Ostomyland's Wicked Wiki: Articles which explain aspects of Colorectal Cancer, why it develops in the first place etc.

Most recent edit on 2007-11-23 13:05:49 by KathyFromEngland

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~*Colorectal Tumor Risk Greater For People With Coronary Artery Disease

*Gene For Colon Cancer Found

Gene For Colon Cancer Found
Main Category: Colorectal Cancer News
Several studies published this month by research teams studying populations all over the world report finding a significant link between a gene on human chromosome 8 and the risk of developing colon cancer.
One of these studies is part of a ten-year project between Michigan in the US and Israel called the Molecular Epidemiology of Colorectal Cancer involving thousands of Israeli Jews and Arabs. The study is published in the July issue of Cancer Biology and Therapy.
Researchers from the University of Michigan (U-M) Medical School and U-M School of Public Health, the Catalan Institute of Oncology in Spain, the CHS National Israeli Cancer Control Center and Technion (the Israel Institute of Technology) compared the genetic material and family history of 1,800 colorectal cancer patients and 1,900 healthy people. Both groups had the same distribution of age, gender and ethnicity which was either Ashkenazi Jew, Sephardic Jew or Arab/non-Jew.
They also tested tumour tissue from many of the cancer patients.
The results showed that people who carry a genetic variation known as the C allele of rs10505477 were 23 per cent more likely to have colon cancer than those without it. The genetic variant is located on a small area of chromosome 8 called 8q24.
The 8q24 link was particularly strong for those patients diagnosed with colon cancer before they reached the age of 50.
The researchers concluded that this variation may account for 14 per cent of colorectal cancer cases in Israel, where colon cancer is the leading cause of death among cancer patients.
Other research teams are reporting similar findings about 8q24 in other populations, suggesting this genetic marker is significant across ethnic groups. Those studies are published in the journal Nature Genetics.
One of the co-leaders of the Michigan Israeli team and first author of the paper is Dr Stephen Gruber, an associate professor of internal medicine and of human genetics in the U-M Medical School, and of epidemiology in the U-M School of Public Health. He also leads the Cancer Genetics program in the U-M Comprehensive Cancer Center, which examines inherited cancer risks.
Gruber said the new discovery was particularly interesting when taken together with other recent findings about this genetic region in prostate and breast cancer:
"The same genetic region that predisposes to colon cancer has also recently been shown to be an important region predisposing to breast cancer and prostate cancer."
"The specific genetic cause for this joint susceptibility to three different cancers has not yet been discovered, but several groups are working to close in on the mechanism that might cause these cancers," he added.
This is yet another in a series of genetic studies that have been unravelling links between disease susceptibility and particular gene variants since the human genome was sequenced in 2003.
"The mystery of the relationship between our genetic code and disease is now starting to become clear, and many scientists are turning to the same chapter to find important clues to colorectal cancer," said Gruber.
Gruber and colleagues will be conducting further research in this area.
The researchers said that while there was no genetic screening test for the variant they have discovered, there are tests for other variants known to be linked to colon cancer.
They said that people with a strong family history of colon cancer, particularly if their relatives got it while young, before they reached the age of 50, should be screened, have a colonoscopy and genetic counselling before they too reached the age of 50.
"Colon cancer is one of the most common cancers in the United States, and the good news is that it's largely preventable with early screening," said Gruber.
According to the American Cancer Society, 150,000 new cases of colon cancer will be diagnosed in the United States in 2007, and more than 50,000 Americans will die from it.
http://www.medicalnewstoday.com/articles/76256.php∞

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~*Colorectal Tumor Risk Greater For People With Coronary Artery Disease

Edited on 2007-11-23 09:47:05 by KathyFromEngland

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~*Researchers Identify Genetic Mutation That May Alter Patients' Response To Cancer Therapeutics

*Colorectal Tumor Risk Greater For People With Coronary Artery Disease

Colorectal Tumor Risk Greater For People With Coronary Artery Disease
Article Date: 25 Sep 2007 - 13:00 PDT
People with coronary artery disease have nearly twice the risk of developing colorectal tumor cancers, compared to people without the disease - the link is even stronger for people with coronary artery disease (CAD) who also smoke(d) or have metabolic syndrome, says a report in the Journal of the American Medical Association (JAMA).
Approximately one in every twenty people worldwide will develop colorectal cancer; it is the second most common cancer. CAD is the foremost cause of death in industrialized countries, write the authors as background to the article. Precancerous tumors or cancer (colorectal neoplasm) or CAD share similar risk factors, therefore their co-occurrence may be linked.
Annie On On Chan, M.D., Ph.D., of the University of Hong Kong, China, and team wanted to see how close the link between colorectal cancer and colorectal neoplasms was in patients who had recently been diagnosed with CAD.
The study participants, all from Hong Kong, were recruited for screening colonoscopy after undergoing coronary angiography for suspected CAD during the period November 2004 to June 2006. They defined CAD as a narrowing of 50% or more in any one of the major coronary arteries - otherwise, the subjects were considered CAD-negative. 206 were CAD-positive, while 208 were CAD negative. A control group of 207, matched for age and sex was recruited from the general population.
Below is what the researchers found:
CAD-Positive Group
-- prevalence of colorectal neoplasms - 34%
-- prevalence of advanced lesions - 18.4%
-- prevalence of cancer - 4.4% (half were early stage)
CAD-Negative Group
-- prevalence of colorectal neoplasms - 18.8%
-- prevalence of advanced lesions - 8.7%
-- prevalence of cancer - 0.5%
Control Group
-- prevalence of colorectal neoplasms - 20.8%
-- prevalence of advanced lesions - 5.8%
-- prevalence of cancer - 1.4%
It was also found that a history of smoking and/or metabolic syndrome were significant independent predictive factors for the positive link between advanced lesions and CAD.
The authors wrote "Both colorectal neoplasm and CAD probably develop through the mechanism of chronic inflammation. Inflammation is now recognized as being pivotal in the pathogenesis of atherosclerosis and, hence, CAD. Colorectal cancer is also thought to progress through the pathway of inflammation."
http://www.medicalnewstoday.com/articles/83604.php∞

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~*Researchers Identify Genetic Mutation That May Alter Patients' Response To Cancer Therapeutics

Edited on 2007-11-23 07:43:15 by KathyFromEngland

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~*Improving Colorectal Cancer Treatment

*Researchers Identify Genetic Mutation That May Alter Patients' Response To Cancer Therapeutics

Researchers Identify Genetic Mutation That May Alter Patients' Response To Cancer Therapeutics
Article Date: 09 Jul 2007 - 0:00 PDT
Researchers from Eli Lilly & Company and the Phoenix-based Translational Genomics Research Institute (TGen) today announced finding a novel recurring mutation of the gene AKT1 in breast, colorectal and ovarian cancers. The altered form of AKT1 appears to cause tumor cell proliferation and may play a role in making cells resistant to certain types of therapies. The findings are reported in an advance online publication (AOP) of the journal Nature.
The PI3-Kinase/AKT pathway is among the most commonly activated cellular pathways in human cancers and members of this pathway are among the most frequently targeted for new cancer drug discovery efforts. Activation of this pathway results in cancer cell growth and cell survival. Although AKT1 is central to pathway activation, its role in cancer has been that of an intermediary between mutated upstream regulatory proteins and downstream survival signaling proteins. This is the first evidence of direct mutation of AKT1 in human cancer tumors: it was discovered in clinical samples from cancer patients, yet has never been detected in cancer cell lines.
"This discovery is a seminal finding in cancer biology that confirms AKT1 as an oncogene in breast, colorectal and ovarian cancer. The mutation alters the electrostatics of binding pocket in the pleckstrin homology domain, the portion of the enzyme that docks with phospholipids on the cell membrane," said Kerry L. Blanchard, PhD, MD, Executive Director, Discovery Biology Research, Eli Lilly & Company.
To identify the AKT1 mutation, the researchers analyzed 150 tumor samples from patients with either breast, colorectal or ovarian cancer (50 samples from each tumor type). Analysis of the data showed that 8 percent of breast, 6 percent of colorectal and 2 percent of ovarian tumors had the AKT1 mutation in the samples that were screened in their study.
"Recently, molecular features such as the AKT1 mutation are beginning to change drug development efforts. This discovery adds to the short but growing list of molecular features that may help guide both current and future cancer drug development," said John Carpten, PhD, Senior Investigator and Director of TGen's Integrated Cancer Genomics Division and the study's lead author. "The next step is to determine the prevalence of the AKT1 mutation in different populations and, hopefully, use the information gained to stratify patients going into clinical trials for AKT inhibitors."
If validated by further studies, the identification of this recurring mutation has the potential to impact cancer treatment and drug development.
"This is a gorgeous study that used a variety of sophisticated techniques to provide new insights into the tumorigenic process," said Bert Vogelstein, MD, Director of the Ludwig Center for Cancer Genetics & Therapeutics at The Johns Hopkins Kimmel Cancer Center.
James E. Thomas, PhD, of Lilly's Cancer Discovery Research division, ex- plained, "AKT1 is a protein kinase or enzyme that plays a key role in activating survival, proliferation and metabolic pathways. Interestingly, other cellular proteins that regulate this network have also been shown to be mutated in a variety of cancers including lung, breast ovary, prostate, colorectal and brain cancers. This mutation in AKT1 is striking direct evidence for the role of AKT1 in cancer formation."
The identification of the AKT1 mutation was a collaborative effort between Eli Lilly & Company and TGen. "This discovery demonstrates the importance of studying the genetic make up of cancers at the clinical level rather than re- lying on model systems," adds Jeffrey Trent, PhD, Scientific Director of TGen.
"This is a key study highlighting Lilly's commitment to translational re- search approaches in cancer drug discovery and development. Furthermore, this work is a great example of a successful public-private partnership at a global level that involves Lilly Research Laboratories in Indianapolis, TGen in Phoenix, Lilly Singapore Centre for Drug Discovery, and the Economic Development Board of Singapore," adds Richard Gaynor, MD, Vice President of Oncology Discovery at Eli Lilly & Company. He added, "This mutation further validates AKT1 as an attractive drug target, and it also will be a valuable tool for the stratification of patients for targeted therapies. This paradigm of identifying specific defects in cancer cells to successfully develop innovative therapies has been validated with oncology drugs such as Gleevec in leukemia and Herceptin in breast cancer."
http://www.medicalnewstoday.com/articles/76253.php∞

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~*Improving Colorectal Cancer Treatment

Edited on 2007-11-23 07:32:49 by KathyFromEngland

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~*Whole Grain, Not "Fiber", Lowers Colorectal Cancer Risk

*Improving Colorectal Cancer Treatment

Improving Colorectal Cancer Treatment
Article Date: 29 Jun 2007 - 1:00 PDT
Researchers have provided new information about a protein responsible for colorectal cancer and the target of a potential drug against this cancer.
Called clusterin, this protein has been linked to the development of tumor cells and resistance to cancer therapy, but how it works is not well understood. Pending questions include how this protein is expressed in normal and cancer cells, how it helps cancer cells escape ionizing radiation and chemotherapy, and which patients will benefit from treatment with a drug targeting clusterin.
Claus Lindbjerg Andersen, Torben Falck Orntoft, and colleagues discovered that clusterin is not expressed in normal cells, while in 25 percent of colorectal tumors, the cancer cells contained clusterin. They also showed that the protein is actually made by the cancer cells themselves. These new findings should help improve current therapies against colorectal cancer, especially for patients with tumors producing clusterin, the scientists concluded.
http://www.medicalnewstoday.com/articles/75500.php∞

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~*Whole Grain, Not "Fiber", Lowers Colorectal Cancer Risk

Edited on 2007-11-23 07:28:37 by KathyFromEngland

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~*UK: Genetic Bowel Cancer Trigger Identified

*Whole Grain, Not "Fiber", Lowers Colorectal Cancer Risk

Whole Grain, Not "Fiber", Lowers Colorectal Cancer Risk
Article Date: 21 Jun 2007 - 1:00 PDT
Experts at the American Institute for Cancer Research (AICR) offered praise for a recently published study which showed that whole grain fiber, and not fiber from other food sources, is associated with lower risk of colorectal cancer.
The AICR experts said the study is to be commended because, unlike many earlier investigations, its authors took care to analyze the role of dietary fiber from different food sources. By acknowledging that the fiber one gets from whole grains is different than the fiber one gets from "starchy" foods like white bread and processed cereal, the study represents an important step toward a more precise understanding of a long-standing scientific controversy.
Findings from the Study
The study in question, published this month in the American Journal of Clinical Nutrition, found that consumption of whole grains was associated with lower risk for colorectal cancer. The same study found no significant link between consumption of fiber from other food sources and colorectal cancer risk.
Researchers at the National Institutes of Health (NIH) analyzed survey results from a large prospective cohort study called the NIH-AARP Study, which involves more than 291,000 men and 197,000 women aged 50 to 71.
The scientists analyzed the participant's intake of fiber from many different food sources, but only fiber from whole grains was associated with lower risk of colorectal cancer. In the study, those subjects who ate the most whole grains had a 20 percent lower risk of colorectal cancer than those who ate the least.
The observed protective effect of whole grain consumption was stronger for rectal cancer (35 percent lower risk).
The Fiber Controversy
AICR nutrition experts have been following the conflicting and often contradictory findings on fiber and colorectal cancer for years.
Much of the previous research simply measured the particpants' total fiber intake. But when so much of the American diet is made up of heavily processed grains (in pasta, cereals and breads), it is helpful to distinguish between different food sources of fiber.
Why? Because scientists are learning that there's something different about whole grain fiber.
The "Whole" Story
All grains, from the familiar (wheat, oats, rye, corn) to the less well-known (barley, bulgur, millet, quinoa) start out as kernels. The bran (the outermost layer of the kernel) is where most of the fiber is found. The germ (the kernel's center) is where most of the vitamins, minerals and fatty acids reside. In between lies the endosperm, which contains a few vitamins and minerals and most of the starch.
Because the refining process removes the bran and germ, the main component of white bread and other products made from refined grains or white flour is starch. The reason whole grain products are darker and chewier than refined grain products is because all three layers of the kernel are ground together to make whole grain flour.
This provides the kernel's full complement of protein, antioxidants, fatty acids and a host of phytochemicals. Most importantly, perhaps, the fiber content of whole grains can be as much as four times that of refined grains.
Why Seek Them Out?
The evidence connecting consumption of whole grains to reduced risk for cancer, cardiovascular disease, stroke and diabetes comes chiefly from population studies and laboratory work. Only recently have researchers begun to identify specific ways a diet high in whole grains promotes health.
In February 2006, for example, a study published in the American Journal of Clinical Nutrition found that a high whole-grain intake had an observable, across-the-board effect on a variety of physiological indicators (or markers) associated with both diabetes and cardiovascular disease.
The evidence for whole grains specifically lowering cancer risk is less strong, although a large 2003 European study with over half a million participants found that high consumption of fiber (from fruits, vegetables and whole grains) reduced risk for colon cancer by 25 percent.
Recently, a Cornell University researcher discovered that whole grains are packed with more antioxidants than was previously expected. These potent health-promoting substances bind directly to the two layers (the germ and the bran) that are discarded in the refining process.
The American Institute for Cancer Research (AICR) is the cancer charity that fosters research on diet and cancer and educates the public about the results. It has contributed more than $82 million for innovative research conducted at universities, hospitals and research centers across the country. AICR also provides a wide range of educational programs to help millions of Americans learn to make dietary changes for lower cancer risk. Its award-winning New American Plate program is presented in brochures, seminars and on its website, http://www.aicr.org∞. AICR is a member of the World Cancer Research Fund International.
http://www.medicalnewstoday.com/articles/74750.php∞

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~*UK: Genetic Bowel Cancer Trigger Identified

Edited on 2007-11-23 07:03:12 by KathyFromEngland

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Categories

CategoryCancer

Edited on 2007-06-16 10:26:51 by KathyFromEngland

Additions:
~*Uveal Melanoma Patients At Higher Risk For Colon Cancer

*Colorectal Cancers Use The Protein "Fascin" To Invade The Organism

Colorectal Cancers Use The Protein "Fascin" To Invade The Organism
Colorectal cancer exploits the power of a protein called "fascin" to form metastasis at distant sites. But when secondary tumors are well established, it "fires" the protein by turning off its gene. Fascin, thus, could represent a novel target to halt the dissemination of malignant cells from the primary site to target organs, a typical behavior of metastasis. Finding the way to inhibit either the protein or its gene activity could lead to the establishment of novel therapies aimed at controlling colorectal cancers, the second most frequent cause of tumor death in Europe after lung cancer (with some 655.000 deaths worldwide).
These results stem from a collaborative effort involving scientists from the Institut Curie in Paris, the Weizmann Institute of Science in Rehovot (Israel) and the Department of Surgery of the Technischen Universitat in Munich. The research was presented on May 12th during the first session of the Workshop on Cell Migration: From Molecules to Organisms and Diseases, an event promoted by the European School of Molecular Medicine (SEMM) and the University of Milan, in collaboration with IFOM The FIRC Institute of Molecular Oncology, and IEO European Institute of Oncology. Venue of the Workshop is the IFOM-IEO Campus (via Adamello, 16, Milan) that was recently opened and represents to date the biggest area dedicated to the oncological research in Europe.
Fascin is a protein that serves to aggregate cellular filaments into bundles, in order to rearrange the cellular frame (called cytoskeleton) and promote the motility. In view of this capacity, several groups of scientists have tried to find a correlation between the presence of fascin and the ability to form metastasis that many tumors exhibit. So far, however, its precise role in tumor development and dissemination was little characterized. Danijela Vignjevic from the UMR144/CNRS, at Institute Curie in Paris, who presented the research at the Workshop, explained the new discovery in details: "Cancer cells become metastatic because they acquire the ability to move and to invade other tissues. This new behavior relies on sensory organelles (common to all the cells that able to move) called filopodia, that sense the environment and help the cells to decide where to go. Fascin is a key component of filopodia, and, inside the colorectal cancer cells, it represents the target of a circuitry that leads to the activation of several genes."
Among the key findings, the investigation proved that the concentration of fascin increases according to the tumor stage: in other words, as the tumor progresses fascin becomes more and more active. In vitro tests revealed that its presence promotes cells migration and invasion, and in vivo experiments confirmed its pro-metastatic power. "There is an interesting feature about this protein" pointed out Danijela Vignjevic. "After the tumor has colonized distant sites fascin is no longer active: it is as if the tumor itself recruited it for its purposes until the malignant cells have spread. When it has arrived at its final destination fascin is no longer needed". As next goal, Vignjevic and colleagues hope to generate a transgenic mouse model for colon cancer metastasis that will provide further insight into the molecular mechanisms of this disease.
"It is tempting to speculate about some possible therapeutic intervention that could derive from this discovery" comments Giorgio Scita, leader of the Signaling regulating acting dynamics in cell motility group at IFOM, and among the Workshop organizers. "However more investigations will be needed before we can think of moving from bench to bedside".
IFOM - THE FIRC INSTITUTE OF MOLECULAR ONCOLOGY FOUNDATION
Via Adamello 16
20139 Milano
http://www.ifom-ieo-campus.it∞
http://www.medilexicon.com/medicalnews.php?newsid=70878∞

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~*Uveal Melanoma Patients At Higher Risk For Colon Cancer

Edited on 2007-06-16 10:22:25 by KathyFromEngland

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~*Rice Bran Could Reduce Risk Of Intestinal Cancer University Of Leicester Research Reveals

*Uveal Melanoma Patients At Higher Risk For Colon Cancer

Uveal Melanoma Patients At Higher Risk For Colon Cancer
15 May 2007
Higher Colon Cancer Risk in Uveal Melanoma Patients and Their Relatives Compared to General Population, was presented by Frederick H. Davidorf, MD, during the Association for Research in Vision and Ophthalmology (ARVO) 2007 Annual Meeting in Fort Lauderdale, Fla.
Uveal melanoma is the most common intraocular cancer in adults. This study involved 130 uveal melanoma patients who provided their extended family medical histories. Results showed that a small, but significant, number of uveal melanoma patients and their families are at higher risk for development of other cancers, most significantly colon cancer. "Therefore, ophthalmologists need to advise patients about the necessity of screening for colon cancer both for themselves and for their blood relatives," advised Dr. Davidorf. Identification of specific genetic changes associated with increased risk for uveal melanomas may provide further insight into the molecular pathogenesis of this cancer.
http://www.medilexicon.com/medicalnews.php?newsid=70524∞

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~*Rice Bran Could Reduce Risk Of Intestinal Cancer University Of Leicester Research Reveals

Edited on 2007-05-04 12:34:22 by KathyFromEngland

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~*Mutation To Mismatch Repair Gene Associated With Colorectal Cancer

*Rice Bran Could Reduce Risk Of Intestinal Cancer University Of Leicester Research Reveals

Rice Bran Could Reduce Risk Of Intestinal Cancer University Of Leicester Research Reveals
31 Mar 2007
A study by biomedical scientists at the University of Leicester has revealed for the first time that rice bran could reduce the risk of intestinal cancer.
The research in the University's Department of Cancer Studies and Molecular Medicine has not been tested on humans, but research in the laboratory has produced promising results.
The research has been published in the British Journal of Cancer.
The results of a controlled laboratory study in a preclinical model of gastrointestinal adenoma demonstrated that consumption of a high daily dose of stabilized rice bran caused an average 51% reduction in the number of precancerous adenomas in the intestinal tract.
Professor Andreas Gescher of the University of Leicester in the UK, the principal investigator, said:
"We compared the cancer-preventive efficacy of rice bran with respect to prostate, breast and intestinal cancers. Whilst there was no effect of rice bran on the development of prostate or breast cancer, rice bran significantly retarded the development of intestinal adenomas. The effect was dependent on the fibre content of the bran. The dose we used translates into approximately 200g rice bran per day in humans. We believe a promising area of future research would be to study the potential colorectal cancer-preventing properties of stabilized rice bran.
"It is known that bran from wheat and rye have anti-cancer properties but this is the first time that this has been shown for rice bran. It appears that rice bran may have a role to play in reducing the development of adenomas, which can be a pre-cursor to cancer. No one has compared the efficacy of the different brans, such as rice, wheat, rye or oat and this may be an interesting future direction for researchers."
http://www.medilexicon.com/medicalnews.php?newsid=66437∞

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~*Mutation To Mismatch Repair Gene Associated With Colorectal Cancer

Edited on 2007-03-28 12:43:03 by KathyFromEngland

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~*Mutation To Mismatch Repair Gene Associated With Colorectal Cancer

Mutation To Mismatch Repair Gene Associated With Colorectal Cancer
26 Mar 2007
Patients with a variant of a DNA repair gene, known as MLH1, may have an increased risk of a subtype of colorectal cancer.
Mismatch repair genes fix problems that arise during DNA replication when bases are incorrectly paired. Mutations in these repair genes are associated with increased risks of cancer.
Stavroula Raptis and Miralem Mrkonjic, graduate students at the University of Toronto, and colleagues analyzed two DNA mismatch repair genes, MLH1 and MSH2, in 1,359 colorectal cancer patients and 1,373 controls from Ontario and Newfoundland.
One particular variant in the MLH1 gene, -93G>A, was strongly associated with colorectal cancer. Patients with two copies of this version of the gene had a greater risk of colorectal cancer than patients with only one.
"Decreased levels of MLH1 expression associated with [MLH1 -93G>A] may lead to impaired cell cycle control, allowing cells to proceed with cell division before proper DNA repair can be accomplished. This impaired control would overwhelm the mismatch repair mechanism, leading to the accumulation of mutations," the authors write.
Contact: Nikki Luscombe, Mount Sinai Hospital
http://www.medilexicon.com/medicalnews.php?newsid=65745∞

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Edited on 2007-03-02 00:17:34 by KathyFromEngland

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~*Regular Vigorous Housework Can Reduce Some Types Of Bowel Cancer Risk

*New Test May Better Identify Certain Colorectal Cancer Types

Deletions:
Regular Vigorous Housework Can Reduce Some Types Of Bowel Cancer Risk

*New Test May Better Identify Certain Colorectal Cancer Types

Edited on 2007-02-11 06:00:22 by KathyFromEngland

Additions:
Regular Vigorous Housework Can Reduce Some Types Of Bowel Cancer Risk
*New Test May Better Identify Certain Colorectal Cancer Types

New Test May Better Identify Certain Colorectal Cancer Types
09 Feb 2007
A new test may more accurately identify colorectal cancer patients with a specific type of gene mutation. These mutations usually indicate that a patient has an inherited form of the disease or may respond to certain cancer drugs differently.
Some people with colorectal cancer have defects in their so-called DNA mismatch repair genes. Researchers test for these mutations by looking for a gene marker called microsatellite instability, which is caused by those gene defects. These mutations indicate that the cancer is likely an inherited condition called Lynch syndrome. It's important to identify patients with Lynch syndrome because they and their family members are at an increased risk of colorectal and other cancers. Patients with a non-hereditary form of colorectal cancer that shows microsatellite instability tend to have a better prognosis than other cancer patients, but they don't respond to a common cancer drug called 5-fluorouracil.
Rosa M . Xicola, a graduate student at the Germans Trias i Pujol Hospital in Barcelona, and colleagues tested two different methods, a standard method and an experimental method, of identifying patients with microsatellite instability. They found that the experimental method better identified - and more accurately ruled out - patients with defects in DNA mismatch repair genes. Furthermore, their results suggest that an even simpler test could be developed to identify patients with these mutations.
"The improved test could result in more patients being assigned to proper treatment based on their disease profile," the authors conclude.
Contact: Xavier Llor, M.D. Associate Professor, University of Illinois at Chicago
http://www.medilexicon.com/medicalnews.php?newsid=62524∞

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Regular Vigorous Housework Can Reduce Some Types Of Bowel Cancer Risk

Edited on 2006-12-30 12:39:51 by KathyFromEngland

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-- Be SunSmart: protect yourself from the sun and harmful UV

Deletions:
-- Be SunSmart: protect yourself from the sun and harmful UV

Edited on 2006-12-30 12:39:26 by KathyFromEngland

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Among the 21,500 cases of colon cancer diagnosed each year in the UK, approximately half are detected on the right-hand side of the colon.

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Among the 21,500 cases of colon cancer diagnosed each year in the UK, approximately half are detected on the right-hand side of the colon.

Edited on 2006-12-30 12:38:56 by KathyFromEngland

Additions:
~*Exercise, Aspirin Consumption And Childbirth May Alter Cancer Risk [Article mentions colon, lung, renal and breast cancers.]
Regular Vigorous Housework Can Reduce Some Types Of Bowel Cancer Risk

Regular Vigorous Housework Can Reduce Some Types Of Bowel Cancer Risk
29 Dec 2006
An hour's vigorous housework every day can help to reduce the risk of some types of bowel cancer according to a new Cancer Research UK report.*
Cleaning the kitchen floor and hoovering the stairs can use as much physical energy as a gym session on the treadmill or a brisk walk and all types of activity can cut the risk of colon tumours.
The study, part-funded by Cancer Research UK and the Medical Research Council and published today by the European Prospective Investigation into Cancer and Nutrition (EPIC) scientists, analysed data from 413,000 people in 10 European countries to conclude that physically active people were 22 per cent less likely to develop colon cancer.
For tumours on the right side of the colon the risk was reduced by as much as 35 per cent in the most active people. For active people who are not overweight with a Body Mass Index (BMI) of less than 25 the risk was reduced even further.
Scientists concluded that exercise was most beneficial in reducing right-sided colon cancer risk in both men and women who already had a healthy weight. But it also benefited to a lesser extent those who were overweight but not obese.
One hour a day of vigorous physical activity or two hours of moderate activity would be enough to reduce the risk of colon, though not rectal cancer.
Dr Lesley Walker, Cancer Research UK's director of information, said: "This is a very large study which should remove any doubt about the benefits of exercise in relation to reducing the risk of bowel cancer. It is important for people to understand that they can take steps in their daily routine to reduce cancer risk. You don't need to join a gym to get the benefit of exercise. If regular brisk walking or going for a run doesn't appeal you can take a tip from TV's Kim and Aggie and do some strenuous housework. Cleaning windows, vacuuming and scrubbing floors burn off a lot of calories. So does gardening or cleaning the car. If you combine regular physical activity with a good diet you are more likely to maintain a healthy body weight which will also significantly help to reduce your risk of bowel cancer. What is particularly interesting about this study is the correlation the scientists have found between exercise and cancers on the right side of the colon. We do not know the reason for this although physical activity is known to stimulate waves of muscle contraction down the right side of the colon which accelerates movement of waste and the possible cancer- causing agents in it."
Kim and Aggie welcomed the benefits of housework. "It's amazing how much energy you use just by doing basic housework," they said. "Thorough cleaning involves bending and stretching, climbing stairs, using a vacuum cleaner, scrubbing the bath and lots more. It all adds up to burning off plenty of calories which helps keep weight down. It's good to know that a daily cleaning routine can help keep you fit and healthy."
Dr Christine Friedenreich, of the International Agency for Research on Cancer (IARC) and the Alberta Cancer Board and lead author of the study, said: "This study is significant because of its very large sample size and the different levels of activity that were observed across the European countries. This allowed a more in-depth analysis of how physical activity influences colon cancer risk."
Professor Elio Riboli, of Imperial College London, coordinator of the EPIC, said: "We were particularly interested in the results that we found for different parts of the colon and rectum which were not feasible in previous studies because of the smaller sample sizes and lack of data on the position of tumours. The protective effect of physical activity on colon but not on rectal cancer is in agreement with our previous results on colorectal cancer risk in relation to obesity and insuline resistance that also showed specific association with colon cancer risk. These new results indicate that the behavioural and metabolic factors on which we can operate for prevention are different for the cancer risk at the two anatomical sub-sites. Professor John Toy, medical director of Cancer Research UK, said: "EPIC has carried out much valuable research into the link between diet and cancer and this study has expanded the work by showing the valuable role of physical activity in reducing bowel cancer risk.From a general public health perspective it is also encouraging that physical activity has been shown to reduce colon cancer risk in people who are overweight."
Among the 21,500 cases of colon cancer diagnosed each year in the UK, approximately half are detected on the right-hand side of the colon.
Bowel cancer, often called colorectal cancer, is the third most common cancer in men, and the second most common cancer in women in the UK. Two thirds of these cases are colon cancer (around 21,500) and one third are rectal cancer (around 13,300).
In England and Wales the lifetime risk of being diagnosed with colorectal cancer is 1 in 18 for men and 1 in 20 for women.
If the cancer is caught at an early stage, around eight out of ten cases can be successfully treated. Nowadays, around half of all patients with bowel cancer are cured.
A Body Mass Index (BMI) between 25 and 30 indicates being overweight. A BMI over 30 indicates obesity.
Half of all cancers could be prevented by changes to lifestyle. Cancer Research UK's Reduce the Risk campaign has five simple messages to help people reduce their risk of cancer. These are:
-- Stop smoking: this is the best present you will ever give yourself
-- Stay in shape: cut your cancer risk by keeping a healthy weight
-- Eat and drink healthily: limit alcohol and maintain a healthy diet
-- Be SunSmart: protect yourself from the sun and harmful UV
-- Look after number one; be aware of any body changes and go for screening.
http://www.medilexicon.com/medicalnews.php?newsid=59224∞

Deletions:
~*Exercise, Aspirin Consumption And Childbirth May Alter Cancer Risk [Article mentions colon, lung, renal and breast cancers.]

Oldest known version of this page was edited on 2006-11-21 03:11:08 by KathyFromEngland []

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Articles which explain aspects of Colorectal Cancer, why it develops in the first place etc.

Contents

*Jefferson Researchers Uncover Genetic Signature That Predicts Colon Cancer
*New Research May Explain Why Some Who Receive Growth Hormone Therapy Develop Colon Polyps
*Virtual Colon Screenings Examined
*Abdominal Obesity May Be Associated With Colon Cancer Risk
*Low 5 Year Colon Cancer Recurrence Rates
*Identification Of Key Molecular Signaling Switch Involved In Allergic Disease: May Provide A New Target For Treatment Of Allergic Reactions [colon cancer mentioned]
*Risk After Colon Cancer Higher For The Very Fat And Very Thin
*Soy And Fish Have Cancer Preventing Qualities
*Exercise, Aspirin Consumption And Childbirth May Alter Cancer Risk [Article mentions colon, lung, renal and breast cancers.]

Jefferson Researchers Uncover Genetic Signature That Predicts Colon Cancer

09 Apr 2006

Researchers at Jefferson Medical College in Philadelphia have uncovered a genetic "signature" that accurately identifies colon cancer--a key, they hope, to better understand how the cancer develops.

Colon cancer may begin when processes that regulate adult stem cells in the colon go awry. A handful of stem cells lie in the bottom of tiny tube-like "crypts" in the epithelium (or lining) of the colon. Stem cells produce daughter cells that proliferate, eventually making their way to the top of the crypt, where they become specialized colon cells. Simply put, mutations in the stem cells lead to mutant daughter cells and cancer.

To try to understand some of these processes, Bruce Boman, M.D., Ph.D., director of the Division of Genetic and Preventive Medicine at Jefferson Medical College of Thomas Jefferson University and at Jefferson's Kimmel Cancer Center, and his co-workers used a microarray chip to analyze the expression of microRNAs (miRNAs). MiRNAs are tiny pieces of genetic material discovered in recent years that are thought to be important in regulating gene expression and in the development of cancer. The chip carried complementary genetic "probes" for most of the known miRNAs in human and mouse.

The researchers first compared miRNA expression in the bottom tenth of normal colon crypts, which is where stem cells are located, to the other nine-tenths of the crypt, where daughter cells were proliferating. This approach was designed to tell the difference between stem cell and non-stem cell activity.

They also examined miRNA gene expression in colon cancer tissue, finding changes in expression between normal tissue and cancer. More specifically, they found a pattern of 16 miRNA genes that characterizes the crypt bottom. The pattern accurately predicted which colon tissues were normal and which were cancerous.

Dr. Boman, professor of medicine and director of Jefferson's Hereditary Cancer Center and Gastrointestinal Cancer Program at Jefferson's Kimmel Cancer Center, presents the team's findings April 4, 2006 at the annual meeting of the American Association for Cancer Research in Washington, D.C.

"This will not only give us insights into how tissue dynamics are regulated in normal colonic epithelium, but also in the development of cancer as well, where the normal steady state is disrupted," he says. "It might also help us better understand the stem cell origin of colon cancer.

"If a miRNA is binding to a gene product that is key to differentiation of a cell, and the miRNA is lost, maybe that cell won't be able to undergo differentiation and will become a cancer cell," he says. "We're now looking at the gene targets for the specific miRNAs.

"The exciting part," notes Dr. Boman, "is that by figuring out which of these molecules are lost in cancer, they can theoretically be replaced. This could have tremendous potential for the development of new drugs."
http://www.medilexicon.com/medicalnews.php?newsid=41024∞

New Research May Explain Why Some Who Receive Growth Hormone Therapy Develop Colon Polyps

12 Apr 2006

The use of growth hormone therapy has been linked in some people to the development of colon polyps, a possible precursor to colorectal cancer - but medical researchers have debated the extent of a cancer risk.

In addition, the reason for a polyp link to growth hormone has been unclear. But new research from the University of North Carolina at Chapel Hill indicates the probable answer: loss of function of one of a pair of genes that normally would inhibit growth hormone signals inside the cell.

The study also offers a possible molecular marker that could help determine which people taking growth hormone therapy are at increased risk for colon polyps. Researchers already know that colon polyps tend to occur in people who already have excessive amounts of growth hormone, such as those with a disease called acromegaly, or gigantism.

A report of the study appears in the April issue of the medical journal Endocrinology.

Study senior author Dr. P. Kay Lund, professor of cell and molecular physiology within UNC's School of Medicine and a member of the UNC Lineberger Comprehensive Cancer Center, said she and her team had been interested in looking at the effect of a newly discovered inhibitor of cellular growth hormone signaling, suppressor of cytokine signaling-2, or SOCS2.

This molecule limits growth hormone action on the body and organ growth, but its role in growth hormone action on intestine is unknown, Lund said.

"Much of the work on SOCS2 had been done in cell cultures. We wanted to study it in vivo, in laboratory animals, with a focus on how it stops the action of cellular growth hormone."

The researchers thought an ideal way to study this issue would be to use an animal model of acromegaly, laboratory mice having excessive amounts of growth hormone.

The animals were crossed with animals in which the SOCS2 gene was deleted. The breeding generated animals with excessive growth hormone and one or two functional SOCS2 genes, but none with excessive growth hormone and no SOCS2 genes, an unexpected result.

"This meant that excessive growth hormone and no functional SOCS2 is incompatible with successful embryonic development," Lund said.

But there was another surprise: While colon polyps did not develop in animals with excessive growth hormone and two functional SOCS genes, multiple polyps did develop in animals with excessive growth hormone and only one functioning SOCS2 gene.

"We discovered that losing this one copy of SOCS2, this 'haplotype insufficiency,' is enough to cause spontaneous polyp formation in these animals," Lund said, adding that the findings may have implications for humans.

"Haplotype insufficiency animal models are much closer to the normal human variation. Animals expressing just 50 percent normal levels of a protein can be thought of as reflecting the physiological variation that occurs in the general population."

According to Lund, expression levels of SOCS2 measured in, say, 100 people would almost certainly vary by at least 50 percent.

"So this really raises the issue that in a situation of growth hormone excess, such as acromegaly or, possibly, growth hormone therapy, SOCS2 may really be fundamental to dictating your risk of getting abnormalities in the colon."

On the other hand, Lund's research may apply to the variations found in response to growth hormone therapy for the gastrointestinal tract. This would include people with short-bowel syndrome, a group of problems affecting individuals who have had half or more of their small intestine surgically removed. Many people with short bowel syndrome are malnourished because their remaining small intestine is unable to absorb enough water, vitamins and other nutrients from food.

"What has been a puzzle there is that the response to growth hormone in these patients is very variable. Some seem to respond well and get a great benefit from this therapy, and some people don't respond well," Lund said.

"And we found that animals having 50 percent of normal expression levels of SOCS2 show much greater small intestinal growth to growth hormone therapy. So if low SOCS2 enhances the response of the small intestine to growth hormone, it says that patients that have lower SOCS2 may be the ones who favorably respond to this therapy."

Thus, depending on the clinical situation, levels of SOCS2 would either predict who might be at greater risk for colon polyps in the presence of an excess of growth hormone and who might best respond to growth hormone therapy for gastrointestinal conditions such as short bowel syndrome.

"Our future research with SOCS2 will be aimed at studies on human tissue samples to test variations in levels of SOCS2 in the intestine to predict risk of colonic polyps or the response of short bowel syndrome patients to therapeutic growth hormone. Future animal studies will test the role of SOCS2 in cancer models," Lund said.

UNC co-authors with Lund were lead author Dr. Carmen Michaylira, a former graduate student in Lund's lab and now at the University of Pennsylvania; Nicole Ramocki, graduate student; Dr. James Simmons, research associate in cell and molecular physiology; C. Kirby Tanner, first-year medical student; Kirk McNaughton, research analyst in cell and molecular physiology; and Dr. John Woosley, asssociate professor of pathology and laboratory medicine. Co-author Dr. Christopher Greenhalgh from the Walter and Eliza Hall Institute in Melbourne, Australia, was an essential collaborator on the SOCS2 work.

http://www.medilexicon.com/medicalnews.php?newsid=41330∞

Virtual Colon Screenings Examined

24 May 2006

With more than 100,000 people in the U.S. diagnosed each year with colon cancer, doctors are working to improve screening techniques through more accurate technologies and more comfortable procedures. In research presented today at Digestive Disease Week? 2006 (DDW), studies suggest that virtual screenings may be just as effective as standard colonoscopy at detecting colon polyps in average-risk individuals. DDW is the largest international gathering of physicians and researchers in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery.

Computed tomographic colonography (CTC), sometimes called "Virtual Colonoscopy," is a non-invasive and well-tolerated CT scan, which uses an X-ray to create images of the body. The images are transferred to a computer, creating a detailed picture of the inside of the colon, so that a doctor can search for polyps or other abnormalities that may need to be removed.

A Prospective Evaluation and Classification of Extra-Colonic Abnormalities Identified with Computed Tomographic Colonography Screening in Asymptomatic, Average Risk Individuals [Abstract 209]

Computed tomographic colonography (CTC) screening is becoming a more prevalent option used to screen moderate-risk individuals for colon cancer. Because of the computer assisted technology, this procedure can also detect extra-colonic abnormalities, such as calcified arteries and nodules. This study examined the characteristics of the abnormalities found by the screening and the resulting evaluation and treatment.

The research team from the National Naval Medical Center conducted CTC for cancer screening on 979 asymptomatic, average risk patients and recorded extra-colonic abnormalities, categorizing the findings as critical (requiring therapeutic intervention), moderate (requiring additional diagnostic intervention) or incidental (no further action).

Extra-colonic abnormalities were detected in approximately 16 percent (156 pts) of CTC screenings, the most common being coronary artery calcifications (41 pts) and non-calcified pulmonary nodules (33 pts). Abnormalities were found throughout the body, including the heart and lungs, kidney, liver, bone and other organs. While half (51.6 percent) were classified as incidental, another 33 percent were moderate and 15 percent were critical.

"Significant abnormalities requiring further action accounted for nearly half of the abnormalities we found, suggesting that by screening for colon cancer, we may offer early detection of other potentially morbid conditions in some patients," said Brooks Cash, M.D., of the National Naval Medical Center, and senior author of the study. "However, it is important to note that abnormalities detected by CTC also increase the indirect costs associated with the exam, so we need to evaluate the true outcomes associated with these findings before recommending the routine use of this procedure."

Accuracy of Computed Tomographic Colonography for Colorectal Cancer (CRC) Screening in Asymptomatic Individuals [Abstract 278]

In an attempt to improve rates of screening while maintaining accuracy, researchers have been examining the optimal usage of computed tomographic colonography (CTC) screening, a less invasive and time consuming screening process. Studies have previously suggested that CTC was comparable to optical colonoscopy (OC), and interim results from this study support those findings.

For the current study, researchers recruited participants who were asymptomatic and at average risk for colon cancer. A total of 760 patients have undergone CTC since the start of the study. If the CTC identified a polyp larger than 10 mm or more than three polyps larger than 6 mm, participants underwent same-day OC, while patients with one or two polyps measuring 6-9 mm underwent OC after one year, and patients with no polyps greater than 6 mm had OC within five years. The one year delay in the removal of polyps is a novel feature of this trial, one which the investigators hope will be able to glean some information regarding the natural history of colonic polyps in this patient population.

Findings from the study suggest that CTC is, in fact, comparable in accuracy to OC in detecting polyps larger than 10 mm, with an overall detection sensitivity of 96.4 percent compared to 96.3 percent with OC. While CTC sensitivity falls as polyp sizes get smaller, CTC detection of smaller polyps (6-9 mm in size) was comparable to that of OC with an 83.6 percent accuracy (sensitivity=77.3 percent, specificity=85 percent). OC sensitivity for these polyps was 88.2 percent.

"For patients who are not at high risk for colon cancer or who do not have alarming signs or symptoms, CTC is an effective method to screen for precancerous colorectal lesions at our institution," said Brooks Cash, M.D., of the National Naval Medical Center, and lead author of the study. "However, for patients who are at increased risk or whose screening results are unclear, we still recommend the use of optical colonoscopy to properly evaluate their colon health. It is also important to realize that we are at the vanguard of this technology and our results may not be indicative of the results that would be obtained in the general community. CTC remains an innovative practice that needs more study before it can be widely recommended, though our current results are certainly very promising."

Histopathology of Small Polyps Removed in the Videoendoscopic Era [Abstract T1344]

Colorectal polyps are common in most of the adult population over 50 and while many are benign, others have the potential to develop into cancerous tumors. Current practice standards call for close monitoring of polyps under 1.0 cm, but do not require that these polyps be removed as a precautionary measure. Study authors from the Indiana University Medical Center closely evaluated more than 10,000 polyps under 1.0 cm and found that if all of these polyps are ignored, a substantial majority of colorectal neoplasms will be left in place to grow. Researchers examined 8,798 (81.6 percent) polyps that were smaller than 6.0mm and an additional 1,282 polyps that were between 6.0 mm and 9.9 mm. Analysis showed that almost half of the polyps smaller than 6.0 mm were either adenomas or advanced adenomas (49.86 percent). This rate was even higher for polyps between 6.0 mm and 9.9 mm; adenomas made up 58.7 percent of these polyps and an additional 5.7 percent were advanced adenomas.

"If we move to a policy of leaving polyps less than one centimeter in place, as has been suggested by some experts for patients who undergo virtual colonoscopy, then we'll be leaving more than 90 percent of the neoplasms in the colon in place," said Douglas Rex, M.D., of the Indiana University Medical Center and senior author of the study. "This would be a major paradigm shift in our colorectal cancer prevention strategy, which currently is based on colonoscopy with resection of all detected neoplasms. As such, it requires very careful evaluation."

Impact of a Virtual Colonoscopy Screening Program on Optical Colonoscopy in Clinical Practice: One Year Data [Abstract 288]

Since the introduction of virtual colonoscopy (VC), its potential impact on the use of traditional optical colonoscopy (OC) has been cause for much speculation. University of Wisconsin Medical School researchers have conducted the first "real life" analysis of the effects of VC on utilization rates of OC and found that while there has not been a decrease in the number of OC procedures performed, there has been a significant reduction in OC referrals.

Study authors reviewed data from the three month period before VC screening was introduced at the University of Wisconsin hospital; the period three months before to five months after VC was introduced; the 14 month period after the introduction of VC; and, finally, the six to 14 month period after VC screening was initiated. Period T4 is defined as the time when VC screening has reached its "steady-state," marked by an increase in VC procedures performed and an increase in provider and patient knowledge of the procedure. The average number of OC screenings performed each month did not change significantly after VC was introduced and the percentage of OC involving removal of polyps also remained constant. However, the percentage of OC screening referrals decreased significantly, from 247 per month to 203 per month after VC screening was initiated. According to the researchers, the trend may be an early indicator that there will be an eventual decrease in demand for OC screening.

"This study shows a potential change in the tide of colonoscopy choices. As more medical institutions and health care service providers adopt and reimburse for virtual colonoscopies, we may see a significant decrease in the popularity of more traditional colonoscopy techniques," said Darren C. Schwartz, M.D., University of Wisconsin Medical School and lead study author. "However, differences in accuracy do still exist so it is important for patients and their physicians, especially those at high risk for colon cancer, carefully consider their options when choosing a screening technique."

Digestive Disease Week? (DDW) is the largest international gathering of physicians, researchers and academics in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery. Jointly sponsored by the American Association for the Study of Liver Diseases (AASLD), the American Gastroenterological Association (AGA), the American Society for Gastrointestinal Endoscopy (ASGE) and the Society for Surgery of the Alimentary Tract (SSAT), DDW takes place May 20-25, 2006 in Los Angeles, California. The meeting showcases more than 5,000 abstracts and hundreds of lectures on the latest advances in GI research, medicine and technology.

Aimee Frank
American Gastroenterological Association
http://www.gastro.org/∞
newsroom@gastro.org∞
http://www.medilexicon.com/medicalnews.php?newsid=43935∞

Abdominal Obesity May Be Associated With Colon Cancer Risk

06 Jul 2006

Waist circumference and a person's waist-to-hip ratio were linked to an increased risk of colon cancer, a new study suggests.

Tobias Pischon, M.D., of the German Institute of Human Nutrition in Potsdam, and colleagues examined the link between abdominal obesity and colon and rectal cancer in 368,277 subjects from the European Prospective Investigation into Cancer and Nutrition. The subjects were followed for an average of 6.1 years.

The authors identified 984 patients with colon cancer and 586 patients with rectal cancer. A large waist, high waist-to-hip ratio, and height were associated with an increased risk of colon cancer in both men and women. In men, high weight and body mass index were also associated with increased risk of colon cancer.

Contact: Gisela Olias, olias@mail.dife.de

Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oxfordjournals.org/∞.
http://www.medilexicon.com/medicalnews.php?newsid=46575∞

Low 5 Year Colon Cancer Recurrence Rates

29 Oct 2006

Five years after a colonoscopy which detected no precancerous growths or polyps, the risk of having a potential cancer is very low according to findings of a study by researchers from Indiana University presented at the 71st Annual Scientific meeting of the American College of Gastroenterology (ACG). The risk of advanced adenomas, a type of colon polyp more likely to become cancerous, while still low, was higher in men than in women. These findings suggest a longer interval for follow-up screening may be safe, and support recommendations by the ACG and other groups to re-screen average risk patients after ten years.

Thomas Imperiale, M.D., FACG of Indiana University presented data from patients in a corporate-sponsored screening program supported by Eli Lilly in which employees are screened for colorectal cancer. Among the 2,436 patients who had no precancerous growths upon initial screening, 1,256 returned for screening approximately five years later. No cancers were found upon re-screening, and tests revealed polyps larger than 1 centimeter in 16 percent of the patients. Researchers identified advanced adenomas in 15 patients, or 1.2 percent. Men in the study were more likely to have polyps at all, and to have advanced adenomas.

Colorectal polyps are classified as adenomas (pre-cancerous) or hyperplastic (non-cancerous). According to the ?Polyp Guideline? of the American College of Gastroenterology, ? only a few polyps acquire the additional genetic alterations that make them grow?and turn into cancer.? [ACG Poylp Guideline, Bond et al., American Journal of Gastroenterology, November 2000.]

The risk of colorectal cancer is ?extremely low? five years after a screening exam which found no precancerous changes, according to Dr. Imperiale.
http://www.medilexicon.com/medicalnews.php?newsid=55333∞

Identification Of Key Molecular Signaling Switch Involved In Allergic Disease: May Provide A New Target For Treatment Of Allergic Reactions

01 Nov 2006

A research team has identified a key enzyme responsible for triggering a chain of events that results in allergic reaction, according to new study findings published online this week in Nature Immunology.

The work by researchers from Virginia Commonwealth University, the Hospital for Special Surgery and Weill Cornell Medical College in New York sets the stage for development of new strategies and target therapies that control allergic disease - the sixth leading cause of chronic disease in the United States.

Allergic diseases such as asthma and hay fever are problematic for about 30 percent of the population in the developed world. Researchers have developed various treatments to control allergy, but no cure has been found.

The team has demonstrated, for the first time, the role of a proteolytic enzyme called ADAM10 that releases a major allergy regulatory protein from the surface of cells and thereby promotes a stronger allergic response. The identification of drugs that inhibit ADAM10's ability to release this molecule could revolutionize treatment of asthma and allergic disease.

"Our research, for the first time, may represent a treatment strategy to prevent, rather than simply control IgE-mediated allergy," said Daniel Conrad, Ph.D., a professor in VCU's Department of Microbiology and Immunology. Conrad directed the research conducted at VCU. IgE is an antibody known to trigger Type I allergic disease.

"Understanding ADAM10's role in allergic disease makes it a potential target for the design of drugs to treat asthma and allergic disease," he said.

According to Conrad, the outcome of allergic disease can be modulated by high levels of the regulatory protein, known as CD23, which ultimately results in a decreased production of IgE. He said that when the regulatory protein is released from the cell surface by ADAM10 there is an increase in the production of IgE and therefore, increased allergy.

"These exciting results extend the known functions of ADAMs in development and disease. We hope our results will stimulate new research into how to block or activate the function of ADAMs involved in human disease, including allergic response, cancer and rheumatoid arthritis," said Carl P. Blobel, M.D., Ph.D, chair of the Arthritis and Tissue Degeneration Program at the Hospital for Special Surgery, and professor of Medicine and of Physiology and Biophysics at Weill Cornell Medical College. Blobel directed the research conducted at Weill Cornell.

According to Blobel, in addition to the critical role of ADAM10 in allergic disease through processing of CD23, ADAMs are also key molecules in cancer and rheumatoid arthritis. For example, he said, ADAMs are essential for activating the epidermal growth factor receptor, an established target for the treatment of cancers, such as colon cancer. Moreover, ADAMs release tumor necrosis factor alpha, currently the major target for treatment of rheumatoid arthritis.

Since the 1970s Conrad has been investigating the basic mechanism involved in allergic disease. Blobel has been investigating ADAM proteases since their discovery in the early 1990s.
http://www.medilexicon.com/medicalnews.php?newsid=55360∞

Risk After Colon Cancer Higher For The Very Fat And Very Thin

19 Nov 2006

Even after successful treatment for colon cancer, the very obese are about one-third more likely to have their cancer recur and to die prematurely from cancer than those of normal weight, researchers from the University of Chicago and the University of Pittsburgh report in the Nov. 15, 2006, issue of the Journal of the National Cancer Institute.

For patients with stage II or stage III colon cancer, the difference in long-term survival for leaner patients compared to those with a body mass index (BMI) of 35 or greater -- which physicians refer to as "very obese" -- was comparable to the difference between those who had surgery followed by chemotherapy and those who had only surgery.

The very thin, those with a BMI less than 18.5, were also at increased risk of death, primarily from other cancers, including respiratory cancers possibly connected to smoking, as well as non-cancer causes.

"Given the increasing proportion of Americans with a BMI greater than 35 and the fact that these individuals are over-represented among colon cancer patients, we need to find out why extra weight has such a harmful impact and come up with new ways to counter that," said study author James Dignam, Ph.D., a biostatistician and assistant professor in the Department of Health Studies at the University of Chicago.

"One first step would be to investigate whether modifying diet and exercise habits for patients after treatment would have a positive impact on colon cancer outcomes," he said. "Other studies beginning to explore the effect exercise in colon and other cancers have been promising."

The researchers studied data from 4,288 patients with stage II or stage III colon cancer who enrolled in either of two multi-center clinical trials between July 1989 and February 1994. Both trials, administered by the National Surgical Adjuvant Breast and Bowel Project, headquartered at the University of Pittsburgh, compared different regimens of chemotherapy following surgery. Median follow-up from surgery to last contact with patients who were still alive was 11.2 years.

More than half of the patients in the trial (54%) were overweight and 5.5 percent were very obese. About three percent were underweight.

The researchers focused on the relationship between body mass index at the time of diagnosis and long-term prognosis. They found that the risk of death was increased "at both ends of the adiposity spectrum."

Patients who were very obese were most likely to die from colon cancer recurrence. Patients who were underweight had twice the risk of death, but their increased risk was from non-colon cancer-related causes.

The mechanism connecting excess weight to cancer recurrence and death "is not completely understood," the authors note. Previous studies have suggested a role for insulin, insulin-like growth factors, the hormones that regulate hunger and other obesity-related pathways. Another possibility is the presence of concurrent illnesses associated with obesity, which may interfere with the ability to deliver effective treatment.

"This study provides us with an easy way to predict that certain patients have a higher risk of recurrence and thus might benefit from closer surveillance and additional interventions," said Dignam.
http://www.medilexicon.com/medicalnews.php?newsid=56737∞

Exercise, Aspirin Consumption And Childbirth May Alter Cancer Risk

20 Nov 2006

Personal choices, such as smoking and consumption of fatty foods, have long been linked to increased cancer risk. During recent years, scientists have been seeking to isolate a variety of lifestyle decisions that may stave off the onset of cancer or even reduce tumor formation in their early stages. The latest round of such studies, presented at the American Association for Cancer Research's Frontiers in Cancer Prevention Research Meeting, include the impact of exercise on colon cancer in men, how aspirin consumption may negate the harmful effects of eating flame-broiled meat, and a new link between child bearing and lung cancer.

Effect of a 12-month exercise intervention on apoptosis in colon crypts: a randomized controlled trial

Exercising six days a week reduces the risk of colon cancer in men, according to a study by the Fred Hutchinson Cancer Research Center in Seattle. The study, conducted by Kristin Campbell, Ph.D., postdoctoral fellow, Public Health Sciences, and her colleagues, illustrated the role of exercise in controlling abnormal cell growth in colon tissue.

In men who engaged in moderate to vigorous exercise (an hour a day, six days a week) for a year, more apoptosis (normal cell life and death cycles) was seen in crypt cells in the colon. These cells are indentations in the colon wall and are the wellspring of polyps and other abnormal growths that can result in colon cancer. A protein called bax that promotes apoptosis was seen in higher amounts in the crypt cells among male exercisers. No such differences were seen in women, regardless of their exercise routines. But some changes in apoptosis were seen even among men who exercised less, about four times a week.

"We saw a substantial increase in the potential for cellular apoptosis in areas of the colon most vulnerable to colon cancer," said Campbell. "The increase was most pronounced in men who exercised six hours a week. No change was seen in women, a finding that is consistent with our previous findings of altered proliferation in men, but not women. Therefore, physical activity may play a stronger role in colon cancer risk reduction among men than it does among women."

The researchers examined 101 men and 98 women in one of the first randomized clinical trials to test the effect of exercise on colon cancer. The participants either exercised or maintained their usual non-active lifestyle for one year. At the same time, researchers measured apoptosis by measuring the ratio of bax, the apoptosis promoter protein, to bcl-2, an anti-apoptotic protein. The researchers also determined where in the colon-crypt cells these apoptotic changes were occurring.

Cellular proliferation in the bottom of colon crypt cells is normal. But precancerous polyps (and ultimately, cancer) can develop when the crypt's cells proliferate too quickly. In that case, cells growing too fast creep up from the bottom and spill over the upper sides, resulting in the growths seen in cancer and its predecessors. The researchers previously found lower proliferation on the upper portions of crypt cells in exercising men, while no decreases were found in women or men who did not exercise.

Is the association between flame-broiled food, meat consumption, and breast cancer modified by N-acetytransferases and aspirin use?

By studying the eating patterns of 312 women with breast cancer and 316 who were cancer free in a prospective study, Kala Visvanathan, M.B.B.S., assistant professor of epidemiology at Johns Hopkins University, and colleagues found that women who eat flame-broiled foods more that twice a month may be at increased risk of breast cancer when compared to women who don't usually eat foods prepared that way.

The good news, however, is that taking aspirin negated the potentially harmful effects.

"We are not certain of the mechanism by which aspirin may be helping attenuate these risks. This is an area that further study should elucidate as we search for means to reduce the risk of breast cancer," said Visvanathan.

The researchers first sought to determine if differences in a women's ability to activate the cancer-provoking chemicals in flame-broiled meat, known as heterocyclic amines (HCAs), modified the risk of developing breast cancer.

The NAT2 enzyme, short for N-acteyltransferase, is involved with activating heterocyclic amines. Several genes control NAT2's ability to activate HCAs: slow NAT2 metabolizers tend to produce less active HCAs than fast NAT2 metabolizers. The study found that fast metabolizers who ate more flame-broiled food were more likely to develop breast cancer than slow metabolizers who never ate such food.

"Previous work examining the association between NAT2, flame-broiled food, and breast cancer risk has been inconsistent. We find the relationship between aspirin, flame-broiled food consumption and NAT2 activity intriguing," said Visvanathan.

Nonsteroidal anti-inflammatory drugs and breast cancer risk: the multiethnic cohort

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) had little effect on reducing the risk of breast cancer overall; however, the risk was notably lower among African-American and Caucasian women with long-term use, according to a study by the University of Hawaii and University of Southern California.

The researchers' work is one of the first to explore the relationship between COX-2 inhibitors (aspirin and NSAIDs) and breast cancer in a multiethnic population. The National Cancer Institute is currently studying COX-2 drugs (short for cyclooxygenease-2) for its effect on breast cancer. The COX-2 enzyme is activated in response to inflammation and precancerous and cancerous tissues, and its inhibition has been associated with significant reduction in breast cancer tissue. A few large research studies have also shown a reduction in risk of breast cancer among NSAID users.

While COX-2 research has found a promising association with NSAIDs and cancer, Jasmeet Gill, Ph.D., postdoctoral fellow in the Department of Etiology, and her colleagues found no associations between aspirin and other NSAID (ibuprofen, naproxen, indomethacin, etc) use and breast cancer risk, even if the women's total NSAID use (aspirin plus other NSAIDs) was for 11 or more years. There were two exceptions: African-American women cut their breast cancer risk by more than half if they took NSAIDs other than aspirin for 6 or more years, and Caucasian women likewise cut their cancer risk by 30 percent.

"The COX-2 research and the NSAID studies led us to consider whether anti-inflammatory drugs might have different associations with breast cancer risk across ethnic groups," said Gill. "We are not sure why we didn't see a reduction in breast cancer incidence for aspirin users as other studies have shown, but we are intrigued by the reduced risk we observed among African-American and Caucasian women who used other NSAIDs. We believe more studies with detailed dosage information need to be conducted to resolve the role aspirin and NSAIDs play in the inhibition of breast cancer development." Gill cautioned that their study did not collect information on dose and frequency of aspirin or other NSAID use.

The researchers followed a cohort of 99,553 African-American, Caucasian, Japanese, native Hawaiian and Latina women from Hawaii and Los Angeles County between 1993 and 2002. When examining the risk of breast cancer from aspirin and other anti-inflammatory drugs, they found that body mass, tumor stage, or age had no consistent effect on the NSAID-cancer association.

Parity and risk of lung cancer

Women's reproductive behavior (having children or not) may increase their risk of lung cancer later in life, a study at the Harvard School of Public Health has found.

Jessica Paulus, a graduate student in epidemiology, and her colleagues studied data from 1,075 women with lung cancer and 867 cancer-free women who took part in a research study from 1992 to 2004 at the Massachusetts General Hospital in Boston. The researchers found that women who had any children (one or more) had nearly 40 percent less risk of lung cancer as compared to women without children. That risk of lung cancer also declined in a linear fashion with increasing numbers of children born.

"Patterns of lung cancer incidence suggest that women may be at a greater risk of lung cancer as compared to men," said Paulus. "Given the role of estrogen as a risk factor in other cancers, and the relationship between number of births and estrogen levels in the body, we hypothesized that having children may be associated with lung cancer risk in women."

While the researchers found a linear relationship between lung cancer and number of children, having one child did not significantly decrease the cancer risk compared to women who never had given birth. Having two children reduced the risk of cancer by 20 percent, and having three or more children reduced that risk by 40 percent.

The protective effect of childbearing was strongest -- but not significant statistically -- in women who had never smoked as compared to current and former smokers. Also, the protective effect of childbearing on lung cancer risk was limited to cases of average age of onset, and was not observed in women diagnosed with lung cancer before age 55 years.

"Our study supports the idea of an inverse relationship between having children and the risk of lung cancer among women," Paulus said. "While smoking behavior remains the strongest risk factor for lung cancer in women, our work indicates a need to further examine the role played by reproductive factors in lung cancer."

Risk factors for renal cell carcinoma in the multiethnic cohort study

Moderate alcohol consumption may lower the risk of renal cell carcinoma, but only in men, while exercise may also reduce risk, but only in women.

Renal cell carcinoma, the most common malignant kidney tumor, has no known cause but has been associated with a number of risk factors. A study by the universities of Southern California and Hawaii found that risks of renal cell carcinoma rise sharply with being overweight, smoking or hypertension, and decrease with physical activity and moderate alcohol consumption.

Wendy Setiawan, Ph.D., assistant professor of preventive medicine at USC, and her colleagues studied data from 167,200 ethnically diverse Americans who had participated in a study from 1993 to 1996. During an eight-year follow-up period, the researchers found 246 men and 129 women who were diagnosed with renal cell carcinoma.

"By examining the association between body size, physical activity, smoking, alcohol consumption and medical conditions, we discovered that body mass index (BMI) increases risk, smoking and hypertension had independently higher risks of cancer, while physical activity and drinking appeared to reduce the risks," Setiawan said. "While smoking has long been associated with the cancer, some of the other risk factors are newly found associations and merit further study in preventing the disease."

The risk of renal cell cancer increased incrementally with every rising unit of BMI (measured as weight divided by height squared), especially among women. Being obese with a BMI over 30 posed a 1.5 times higher risk of cancer for men, and more than 2 and a third times higher risk for women. Hypertension increased the risk by one-and-a-half times for men and more than one-and-two-third times for women. Cigarette smoking, long considered a risk factor, was confirmed by the study.

Increased alcohol consumption, however, reduced the risk by about one-third, but only among men. In addition, physical activity reduced risk only among women.

Renal cell carcinoma, marked by the growth of malignant tumors in the lining of the kidney's tubules (which carry urine and other wastes from the blood into the bladder), constitutes 90 percent of all malignant kidney cancers. About 38,900 Americans are diagnosed with the disease each year; of that, about 12,800 die. Its occurrence is increasing by about 1.5 percent each year. The cause of the disease, as well as of its increased occurrence, remains a mystery.
http://www.medilexicon.com/medicalnews.php?newsid=56758∞

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