. adult population. Diabetes mellitus appears to be a risk factor for some cancers, but the effect of pre-existing diabetes on all-cause death in newly diagnosed cancer patients is less clear, as per background information in the article.

Bethany B. Barone, Sc.M., of the Johns Hopkins Bloomberg School of Public Health, Baltimore, and his colleagues conducted a meta-analysis to examine the association of pre-existing diabetes with long-term, all-cause death in cancer patients. The scientists identified 48 articles that met criteria for the study, including 23 articles for which data could be included in the meta-analysis.

The meta-analysis (of these 23 studies) indicated that pre-existing diabetes was linked to an increase in all-cause death following cancer diagnosis, compared with individuals with normal glucose levels, across all cancer types. Additional analyses by type of cancer showed that pre-existing diabetes was significantly linked to increased long-term, all-cause death for cancers of the endometrium, breast, and colorectum. Diabetes was linked to a nonsignificant increase in risk in prostate, gastric, hepatocellular, lung and pancreas cancer.........

Posted by: Andria      Read more         Source


December 11, 2008, 5:13 AM CT

Fluorescence Tomography Of Tumors In Living Animals

Fluorescence Tomography Of Tumors In Living Animals
Vasilis Ntziachristos. Foto: TUM
Fluorescent molecules - i.e. substances which can be stimulated to emit light - are extremely valuable tools in biological research and medical diagnosis. Fluorescence can be used for instance to analyze the regulation and expression of genes, to locate proteins in cells and tissues, to follow metabolic pathways and to study the location and migration of cells. Of particular importance is the combination of fluorescence imaging with novel techniques that allow tomographic three-dimensional visualization of objects in living organisms. At the Helmholtz Zentrum München - German Research Center for Environmental Health together with the Technische Universität München an own institute is concerned with the development and refinement of such new technologies: the Institute for Biological and Medical Imaging headed by Professor Vasilis Ntziachristos.

The quality of optical imaging in tissues is naturally limited, since beyond a penetration depth of a few hundred micrometers the photons are massively scattered due to interactions with cell membranes and organelles which results in blurred images. In the latest issue of the journal Proceedings of the National Academy of Sciences Prof. Ntziachristos and his team, together with colleagues from the Harvard Medical School and the Massachusetts General Hospital in Boston, USA, report on the use of the so-called early arriving photons together with tomographic principles. Early photons are the first photons that arrive onto a photon detector after illumination of tissue by an ultra-short photon pulse and undergo less scattering compared to photons arriving at later times. In comparison to continuous illumination measurements a combination of these less scattered photons with 360-degree illumination-detection resulted in sharper and more accurate images of mice under investigation.........

Posted by: Andria      Read more         Source


December 9, 2008, 10:16 PM CT

Selenium, vitamin E do not prevent prostate cancer

Selenium, vitamin E do not prevent prostate cancer
Scott M. Lippman, M.D., is professor and chair of Thoracic/Head and Neck Medical Oncology at M. D. Anderson.
Findings from one of the largest cancer chemoprevention trials ever conducted have concluded that selenium and vitamin E taken alone or in combination for an average of five and a half years did not prevent prostate cancer, as per a team of scientists coordinated by the Southwest Oncology Group (SWOG) and led by researchers at The University of Texas M. D. Anderson Cancer Center and Cleveland Clinic.

Data and analysis gathered through Oct. 23, 2008, from the Selenium and Vitamin E Cancer Prevention Trial (SELECT) were reported in the Dec. 9 issue of the Journal of the American Medical Association (JAMA) by Scott M. Lippman, M.D., professor and chair of Thoracic/Head and Neck Medical Oncology at M. D. Anderson, Eric A. Klein, M.D., of the Cleveland Clinic Lerner College of Medicine, and 30 coauthors from the United States, Puerto Rico and Canada.

Funded by the National Cancer Institute (NCI) with some additional contribution from the National Center for Complementary and Alternative Medicine, the Phase III trial began recruitment in August 2001 and aimed to determine whether selenium, vitamin E, or both could prevent prostate cancer and other diseases in relatively healthy men. The study followed 35,533 participants from 427 sites in the United States, Canada and Puerto Rico. The randomized, placebo-controlled and double-blind trial divided the participants into four intervention groups: selenium, vitamin E, both selenium and vitamin E, and placebos.........

Posted by: Andria      Read more         Source


December 1, 2008, 6:12 PM CT

European ancestry increases breast cancer risk

European ancestry increases breast cancer risk
Latina women have a lower risk of breast cancer than European or African-American women generally, but those with higher European ancestry could be at increased risk, as per data reported in the December 1 issue of Cancer Research, a journal of the American Association for Cancer Research.

"We need to study the possible factors that are placing Latina women of high European ancestry at greater risk," said Laura Fejerman, Ph.D., a post-doctoral research fellow at the University of California San Francisco. "The increased risk could be due to environmental factors, genetic factors or the interplay of the two".

Latinas are what geneticists refer to as an "admixed" population with most of their genetic ancestry from European or indigenous Americans. Fejerman said the term "indigenous Americans" commonly refers to the groups that lived on the American continent previous to the arrival of the European colonizers.

For the current study, Fejerman and his colleagues identified the genetic ancestry of 440 Latina women with breast cancer and 597 Latina women who did not have breast cancer.

For every 25 percent increase in European ancestry there is a 79 percent increase in the risk of breast cancer. If a woman had an estimated European ancestry of 25 percent she would be 79 percent more likely to have breast cancer than a woman of full indigenous American ancestry.........

Posted by: Andria      Read more         Source


December 1, 2008, 6:07 PM CT

Prostate cancer spurs new nerves

Prostate cancer spurs new nerves
Prostate cancer and perhaps other cancers promotes the growth of new nerves and the branching axons that carry their messages, a finding linked to more aggressive tumors, said scientists from Baylor College of Medicine in the first report of the phenomenon that appears today in the journal Clinical Cancer Research

Prior research showed that prostate cancer follows the growth of nerves, but this is the first time that researchers have demonstrated that the tumors actually promote nerve growth.

"This is the first report of this phenomenon," said Dr. Gustavo Ayala, professor of pathology and urology at BCM and first author of the article. "It represents an important new target in prostate cancer therapy, as prostate cancers are more aggressive when neurogenesis is present".

Ayala noted that this finding is comparable to the discovery of angiogenesis or the growth of new blood vessels. Both are part of the wound repair process.

"We also think that axongenesis and neurogenesis is found not only in prostate cancer, but is potentially a more global phenomenon, especially relating to those cancers that grow along nerve paths," said Ayala, also a researcher in the Dan L. Duncan Cancer Center at BCM.

Ayala and colleagues studied the neurogenesis in tissue culture, in human tissues of patients who had had prostate cancer and in comparison to prostate tissues from patients who had died of other ailments. They calculated the density of nerves in human prostate tissues, including those with prostate cancer. They observed that nerve density was considerably higher in prostate cancer patients and in premalignant lesions. As part of the study, he used an entire prostate gland to reconstruct the prostate and enable researchers to see the growth of nerves and axons in three-dimensions, a computerized process that took substantial continuous computer processing.........

Posted by: Andria      Read more         Source


November 24, 2008, 9:33 PM CT

Potential new drug target for chronic leukemia

Potential new drug target for chronic leukemia
Scientists at the University of California, San Diego (UCSD) and the Moores UCSD Cancer Center have discovered what could be a novel drug target for an often difficult-to-treat form of leukemia. The researchers have identified a unique "signature" or pattern of a specific family of enzymes in patients with chronic lymphocytic leukemia (CLL), the most common form of adult leukemia.

Paul Insel, M.D., professor of pharmacology and medicine at the UC San Diego School of Medicine and his co-workers compared white blood cells in patients with CLL to those of healthy adults. They observed that one form of the group of enzymes, collectively known as cyclic nucleotide phosphodiesterases, was 10 times higher in CLL patients than in normal individuals. The specific type of enzyme, phosphodiesterase 7B (PDE7B), controls the levels of cyclic AMP (cAMP), a molecule that can promote programmed cell death, a process that is defective in CLL. The team reports its findings this week in the Proceedings of the National Academy of Sciences

Typically whereas most cancers have out-of-control cell growth, cll is characterized by an overabundance of white blood cells that do not die when they should, Insel explained.

The researchers subsequently tested the effects of drugs that blocked PDE7B in CLL cells, and observed that this raised cAMP levels and caused CLL cells to undergo cell death. He explained that since PDE7B degrades cAMP, blocking PDE7B in essence takes the clamp off of programmed cell death, enabling CLL cells to die.........

Posted by: Andria      Read more         Source


November 24, 2008, 9:28 PM CT

Suppressing prostate cancer development

Suppressing prostate cancer development
Scientists at the University of Southern California (USC) have observed that inactivating a specific biomarker for aggressive prostate cancer blocks the development of prostate cancer in animal models.

Scientists say the upcoming study in the Proceedings of the National Academy of Sciencesnow available onlinemay lead to a novel cancer treatment for humans.

"This research has far-reaching implications in a wide range for human cancers," says Amy Lee, Ph.D., the study's principal investigator and the associate director for basic research and holder of the Freeman Cosmetics Chair at the USC/Norris Comprehensive Cancer Center, and professor of biochemistry and molecular biology at the Keck School of Medicine of USC. "It is a breakthrough study." .

Prostate cancer is the most common cancer in men and develops through successive stages. The glucose-regulated protein GRP78 has been identified as a crucial entity in the development of prostate cancer by promoting cancer cell proliferation, mediating oncogenic signaling and protecting cancer cells against cell death resulting from the stress of tumor development, Lee explains. By suppressing GRP78 expression or activity, the USC scientists observed that they could block prostate cancer activation and development resulting from the loss of PTEN, a powerful tumor suppressor gene for many human cancers.........

Posted by: Andria      Read more         Source


November 18, 2008, 5:28 AM CT

Role of vitamin D in cancer therapy

Role of vitamin D in cancer therapy
A colon cancer cell isn't a lost cause. Vitamin D can tame the rogue cell by adjusting everything from its gene expression to its cytoskeleton. In the Nov. 17 issue of the Journal of Cell Biology, Ordez-Morn et al. show that one pathway governs the vitamin's diverse effects. The results help clarify the actions of a molecule that is undergoing clinical trials as a cancer treatment.

Vitamin D stymies colon cancer cells in two ways. It switches on genes such as the one that encodes E-cadherin, a component of the adherens junctions that anchor cells in epithelial layers. The vitamin also induces effects on the cytoskeleton that are mandatory for gene regulation and short-circuiting the Wnt/b-catenin pathway, which is overactive in most colon tumors. The net result is to curb division and prod colon cancer cells to differentiate into epithelial cells that settle down instead of spreading.

To delve into the mechanism, the team dosed colon cancer cells with calcitriol, the metabolically active version of vitamin D. Calcitriol triggered a surge of calcium into the cells and the subsequent switching on of RhoARhoGTPases, which have been implicated in the cytoskeletal changes induced by vitamin D. The activated RhoA in turn switched on one of its targets, the rho-associated coiled kinase (ROCK), which then roused two other kinases. Each step in this nongenomic pathway was necessary to spur the genomic responses, the scientists showed. The team also nailed down the contribution of the vitamin D receptor (VDR). The receptor was crucial at the beginning of the pathway, where it permitted the calcium influx, and at the end, where it activated and repressed genes.........

Posted by: Andria      Read more         Source


October 29, 2008, 10:07 PM CT

If the diabetes has a direct carcinogenetic effect?

If the diabetes has a direct carcinogenetic effect?
The association of DM2 with solid tumors, and especially with HCC, has been long suspected and several studies have reported increased mortality rates for neoplastic diseases in patients with DM2. However, the temporal relationship between onset of diabetes and development of HCC, and the clinical and metabolic characteristics of patients with DM2 and HCC have not been well examined.

A research article would be published on October 7, 2008 in the World Journal of Gastroenterology addresses this question. The research team led by Dr. Valter Donadon from Pordenone Hospital of Italy investigated the relationships between DM2 and risk of HCC in a large population based case-control study. They enrolled 465 consecutive patients with HCC compared with an age and sex matched control group of 490 subjects.

Their results confirm that patients with DM2 have a significantly increased risk of HCC, independent of cofactors such as HBV and HCV infection and alcohol intake, and demonstrate that DM2 pre-exists to the development of HCC in most cases, suggesting that DM2 is more likely a concourse rather than merely a consequence of the liver tumor. This conclusion is also supported by the finding of a similar frequency and severity of DM2 in patients with small HCC detected during follow-up of cirrhosis and in those with more advanced and diffuse cancers detected outside of a surveillance program. The observation that patients with DM2, especially males, treated with insulin had an increased frequency of HCC is intriguing and clinically relevant. These patients are those often showing the highest insulin blood levels, and this might contribute to facilitate the development of HCC.........

Posted by: Andria      Read more         Source


October 15, 2008, 5:23 PM CT

Scientists close in on method to fight deadly childhood cancer

Scientists close in on method to fight deadly childhood cancer
A multicenter team of researchers, including researchers from the University of Florida, has discovered a way to potentially block the growth of neuroblastoma, a type of cancer responsible for 15 percent of all cancer deaths in children.

Working with human cell lines and tissue samples, scientists describe in Thursday's (Oct. 16, 2008) online issue of Nature how they were able to short-circuit genetic processes that apparently contribute to neuroblastomas tumors that arise from the developing nervous system in children and often appear in the abdomen, chest or neck.

Concentrating on a gene known as ALK, the researchers used a small-molecule inhibitor a technique common to a number of drugs to block abnormalities that apparently cause neuroblastomas.

Neuroblastomas are extremely rare, appearing in about 600 patients annually in the United States, as per the National Institutes of Health. About half of the patients with neuroblastoma are diagnosed before the age of 18 months. In 40 percent of cases, the cancer has spread to other parts of the body by the time doctors discover it.

Treatment commonly involves surgery, chemotherapy and radiation, and transplantation for high-risk patients.

"We need to find a home run for these kids," said Wendy B. London, Ph.D., a research associate professor of epidemiology, biostatistics and health policy research at the UF College of Medicine and a member of the UF Shands Cancer Center. "A targeted treatment to treat patients with ALK mutations would be a real breakthrough".........

Posted by: Andria      Read more         Source


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