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duminică, 5 august 2012

Researchers Develop First Potential Medicine For Patients With Most Severe Form Of Congenital Hyperinsulinism

A pilot study in adolescents and adults has found that an investigational drug shows promise as the first potential medical treatment for children with the severest type of congenital hyperinsulinism, a rare but potentially devastating disease in which gene mutations cause insulin levels to become dangerously high.

"There is currently no effective medicine for children with the most common and most severe form of hyperinsulinism," said study leader Diva D. De Leon, M.D., a pediatric endocrinologist at The Children's Hospital of Philadelphia. "Our new research shows that this investigational drug, a peptide called exendin-(9-39), controls blood sugar levels in people, a very promising result."

The study appears online ahead of print in the journal Diabetes.

In congenital hyperinsulinism (HI), mutations disrupt the insulin-secreting beta cells in the pancreas. Uncontrolled, excessive insulin levels thus sharply reduce blood glucose levels, a condition called hypoglycemia. If untreated, hypoglycemia may cause irreversible brain damage or death in children. Congenital HI occurs in an estimated one in 50,000 U.S. children, with a higher incidence among Ashkenazic Jews and certain other groups.

The standard treatment for some forms of congenital HI is diazoxide, a drug that controls insulin secretion by opening potassium channels in beta cells. However, this drug does not work in the most common types of HI, in which mutations prevent these potassium channels from forming.

When abnormal beta cells occur only in a discrete portion of the pancreas, precise surgery on the tiny organ can remove the lesion and cure HI. The Congenital Hyperinsulinism Center at The Children's Hospital of Philadelphia is a world leader in diagnosing such lesions and performing the curative surgery on newborns.

However, in roughly half of congenital HI cases, abnormal cells are diffused through the pancreas, and surgeons must remove nearly the entire pancreas. This leaves the majority of patients at high risk of developing diabetes.

The current study, which builds on previous research by De Leon and colleagues in animals, uses exendin-(9-39), which blocks the action of a hormone receptor, glucagon-like peptide-1 (GLP-1), in beta cells. The GLP-1 receptor is currently the target of drugs that treat diabetes, using the opposite effect from that investigated in this HI study.

The current pilot study included nine subjects, aged 15 to 47 years old, who had hyperinsulinism caused by mutations in potassium channels. None were being treated for HI at the time of the study, but all were at risk of hypoglycemia during periods of fasting.

In all nine subjects, the drug controlled blood glucose levels during fasting. Exendin also controlled insulin secretion in cell studies of beta cells taken from newborns with HI. The current research did not focus on the biological mechanisms that occurred, but De Leon said the results are encouraging enough to progress to a clinical study in children with HI over the next year.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our diabetes section for the latest news on this subject. Financial support for this study came from the National Institutes of Health (grant 1R03DK07835), the Lester and Liesel Baker Foundation, and the Clifford and Katherine Goldsmith Foundation. De Leon's co-authors, all from Children's Hospital, were Charles A. Stanley, M.D., Andrew C. Calabria, M.D., Changhong Li, M.D., and Paul R. Gallagher In addition to their positions at Children's Hospital, De Leon, Stanley and Li also are in the Perelman School of Medicine at the University of Pennsylvania.
"The GLP-1 Receptor Antagonist Exendin-(9-39) Elevates Blood Fasting Glucose Levels in Congenital Hyperinsulinism due to Inactivating Mutations in the ATP-sensitive Potassium Channel," Diabetes, published online Aug.1, 2012, to appear in print, October 2012. doi: 10.2337/db12-0166.
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marți, 13 decembrie 2011

How Do BRCA1 Mutations Harm Breast Cells? Researchers Demonstrate

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Academic Journal
Main Category: Breast Cancer
Also Included In: Cancer / Oncology; Genetics
Article Date: 13 Dec 2011 - 9:00 PST

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Researchers at the Johns Hopkins Kimmel Cancer Center have demonstrated during their work with breast cells that breast cells become vulnerable to cancer if a single copy of the breast cancer gene BRCA1 is inactivated. It causes genetic instability in the cells through reducing their ability to repair DNA damage.

The leading risk factor for hereditary breast cancer is an inherited mutation in the BRCA1 gene which requires close monitoring or prompt preventive mastectomy.

The breakthroughs might help researchers develop a drug that prevents hereditary breast cancer, as well as tools to identify those who benefit most from prophylactic treatments. The study is published in the Proceedings of the National Academy of Sciences Oct. 25.

Exactly how BRCA1 inactivation increases the risk of cancer has remained a mystery. BRCA1 is believed to be a "tumor suppressor" gene. Usually, cancer is not caused by the loss of one copy of such genes, as each individual is born with two copies of each gene (one from each parent), and the second copy is sufficient in keeping cells healthy in a similar way that a car can stop safely after losing control of the front brakes as the rear brakes are still working.

According to the researchers, cancer seems to develop in such cases only after the second copy of the gene is damaged, i.e. random mutation during cell division, resulting in uncontrolled cell growth.

Mouse models of BRCA-related cancers have demonstrated that damage to genes, such as TP53, occurred prior to damage to the second copy of BRCA.

Ben Ho Park, M.D., Ph.D., associate professor of oncology at the Johns Hopkins Kimmel Cancer Center, explained:

"In theory, this process would take a long time and BRCA-related breast cancers
occur at an early age."

For the investigation, the team used novel technology in order to insert a single copy of a typical BRCA1 mutation into normal breast cells.

The main theory has been that the original inactivation of a single copy of BRCA1 produces additional DNA mutations to expand more rapidly than normal - a condition called "genomic instability."

Park explains:

"The protein coded by BRCA1 is involved in repairing major DNA breaks, so it would make sense that its inactivation could weaken a cell's resistance to DNA mutations."

However, Park adds that the consequence of losing a single copy of BRCA1 was hard to model and difficult to investigate. Results from prior attempts to produce mice with single-copy BRCA1 mutations were uncertain as the mice were unable to demonstrate the pattern of human cancers. Furthermore, it has been hard for investigators to create human cell lines in which the only flaw is a single mutated copy of BRCA1.

In order to test their theory, the team first selected cell lines obtained from non-cancerous human breast epithelial cells - where BRCA1 breast cancers originate. An advanced gene-targeting method was then used to generate novel cell lines that have a typical cancer-associated BRCA1 mutation in just one copy of the gene.

? Following this, tests were conducted on both cell types - cells with the BRCA1 mutation, and the original cells with two healthy copies of BRCA1 - to compare their DNA repair activity. The team demonstrated that cells with BRCA1 mutations were not as effective at carrying out the type of DNA repair known to involve the BRCA1 protein.

They found that when exposed to a DNA-damaging chemotherapy medication or radiation the BRCA1-mutated cells were more likely to die. In addition, BRCA1-mutated cells that were allowed to divide for many weeks were more likely to lose additional genes, includes those frequently mutated in breast tumors. Similar genetic losses were observed on non-cancerous breast cells taken from women with BRCA1 mutations.

Park said:

"What this shows is that having only a single working copy of BRCA1 really does bring about changes in a cell that would be expected to give rise to cancer.
We hope to use this new system to introduce other known BRCA1 mutations, to get a better idea of the relative cancer risk each individual mutation represents, because right now there are few good ways to do that. In the future, we hope to further define risk so that family members with one type of BRCA1 mutation may be advised to get preventative treatment or surgery, and those with other BRCA1 mutations could rely on careful screening."

In addition, the cell models might be helpful in determining the susceptibility of various BRCA1 mutations to drugs, Park adds. At present, anti-cancer medications known as PARP inhibitors are in clinical trials against tumors with BRCA1-mutations.

The lifetime risks of developing breast cancer has been shown among women born with a mutated copy of BRCA1 to range between 50% to 90%. In addition, they have high, but variable risks of ovarian and other cancers.

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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Researchers Identify Genetic Mutation Responsible For Most Cases Of Waldenstrom's Macroglobulinemia

Main Category: Lymphoma / Leukemia / Myeloma
Also Included In: Genetics
Article Date: 13 Dec 2011 - 1:00 PST

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Scientists at Dana-Farber Cancer Institute have identified a gene mutation that underlies the vast majority of cases of Waldenstrom's macroglobulinemia, a rare form of lymphoma that has eluded all previous efforts to find a genetic cause.

The research (abstracts 261, 300, 434 and 597), to be presented at the American Society of Hematology's 2011 annual meeting on Monday, Dec. 12 at 2:45 p.m. PST, points to an error in a single digit of DNA one of three billion letters in the human genetic code as the leading culprit in Waldenstrom's, and a prime target for new therapies against the disease. The discovery was made by sequencing the genome of tumor cells in Waldenstrom's patients, ¬ reading the cells' DNA letter by letter and seeing where it differed from that of the patients' normal cells.

"We found that tumor cells in 90 percent of the patients we tested contained a single point mutation, an error in one of the bases that make up the 'rungs' of the DNA helix," says Steven Treon, MD, PhD, who led the research with his Dana-Farber colleague Zachary Hunter. "In subsequent experiments, when we treated the tumor cells with drugs that target the pathway activated by the mutated gene, the cells underwent apoptosis, or programmed cell death. These results suggest that new, effective treatments that target the tumor cells directly are now possible for people with the disease."

Waldenstrom's macroglobulinemia is a slow-growing form of non-Hodgkin lymphoma that originates in white blood cells known as B lymphocytes. When abnormal B cells begin to multiply out of control, they produce excessive amounts of a protein called monoclonal immunoglobulin, which causes the blood to thicken and flow less smoothly.

In some patients, the disease produces no major symptoms; in others, problems can include weakness, fatigue, excessive bleeding, and weight loss. In severe cases, vision and neurological problems can occur. Approximately 2,000 to 3,000 people are diagnosed with Waldenstrom's each year in the United States; it is more common in men than women, more prevalent in people of Ashkenazi (Eastern European Jewish) descent, and arises more often in older people than young.

Although there isn't a cure for Waldenstrom's, treatments include drugs such as rituximab, bortezamib, and bendamustine. High-dose chemotherapy with autologous stem cell transplantation is infrequently also used.

Since the disease was first described 70 years ago, all previous efforts to track down a genetic cause have been fruitless, Treon remarks. For the current research, Treon and his colleagues conducted whole genome sequencing of tumor cells and normal cells from 30 patients with Waldenstrom's. In collaboration with Complete Genomics of Mountain View, Calif., researchers "lined up" the sequences of the tumor and non-tumor cells to identify differences. Ninety percent of the tumor cells had a point mutation in the gene MYD88.

"The mutation causes the cells to produce a distorted protein, which switches on the IRAK complex pathway, leading to activation of NF-kB, a protein that is essential for the growth and survival of Waldenstrom's tumor cells," Treon comments. "When we shut down the pathway by blocking the abnormal protein with drug molecules, the tumor cells entered apoptosis." Equally important, the tested molecules had no adverse effect on normal cells.

The discovery of a genetic signature for Waldenstrom's will enable doctors to definitively determine which patients have the disease and not a similar condition such as other forms of lymphoma or multiple myeloma, Treon says. Drugs that block the abnormal protein or other proteins in the NF-kB pathway could, theoretically, short-circuit the disease process in many patients. Some of these drugs already exist, having been developed for other conditions. Treon and his colleagues are currently working to develop others and are testing them in experimental models.

Funding for the research was provided by the International Waldenstrom's Macroglobulinemia Foundation and the Bing family.

Article adapted by Medical News Today from original press release. Source: Dana-Farber Cancer Institute
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Researchers Say Scar Findings Could Lead To New Therapies

Main Category: Dermatology
Also Included In: Immune System / Vaccines
Article Date: 13 Dec 2011 - 0:00 PST

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Researchers at the Stanford University School of Medicine report that they have identified the molecular pathway through which physical force contributes to scarring in mice.

"Our study exposes one of the fundamental mechanisms by which the mechanical environment can directly increase inflammation, which is strongly implicated in scarring," said Geoffrey Gurtner, MD, professor and associate chair of surgery.

Mice genetically engineered to lack an enzyme that is activated by mechanical force demonstrated less inflammation and fibrosis - the formation of excess fibrous connective tissue - in their incisions than mice in a control group, the study found. Inflammation and scar formation also were reduced among mice injected with an organic compound, a small molecule called PF-573228, that blocks this enzyme, which helps cells sense changes in the mechanical environment.

While further testing is needed to determine the validity of the findings in humans, the researchers say they hope their work will pave the way for new treatments of fibrotic diseases - disorders caused by excess scarring, such as pulmonary fibrosis (the buildup of scar tissue in the lungs) - as well as inflammatory diseases, such as rheumatoid arthritis.

The study was published online in Nature Medicine. Gurtner is the senior author. The lead author is postdoctoral scholar Victor Wong, MD.

Inflammation, an important part of healing, occurs when white blood cells and the chemicals they release try to kill bacteria and eat up damaged tissue at the site of an injury. However, inflammation is also linked to scarring. Excessive scarring is known as fibrosis. And while there are chemical mechanisms that lead to inflammation, mechanical forces generally have been overlooked as a key stimulator of this biological response and as a possible therapeutic target, the researchers say. An example of such a force would be the pulling on an incision when a patient moves; it's the reason stitches are sometimes needed.

"We just haven't taken the physical environment - the environment of mechanical forces that hold all our cells together - seriously enough as a source of inflammation and fibrosis," Gurtner said.

Previous studies have implicated the enzyme, known as focal adhesion kinase, in cellular responses to force, but whether it played a role in inflammation and scarring remained unclear. When the researchers had it genetically engineered out of mice for the current study, incisions in those mice healed normally but scarring was markedly diminished. Ten days after the mice sustained a skin incision, 48 percent fewer scar-tissue cells had formed around it compared with incisions in a control group, according to the study.

The researchers found that the enzyme appears to modulate protein molecules often used by cells to communicate with one another. In test tube studies, mouse scar tissue missing the enzyme did not respond normally to mechanical stimuli and released far lower levels of inflammatory mediators.

The researchers also tested the effects of the enzyme-inhibiting molecule (PF-573228) on human cells that play a key role in wound healing and found that the molecules that stimulate inflammation were not released.

Tests on humans are needed before researchers can evaluate whether this approach could serve as the basis for a valid therapy. The researchers said they hope their findings can eventually be used to develop treatments for diseases that involve excess scarring throughout the body. "These results suggest that targeted strategies to uncouple mechanical force from inflammation and fibrosis may prove clinically successful across diverse organ systems," they concluded.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our dermatology section for the latest news on this subject. Other Stanford co-authors were Michael Longaker, MD, MBA, the Deane P. and Louise Mitchell Professor at the School of Medicine; Satoshi Akaishi, MD, a visiting surgeon from Japan; postdoctoral fellows Michael Sorkin, MD, Kemal Levi, MD, and Jason Glotzbach, MD; bioinformatics student Michael Januszyk, MD; and medical students Emily Nelson, Kristine Rustad, Josemaria Paterno and Ivan Vial.
The study was funded by grants from the Armed Forces Institute of Regenerative Medicine and the Oak Foundation. Information about Stanford's Department of Surgery, which also supported the work, is available at http://surgery.stanford.edu.
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duminică, 11 decembrie 2011

Researchers Design Alzheimer's Antibodies

Main Category: Alzheimer's / Dementia
Article Date: 10 Dec 2011 - 1:00 PST

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Researchers at Rensselaer Polytechnic Institute have developed a new method to design antibodies aimed at combating disease. The surprisingly simple process was used to make antibodies that neutralize the harmful protein particles that lead to Alzheimer's disease.

The process is reported in the Dec. 5 Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS). The process, outlined in the paper, titled "Structure-based design of conformation- and sequence-specific antibodies against amyloid ß," could be used as a tool to understand complex disease pathology and develop new antibody-based drugs in the future.

Antibodies are large proteins produced by the immune system to combat infection and disease. They are comprised of a large Y-shaped protein topped with small peptide loops. These loops bind to harmful invaders in the body, such as a viruses or bacteria. Once an antibody is bound to its target, the immune system sends cells to destroy the invader. Finding the right antibody can determine the difference between death and recovery.

Scientists have long sought methods for designing antibodies to combat specific ailments. However, the incredible complexity of designing antibodies that only attached to a target molecule of interest has prevented scientists from realizing this ambitious goal.

When trying to design an antibody, the arrangement and sequence of the antibody loops is of utmost importance. Only a very specific combination of antibody loops will bind to and neutralize each target. And with billions of different possible loop arrangements and sequences, it is seemingly impossible to predict which antibody loops will bind to a specific target molecule.

The new antibody design process was used to create antibodies that target a devastating molecule in the body: the Alzheimer's protein. The research, which was led by Assistant Professor of Chemical and Biological Engineering Peter Tessier, uses the same molecular interactions that cause the Alzheimer's proteins to stick together and form the toxic particles that are a hallmark of the disease.

"We are actually exploiting the same protein interactions that cause the disease in the brain to mediate binding of antibodies to toxic Alzheimer's protein particles," Tessier said.

Alzheimer's disease is due to a specific protein the Alzheimer's protein sticking together to form protein particles. These particles then damage the normal, healthy functions of the brain. The formation of similar toxic protein particles is central to diseases such as Parkinson's and mad cow disease.

Importantly, the new Alzheimer's antibodies developed by Tessier and his colleagues only latched on to the harmful clumped proteins and not the harmless monomers or single peptides that are not associated with disease.

Tessier and his colleagues see the potential for their technique being used to target and better understand similar types of protein particles in disorders such as Parkinson's disease.

"By binding to specific portions of the toxic protein, we could test hypotheses about how to prevent or reverse cellular toxicity linked to Alzheimer's disease," Tessier said.

In the long term, as scientists learn more about methods to deliver drugs into the extremely well-protected brain tissue, the new antibody research may also help to develop new drugs to combat disorders such as Alzheimer's disease.

The research was funded by the Alzheimer's Association, the National Science Foundation (NSF), and the Pew Charitable Trust.

Article adapted by Medical News Today from original press release. Source: Rensselaer Polytechnic Institute
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vineri, 9 decembrie 2011

Researchers Find Smoking Is Strongly Associated With Squamous Cell Carcinoma Among Women

Main Category: Women's Health / Gynecology
Also Included In: Cancer / Oncology
Article Date: 09 Dec 2011 - 2:00 PST

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Women who have non-melanoma skin cancers are more likely to have smoked cigarettes compared to women without skin cancer, said researchers at Moffitt Cancer Center in Tampa, Fla., who published study results in a recent issue of Cancer Causes Control.

The study investigated the relationship between cigarette smoking and non-melanoma skin cancers, including basal cell carcinoma (BCC) and squamous cell carcinomas (SCC). Smoking histories were assessed and compared between patients diagnosed with BCC and/or SCC, and a group of controls comprised of patients who were screened for skin cancers, but who were not diagnosed with and had no history of skin cancer.

The study's 698 participants were recruited through Moffitt's Lifetime Screening and Prevention Center and the University of South Florida's Dermatology and Family Medicine Clinics. Participants were asked about their smoking behaviors in terms of years smoked, how many cigarettes per day they smoked, and when those who once smoked quit smoking. The results were stratified by sex.

Study results showed that cigarette smoking was associated with non-melanoma skin cancer overall, and that the risk increased with numbers of cigarettes per day, total years of smoking, and pack-years smoked. Associations were particularly strong for SCC, with SCC being more than two times as likely in those who have smoked for 20 or more years compared to controls.

"Among men, positive associations with smoking of equal magnitude were observed for BCC and SCC, although none of the associations were statistically significant," said Dana E. Rollison, Ph.D., study lead author and an associate member in the Moffitt Department of Cancer Epidemiology. "However, among women, smoking was not associated with BCC, while highly statistically significant associations were observed with SCC. Women with SCC were almost four times more likely than controls to have smoked for 20 or more years."

The researchers concluded that:

Cigarette smoking was associated with non-melanoma skin cancer, and the risk increased with increasing dose (cigarettes per day) and number of years smoked.

Among men, smoking was modestly associated with BCC and SCC.

Among women, smoking was strongly associated with SCC, but not BCC.

Why women smokers should be more likely than men to be diagnosed with SCC is not clear, said the researchers.

"Observations from the lung cancer literature may provide possible explanations for why smoking was a higher risk factor for SCC in women," wrote Rollison and co-authoring colleagues both at Moffitt and across USF's College of Medicine. "Female current smokers have higher lung cancer risks than men. Women have been shown to have more active CYP enzyme activity in the lung, where CYP is responsible for metabolizing 70-80 percent of nicotine. In addition, the up-regulation of CYP by estrogen may play a role."

Also, women have been shown to have higher levels of DNA adducts and lower levels of DNA repair in the lung as compared to men, said Rollison.

"Further study is needed to shed more light on the sex-based differences and the role of smoking in non-melanoma skin cancers," concluded Rollison.

Article adapted by Medical News Today from original press release. Source: Moffitt Cancer Center
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joi, 8 decembrie 2011

Researchers Link 'Epigenetic' Changes To Inflammation-Induced Colon Cancer

Main Category: Colorectal Cancer
Article Date: 08 Dec 2011 - 3:00 PST

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Johns Hopkins Kimmel Cancer Center scientists report that sharp rises in levels of reactive oxygen molecules, and the inflammation that results, trigger biochemical changes that silence genes in a pattern often seen in cancer cells. The researchers confirmed this gene-silencing effect in mice that develop inflammation-induced colon cancer.

The study, reported Nov. 14 in Cancer Cell, is believed to be the first to identify a specific molecular mechanism linking inflammation to cancer epigenetics. Epigenetic changes alter the usual patterns of gene expression in cells and typically cause the silencing of tumor-suppressor genes.

"Our finding could explain why epigenetic changes are found in cancer cells and one important reason inflammation is so frequently linked to cancer," says Stephen Baylin, M.D., the Virginia and D.K. Ludwig Professor for Cancer Research and deputy director of the Johns Hopkins Kimmel Cancer Center.

In the past several years, researchers have noted that cancers linked to chronic inflammation, such as some colon tumors, appear to be enabled by early changes in patterns of DNA methylation, the addition of a molecule known as a methyl group to the "engine-starter" region of a gene known as a promoter. Methylation events reduce or completely shut down the gene's ability to make functional proteins. Cancer cells typically show abnormal patterns of DNA methylation.

How inflammation brings about these epigenetic abnormalities has not been clear, but in a study reported in 2008, scientists led by Baylin and research associate Heather M. O'Hagan found an important hint. Working on lab-grown cells, they created a model of DNA damage caused by severe inflammation and found that methylating enyzmes known as DNA methyltransferases soon appeared on the scene, as part of the cellular DNA-repair crew.

For the new study, Baylin's team exposed cells to high levels of hydrogen peroxide, a strongly reactive molecule known as a reactive oxygen species which is emitted by a variety of cells during episodes of inflammation. Hydrogen peroxide can damage DNA, as well as other proteins and structures within cells. Baylin's team, in experiments led by O'Hagan and graduate student Wei Wang, found that peroxide-induced damage recruited methyltransferases to damage sites. The enzymes also appeared to form large, molecular complexes with other proteins involved in epigenetic gene-silencing.

These effects did not appear when DNA was damaged by gamma or ultraviolet radiation, suggesting that they are largely a result of reactive oxygen damage induced by inflammation.

The team also saw rapid abnormal DNA methylation in several genes whose promoter regions contain dense groupings of cystine and guanine molecules known as CpG islands. Their epigenetic silencing also is known to contribute to cancer. Further studies with Johns Hopkins colleagues Cynthia Sears and Robert Casero showed that these protein interactions are seen in mice with a bacterially induced form of colon inflammation a condition that accelerates the development of colon cancer in the animals.

Baylin and his colleagues suspect that epigenetic silencing evolved to temporarily give inflamed tissue an opportunity to repair and renew itself. However, when inflammation becomes chronic and lasts too long, Baylin says the silencing process may "become locked-in for some vulnerable genes." The loss of these genes may allow uncontrolled cell division and growth, bringing them one step closer to cancer, he says.

Chronic inflammation induced by viruses, bacteria, toxins and autoimmune processes is well known to promote common types of cancer, including colon, lung and liver cancer. "Our hope is that by understanding how inflammation brings about this abnormal epigenetic process, we might be able to use drugs to target it and thereby prevent many cancers," Baylin says.

The research was supported by the National Cancer Institute, the National Institute of Environmental Health Sciences and the National Institutes of Health.

Article adapted by Medical News Today from original press release. Source: Johns Hopkins Medicine
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Users Of Game Designed By McGill Researchers Contributing To Analysis Of DNA Sequences

Main Category: IT / Internet / E-mail
Also Included In: Genetics; Alzheimer's / Dementia
Article Date: 08 Dec 2011 - 1:00 PST

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Thousands of video game players have helped significantly advance our understanding of the genetic basis of diseases such as Alzheimer's, diabetes and cancer over the past year. They are the users of a web-based video game developed by Dr. Jérôme Waldispuhl of the McGill School of Computer Science and collaborator Mathieu Blanchette. Phylo is designed to allow casual game players to contribute to scientific research by arranging multiple sequences of coloured blocks that represent human DNA. By looking at the similarities and differences between these DNA sequences, scientists are able to gain new insight into a variety of genetically-based diseases.

The researchers are releasing the results computed from the solutions collected over the last year today, together with an improved version of Phylo for tablets.

Over the past year, Phylo's 17,000 registered users have been able to simply play the game for fun or choose to help decode a particular genetic disease. "A lot of people said they enjoyed playing a game which could help to trace the origin of a specific disease like epilepsy," said Waldispuhl. "There's a lot of excitement in the idea of playing a game and contributing to science at the same time," Blanchette agreed. "It's guilt-free playing; now you can tell yourself it's not just wasted time."

Waldispuhl and his students came up with the idea of using a video game to solve the problem of DNA multiple sequence alignment because it is a task that is difficult for computers to do well. "There are some calculations that the human brain does more efficiently than any computer can. Recognizing and sorting visual patterns fall in that category," explained Waldispuhl. "Computers are best at handling large amounts of messy data, but where we require high accuracy, we need humans. In this case, the genomes we're analyzing have already been pre-aligned by computers, but there are parts of it that are misaligned. Our goal is to identify these parts and transform the task of aligning them into a puzzle people will want to sort out."

So far, it has been working very well. Since the game was launched in November 2010, the researchers have received more than 350,000 solutions to alignment sequence problems. "Phylo has contributed to improving our understanding of the regulation of 521 genes involved in a variety of diseases. It also confirms that difficult computational problems can be embedded in a casual game that can easily be played by people without any scientific training," Waldispuhl said. "What we're doing here is different from classical citizen science approaches. We aren't substituting humans for computers or asking them to compete with the machines. They are working together. It's a synergy of humans and machines that helps to solve one of the most fundamental biological problems."

With the new games and platforms, the researchers are hoping to encourage even more gamers to join the fun and contribute to a better understanding of genetically-based diseases at the same time.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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McGill University. "Users Of Game Designed By McGill Researchers Contributing To Analysis Of DNA Sequences." Medical News Today. MediLexicon, Intl., 8 Dec. 2011. Web.
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