Gene key to common kidney cancer identified

May 21, 2010 By Leave a Comment

Washington, May 21 (ANI): Scientists have found a key gene that, when turned off, promotes the development of common kidney cancer.

Their findings suggest that a combination of agents now being tested in other cancers may turn the gene back on, providing a much-needed therapy for the difficult-to-treat cancer.

Researchers at Mayo Clinic”s campus in Florida describe a gene called GATA3 that has been silenced in clear cell renal cell carcinoma (ccRCC), the most common kind of kidney cancer, and is a key gene also lost in breast cancer.

GATA3 controls many genes and proteins that regulate cell growth, and one of them, a receptor known as the type III transforming growth factor-ß receptor (TßRIII), is absent in a number of cancers.

According to the study”s senior investigator, John Copland, a cancer biologist at the Mayo Clinic campus at Florida, these findings will surprise many in the cancer field.

“Cancer researchers know that GATA3 is essential for immune T cell development and function. As well, very recent studies show that GATA3 is also critical to breast cancer development, where GATA3 expression is limited to mammary luminal epithelial cells. GATA3 is lost during breast cancer progression and its loss is a strong predictor of poor clinical outcome in luminal breast cancer. GATA3 also plays an important role in renal development and differentiation during embryogenesis, but little is known about the role of GATA3 in the adult human kidney,” he said.

“Now it looks like GATA3 regulates the expression of genes that are critical to cancer control in the kidney, and silencing it appears to be very important to the growth of kidney cancer and probably to others tumors, as well. No one could have guessed that would be the case in kidney cancer. This is a completely novel finding,” he added.

The study has been published in the May 20, 2010 issue of Oncogene. (ANI)

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Mice study shows slight changes in 2 genes launches breast cancer development

May 13, 2010 By Leave a Comment

Washington, May 13 (ANI): Scientists have made a new breakthrough in the fight against breast cancer.

Researchers at Georgetown Lombard Comprehensive Cancer Center have been able to show, in mice, how just a little adjustment in the expression of two common genes can promote the kind of cellular changes that led to breast cancer.

They say these tweaks likely mimic natural variation women have in expression of the two genes.

The researchers say that a readout of these two genes – estrogen receptor alpha and p53 – in healthy women could provide an “interacting biomarker” that might predict future breast cancer risk.

“It was believed that both of these genes only act once breast cancer had developed – p53 mutations are found in many cancers, including breast cancer, and the majority of women with breast cancer have over-expression of this common estrogen receptor,” says the study”s lead investigator, Priscilla A. Furth, a professor of oncology and medicine with Lombardi at Georgetown University Medical Center.

“What wasn”t known is that different levels of expression of these genes can help launch the cellular changes that lead to breast cancer.

“That suggests that testing women for their own variations in these genes might potentially give us a clue as to which women are at higher risk for development of breast cancer,” Furth adds.

In the study, the researchers developed mice in which one copy of the p53 gene was silenced (mice, and humans, inherit two copies, one from each parent), and tested the effect on what is known as development of preneoplasia, or early breast cancer progression.

The p53 gene, long called the ”guardian of the genome,” is known as a very powerful tumour suppressor because it regulates cell growth. Alterations to p53 are reported in 30-40 percent of human breast cancers, and this loss is linked to increased cancer aggressiveness, poor prognosis, and chemotherapy resistance.

The researchers also increased expression of the estrogen receptor by two-fold, an equivalent elevation sometimes seen in women. Almost 70 percent of women with breast cancer have estrogen receptor-positive breast cancer, meaning that the estrogen hormone is driving cell growth because it is binding to, in some cases, an over abundance of its receptors on the outside of breast cells.

Both mouse models showed significant precancerous changes in breast tissue. They then compared those effects with changes seen in mice that had one p53 gene as well as twice as much estrogen receptor expression, and found substantially higher evidence of early stage breast cancer progression.

“Normal breast tissue functioning requires a balance of cell growth and cell death, and in this study we found that both deregulated estrogen receptor function and p53 expression independently, and in combination, altering this balance and transforming cells,” Furth says.

The study has published in the May 15 issue of Cancer Research. (ANI)

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New protein involved in longevity identified

May 8, 2010 By Leave a Comment

Washington, May 8 (ANI): The level of a single protein in the tiny roundworm C. elegans determines how long it lives, researchers in the Department of Biochemistry and Molecular Biology at Thomas Jefferson University have found.

Worms born without this protein, called arrestin, lived about one-third longer than normal, while worms that had triple the amount of arrestin lived one-third less.

The research also showed that arrestin interacts with several other proteins within cells to regulate longevity.

The human version of one of these proteins is PTEN, a well-known tumor suppressor. The study, to be published in the online edition of the Journal of Biological Chemistry, was chosen by the journal as the “Paper of the Week” – considered in the top one percent of published articles.

Because most proteins in worms have human counterparts, these findings may have relevance to human biology and the understanding of cancer development, said Jeffrey L. Benovic, Ph.D., professor and chair of the department.

“The links we have found in worms suggest the same kind of interactions occur in mammals although human biology is certainly more complicated. We have much work to do to sort out these pathways, but that is our goal,” said Dr. Benovic.

Researchers use the roundworm as a model because it offers a simple system to study the function of genes and proteins that are relevant to human biology. (ANI)

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Lactate”s role in development of breast cancer

April 20, 2010 By Leave a Comment

Washington, April 19 (ANI): Researchers from The Cancer Institute of New Jersey (CINJ) have revealed the role lactate plays in the development of breast cancer cells and surrounding connective tissue.

A known energy source for cancer cells is blood sugar (glucose), which helps convert food into a useable resource for the cell.

Cancer cells also can convert glucose into lactic acid (or lactate), which can result in excess accumulation of this chemical in the cell. In order for tumor cells to thrive, the lactate needs to be expelled from the cell.

This function is carried out by a family of proteins (monocarboxylate transporters) that transport this lactic acid across cell membranes.

Previous study shows that breast cancer development and disease spread are highly dependent on specialized connective tissue (stroma), particularly carcinoma associated fibroblasts (CAFs), as tumors rarely develop in the absence of this tissue.

CAFs are known to support tumor growth and may cause tumor cells to be drug resistant. The exact role of stroma in the development of breast cancer remains unclear and is an area of intense investigation.

To explore whether lactate produced by tumor cells is used as an energy source for stromal cells — in effect forming a small ecosystem where lactate is an essential element — the team developed an experimental system to generate CAFs from bone marrow-derived mesenchymal stem cells (MSCs), which make up the outer connective tissue of a cancer tumor.

Investigators have demonstrated the ability of these CAFs to promote tumor growth both in laboratory and experimental models using a cell line that represents the basal subtype of human breast cancer.

They found that CAFs can remove lactate from the tumor environment and utilize it as an energy source by increased activity of monocarboxylate transporters.

In exchange, the CAFs support tumor growth by providing the tumor with the stimulation necessary to secrete proteins in order to regulate certain cellular functions. One of these functions is the recruitment of MSCs through cell migration, in essence, directing strategic placement of these cells.

“These studies will increase our understanding of metabolic cooperation between two of the principal players in the tumor environment and will yield information regarding important targets permitting future development of focused therapies for stroma reliant tumors,” said Debabrata Banerjee, a scientist at CINJ and associate professor of medicine at UMDNJ-Robert Wood Johnson Medical School, is the senior investigator.

The findings have been presented this week at the 101st Annual Meeting of the American Association for Cancer Research (AACR). (ANI)

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Lactate”s role in development of breast cancer

April 19, 2010 By Leave a Comment

Washington, April 19 (ANI): Researchers from The Cancer Institute of New Jersey (CINJ) have revealed the role lactate plays in the development of breast cancer cells and surrounding connective tissue.

A known energy source for cancer cells is blood sugar (glucose), which helps convert food into a useable resource for the cell.

Cancer cells also can convert glucose into lactic acid (or lactate), which can result in excess accumulation of this chemical in the cell. In order for tumor cells to thrive, the lactate needs to be expelled from the cell.

This function is carried out by a family of proteins (monocarboxylate transporters) that transport this lactic acid across cell membranes.

Previous study shows that breast cancer development and disease spread are highly dependent on specialized connective tissue (stroma), particularly carcinoma associated fibroblasts (CAFs), as tumors rarely develop in the absence of this tissue.

CAFs are known to support tumor growth and may cause tumor cells to be drug resistant. The exact role of stroma in the development of breast cancer remains unclear and is an area of intense investigation.

To explore whether lactate produced by tumor cells is used as an energy source for stromal cells — in effect forming a small ecosystem where lactate is an essential element — the team developed an experimental system to generate CAFs from bone marrow-derived mesenchymal stem cells (MSCs), which make up the outer connective tissue of a cancer tumor.

Investigators have demonstrated the ability of these CAFs to promote tumor growth both in laboratory and experimental models using a cell line that represents the basal subtype of human breast cancer.

They found that CAFs can remove lactate from the tumor environment and utilize it as an energy source by increased activity of monocarboxylate transporters.

In exchange, the CAFs support tumor growth by providing the tumor with the stimulation necessary to secrete proteins in order to regulate certain cellular functions. One of these functions is the recruitment of MSCs through cell migration, in essence, directing strategic placement of these cells.

“These studies will increase our understanding of metabolic cooperation between two of the principal players in the tumor environment and will yield information regarding important targets permitting future development of focused therapies for stroma reliant tumors,” said Debabrata Banerjee, a scientist at CINJ and associate professor of medicine at UMDNJ-Robert Wood Johnson Medical School, is the senior investigator.

The findings have been presented this week at the 101st Annual Meeting of the American Association for Cancer Research (AACR). (ANI)

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Therapeutic target to stop cancer metastases found

April 1, 2010 By Leave a Comment

Washington, Apr 1 (ANI): Scientists from New York University have found therapeutic target to stop cancer metastases.

Published in the Journal of Leukocyte Biology, the new research suggests that combating immune suppressive cells in the liver early after a cancer develops may keep the disease from spreading to the liver.

“Our work may open a new field of experimental therapeutics as combating the eventual development of liver metastases by targeting immune suppressive cells in the livers in patients with early cancer can have great benefit,” said George Miller, a scientist involved in the work from the Departments of Surgery and Cell Biology at the New York University School of Medicine.

Miller and colleagues reached this conclusion after conducting experiments in mice.

In the experiments, the researchers used mice that spontaneously developed pancreatic cancer because of a mutation (Kras-mutation) in the progenitor cells of the pancreas, as well as mice with advanced colon cancers that spread to the abdomen. They then studied the expansion of immune suppressive cells in the liver from a very early stage in the cancer development to determine the immune phenotype, stimulus for recruitment, inhibitory effects and tumor-enabling function of these cells. Results suggest that combating immune suppressive cells in the liver early after cancer development may prevent the spread of cancer to this vital organ.

“This study could represent one of those ”a-ha” moments in science where one idea or experiment opens up entirely new ways of approaching and understanding a problem,” said Luis Montaner, Editor-in-Chief of the Journal of Leukocyte Biology. “Physicians have known that the spread of cancer to the liver is far too common to occur by chance. Now we know that the immune system likely plays a role in facilitating this process. The next step, obviously, is to learn more so we can prevent it from happening.” (ANI)

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Experimental vaccine may delay bowel inflammation and colon cancer

March 25, 2010 By Leave a Comment

Washington, March 25 (ANI): A new experimental vaccine could delay bowel inflammation and colon cancer, researchers at the University of Pittsburgh School of Medicine say.

Their findings have appeared in Cancer Prevention Research, a journal of the American Association for Cancer Research.

According to senior author Olivera Finn, professor and chair, Department of Immunology, Pitt School of Medicine, people with chronic inflammatory disorders such as IBD are at greater risk for developing cancer at the inflamed site. In other cases, genes that develop cancerous changes can trigger inflammation.

The vaccine made by her team is directed against an abnormal variant of a self-made cell protein called MUC1, which is altered and produced in excess in both IBD and colon cancer.

Dr. Finn said: “Our experiments indicate that boosting the immune response against this protein early in the disease can delay IBD development, control inflammation and thereby reduce the risk of future cancers.

“These findings suggest also that the early stages of chronic inflammation might be considered a premalignant condition.”

For the study, the scientists tested transgenic mice that spontaneously develop IBD and then progress to colitis-associated colon cancer, producing the human version of MUC1 in both disease states. It was seen that animals that received the vaccine showed the first signs of IBD significantly later than those in two control groups that did not get the vaccine.

Microscopic evaluation of the colon tissue demonstrated less inflammation in the vaccinated mice, and no indication of cancerous changes. Nearly half of the animals in each of the control groups had evidence of abnormal tissue, and two had colon cancer.

Dr. Finn said: “The MUC1 vaccine seems to change the local environment from one that promotes cancer development to one that inhibits it.

“Certain immune cells that we usually see in the inflamed colon aren”t present, and that could make the surroundings less friendly for potentially cancerous cells that also are directly targeted by the vaccine for destruction.” (ANI)

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High dietary phosphate intake may increase skin cancer risk

March 24, 2010 By Leave a Comment

Washington, March 24 (ANI): A new study by researchers at Emory University School of Medicine has shown that a high intake of phosphates can contribute to tumor growth in skin cancer.

In the study, the researchers applied dimethylbenzanthracene, a carcinogen found in cigarette smoke, to the skins of mice, followed by another chemical that stimulates cell growth.

Feeding these mice a high phosphate diet (1.2 percent by weight) increased skin papilloma number by 50 percent compared with a low phosphate diet (0.2 percent).

Skin papillomas are the initial stage of skin cancer development, which may progress to full carcinoma.

“This is a very well established model for the initiation and progression of cancer, and the effects of many physiological conditions on cancer initiation have been measured this way,” said senior author George Beck, assistant professor of medicine (endocrinology) and a member of the Winship Cancer Institute, Emory University.

The study has been published in the journal Cancer Prevention Research. (ANI)

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Gene linked to lung cancer in non-smokers identified

March 22, 2010 By Leave a Comment

London, March 22 (ANI): Scientists have identified a gene that is specifically associated with lung cancer in people who have never smoked.

The research team, co-led by scientists at the Mayo Clinic campus in Minnesota, Harvard University, University of California at Los Angeles (UCLA), and MD Anderson Cancer Center, found that about 30 percent of patients who never smoked and who developed lung cancer had the same uncommon variant, or allele, residing in a gene known as GPC5.

The researchers found in laboratory studies that this allele leads to greatly reduced GPC5 expression, compared to normal lung tissue.

The finding suggests that the gene has an important tumor suppressor-like function and that insufficient function can promote lung cancer development.

“This is the first gene that has been found that is specifically associated with lung cancer in people who have never smoked,” says the study”s lead investigator, Ping Yang, Mayo Clinic genetic epidemiologist.

“What”s more, our findings suggest GPC5 may be a critical gene in lung cancer development and genetic variations of this gene may significantly contribute to increased risk of lung cancer. This is very exciting,” Yang added.

The research teams scanned and analyzed the genomes of 2,272 participants who have never smoked, nearly 900 of whom were lung cancer patients. It took researchers 12 years to identify and enroll these study participants.

“It has been very hard to do this research because never smokers have been mingled with smokers in past studies, and what usually pops up are genes related to nicotine dependence,” Yang said.

“Findings from this study concern pure lung cancer that is not caused by smoking, and it gives us some wonderful new avenues to explore,” Yang added.

The research has been published in the March 22 online issue of Lancet Oncology. (ANI)

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Weight gain in adulthood linked to prostate cancer risk

September 12, 2009 By Leave a Comment

Washington, Sep 12 (ANI): Body size and weight gain in younger and older adulthood may help weigh a man’s proneness to prostate cancer, according to a study by researchers at the University of Hawaii at Manoa’s Cancer Research Center of Hawaii.

Led by Dr. Brenda Hernandez, the researchers said that the risk varies among different ethnic groups

For the study, the researchers studied the relationship in a multiethnic population consisting of blacks, Japanese, Hispanics, Native Hawaiians and whites, and compared differences among age groups using the Multiethnic Cohort, a longitudinal study of men 45-75 years of age established in Hawaii and California from 1993-1996.

Of the 83,879 men who participated in the study, 5,554 developed prostate cancer.

Overall, men who were overweight or obese by age 21 had a decreased risk of localized and low-grade prostate cancer, according to Hernandez.

Their results suggested that being overweight in older adulthood was associated with increased prostate cancer risk among white and Native Hawaiian men, but a decreased risk among Japanese men.

While excessive weight gain between younger and older adulthood was observed to increase the risk of advanced and high-grade prostate cancers in white men and increase the risk of localized and low-grade disease in black men, it appeared to decrease the risk of localized prostate cancer in Japanese men.

“The relationship of certain characteristics, such as body size, with cancer risk may vary across ethnic groups due to the combined influence of both genes and lifestyle,” said Hernandez.

However, the relationship between body size and prostate cancer risk is not entirely understood.

Excess fat is associated with a number of conditions that contribute to cancer development including low-grade chronic inflammation, insulin resistance, metabolic abnormalities, and hormone imbalances.

These conditions may in turn contribute to more aggressive prostate malignancies.

Ethnic differences in cancer risk may be explained by differences in the distribution of stored body fat that could have a differential effect on the development of prostate cancer.

And the distribution of body fat may influence the specific way that excess fat influences cancer risk.

The study has been published in Cancer Epidemiology, Biomarkers and Prevention, a journal of the American Association for Cancer Research. (ANI)

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Turning off oncogene may inhibit lung cancer stem cells’ growth

September 10, 2009 By Leave a Comment

Washington, Sep 9 (ANI): A lung cancer oncogene, called PKCiota, is necessary for the proliferation of lung cancer stem cells, and turning it off could act as a key for the treatment of this deadly disease, according to scientists at the Mayo Clinic campus in Florida.

These stem cells are rare and powerful master cells that manufacture the other cells that make up lung tumours, and are resistant to chemotherapy treatment.

The study also shows that an agent, aurothiomalate, being tested at Mayo Clinic in a phase I clinical trial substantially inhibits growth of these cancer stem cells.

“Our data indicate that PKCiota is required for the earliest steps in the development of lung cancer, which is the expansion of tumor-initiating cells or cancer stem cells,” said the study’s senior author, Dr. Alan Fields.

“Lung cancer stem cells appear to be the major drivers in many common lung cancers, and in order for a therapeutic treatment to be effective, it has to disrupt these cancer stem cells. We show that aurothiomalate, the agent now being tested in lung cancer patients, can, in fact, target these cells,” he added.

While aurothiomalate was once used to treat rheumatoid arthritis, the researchers have now discovered that it can also target PKCiota.

Currently, the agent is being tested in patients at Mayo Clinic’s sites in Minnesota and Arizona and, based on this phase I trial, a phase II human clinical trial is planned to combine aurothiomalate with agents targeted at other molecules involved in cancer growth.

“We had previously shown that PKCiota is required to maintain tumor growth, but what this study sought to determine is whether PKCiota is involved in the initial steps of lung cancer development,” said Fields.

Fields said that, in mice, an oncogene known as Kras is thought to transform normal lung stem cells into cancer stem cells, thereby initiating lung cancer.

In the present study, the researchers established a strain of mice in which Kras can be activated at the same time that the PKCiota gene is inactivated.

They found that when the PKCiota gene is inactivated, Kras was unable to cause errant growth and expansion of lung stem cells in mice, the process that initiates tumour formation.

“What this told us is that Kras requires PKCiota to transform the lung stem cells and make them proliferate. In other words, PKCiota is downstream from Kras, and is necessary for Kras to initiate lung tumor formation,” said Fields.

After discovering that aurothiomalate disables PKCiota, the researchers tested whether this agent is effective against lung cancer that develops due to Kras mutation.

“The drug showed potent inhibitory effects on the Kras-dependent proliferation of lung cancer stem cells both in cell culture and in animals,” said Fields.

“That further suggests that a drug like aurothiomalate could have an effect on tumors that are dependent on either Kras or PKCiota for growth and survival, and that is potentially a lot of cancers.

Aurothiomalate appears to be one of the few drugs available that can effectively target these critical cancer stem cells. In the clinic, however, it is likely that aurothiomalate will be most effective when combined with other agents designed to target other tumor survival pathways,” he added.

The study has been published in Cancer Research. (ANI)

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Protein’s ‘Jekyll and Hyde’ role in cancer discovered

September 4, 2009 By Leave a Comment

Washington, September 4 (ANI): American scientists have discovered a protein’s “Jekyll and Hyde” role in cancer development.

While the protein called FOXO3a is thought to protect against cancer development, researchers from the Mayo Clinic campus in Florida and Harvard Medical School have found that it can actually spur the spread of tumours.

They point out that FOXO3a, a transcription factor that regulates gene expression, becomes active when growing cancer cells begin to starve.

Their study suggests that this protein then turns on molecular switches that allow the cancer cells to invade surrounding tissues.

“This is a complete reversal of what everyone thought about FOXO3a – that we should find a way to activate this transcription factor so as to fight cancer growth,” says cancer biologist Dr. Peter Storz, the study’s lead investigator from Mayo Clinic in Florida.

Funded in part by the Florida Department of Health, the study illustrates the growing recognition in the research community that proteins can play multiple roles with respect to tumour progression.

A research article describing the study has been published in the journal Molecular and Cellular Biology. (ANI)

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How diarrhoeal bacteria may cause some colon cancers

August 25, 2009 By Leave a Comment

London, August 24 (ANI): Johns Hopkins scientists have gained significant insights into how bacteria that cause diarrhoea may also be responsible for some colon cancers.

The researchers have found that strains of the common Bacteroides fragilis (ETBF) dupe immune system cells into permitting runaway colon tissue inflammation, a precursor for malignant growth.

“This could be the H. pylori of colon cancer,” Nature magazine quoted Dr. Cynthia Sears, Johns Hopkins infectious disease specialist, as saying, referring to the bacteria long known to cause stomach ulcers and suspected of causing the majority of stomach cancers.

During the study, she and her colleagues observed that ETBF uses tissue inflammation to cause colon cancer in a similar way that H. pylori causes stomach tumours.

In their study report, the researchers have highlighted the fact that a so-called enterotoxigenic bacterium is widely known to cause diarrhoea in children and adults, and that a previous study in Turkey has linked it to colon cancer.

While the bacteria does not cause any symptoms in some individuals, others develop diarrhoea and colon inflammation, which has been linked to cancer growth.

Unlike the case with H. pylori, it is unknown whether standard antibiotics can eradicate the microbe, experts say.

With a view to finding the link between ETBF and colon cancer, the researchers conducted a series of tests in mice bred to carry mutations in a colon cancer-causing gene called APC.

They observed that mice infected with ETBF developed diarrhoea that resolved quickly, but within a week, the animals developed inflammation and small tumours in the colon.

One month later, the colons were pockmarked with tumours.

Mice infected with a non-toxin producing strain of the bacteria were free of diarrhoea, inflammation, and tumours.

While evaluating the bacteria’s effect on immune responses that may contribute to cancer development, the researchers observed that in ETBF-infected mice, there were high levels of a protein called pStat3, which, in its normal role, acts as a signal to trigger inflammation.

One of those signals activates an immune cell called T-helper 17 (Th17). Th17 cells produce molecules that have been implicated in fostering inflammation of tissues.

The researchers said that Th17 activity in the gut of germ-bearing mice was 100 times greater than normal, and when it was blocked, inflammation and tumour growth in the animals was reversed.

Dr. Drew Pardoll, an immunologist and cancer researcher at Johns Hopkins, speculates that in humans, infection with ETBF “produces a low-level inflammation that persists for a long time.”

“If what we are seeing in mice holds true in humans, the chronic inflammation damages genetic material in the colon cells, allowing them to grow uncontrollably and develop into tumors earlier and more progressively than if they were not infected with ETBF,” Pardoll says.

Sears and Pardoll believe that ETBF may collude with other types of normal bacteria in the gut to promote cancer.

Given that the microbe itself is difficult to culture from stool specimens, th eresearchers are working on blood tests to detect antibodies to the pathogen’s toxin, which may show whether an individual has been exposed to it and perhaps determine who may be at risk for colon cancer.

The investigators also envision vaccines and drug therapies that neutralize the pathogen’s toxin and its ability to inflame tissues.

The study has been published in the journal Nature Medicine. (ANI)

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Gastrin levels vital in bacterial-induced stomach cancer

June 26, 2009 By Leave a Comment

Washington, June 24 (ANI): Gastrin levels have a very important role to play in the development of Helicobacter-induced stomach cancer, according to a study.

Over 50 percent of the world’s population is infected with Helicobacter pylori, which causes chronic inflammation of the stomach lining, and is strongly linked to the development of gastric ulcers and stomach cancer.

Stomach cancer is the second leading cause of cancer-related deaths worldwide.

Helicobacter infection results in increased expression of gastrin, a hormone that stimulates secretion of gastric acid.

However, the role of gastrin in cancer development still remains unclear.

While high levels of gastrin lead to the development of stomach cancer, but absence of gastrin has been shown to increase the numbers of tumours in the gastric antrum- the lower section of the stomach that empties into the small intestine.

Thus, for explaining this apparent disparity, a group led by Dr. Timothy Wang at the Columbia University Medical Center in New York, NY examined the contribution of Helicobacter infection to gastric cancer in animal models with either high expression of gastrin or no gastrin at all.

It was found that Helicobacter infection in mice with high levels of gastrin resulted in cancer of the gastric corpus (main body of the stomach).

On the other hand, infection in gastrin-deficient mice led to cancer in a different part of the stomach- the gastric antrum.

Thus, the researchers concluded that gastrin plays a key role in the development of Helicobacter-induced stomach cancer, but may have distinct effects on carcinogenesis in different parts of the stomach.

The related report by Takaishi et al, ‘Gastrin is an essential cofactor for Helicobacter-associated gastric corpus carcinogenesis in C57BL/6 mice’, is appearing in the upcoming issue of The American Journal of Pathology. (ANI)

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‘Vitamin D deficiency tied to cancer development’

May 22, 2009 By Leave a Comment

Washington, May 22 (ANI): Researchers at Moores Cancer Centre at the University of California, San Diego have found that low levels of vitamin D may play a crucial role in cancer development.

Lead researcher Cedric Garland, professor of family and preventive medicine at the UC San Diego School of Medicine, said that vitamin D may halt the first stage of the cancer process by re-establishing intercellular junctions in malignancies having an intact vitamin D receptor.

The research team claim to have developed a model, called DINOMIT that hinges on a loss of cancer cells’ ability to stick together.

“The first event in cancer is loss of communication among cells due to, among other things, low vitamin D and calcium levels,” said Garland.

“In this new model, we propose that this loss may play a key role in cancer by disrupting the communication between cells that is essential to healthy cell turnover, allowing more aggressive cancer cells to take over,” he added.

The researchers suggest that such cellular disruption could account for the earliest stages of many cancers.

“Competition and natural selection among disjoined cells within a tissue compartment, such as might occur in the breast’s terminal ductal lobular unit, for example, are the engine of cancer,” Garland said.

Garland revealed that each letter in DINOMIT stands for a different phase of cancer development. “D” stands for disjunction, or loss of intercellular communication; “I,” for initiation, where genetic mutations begin to play a role; “N” for natural selection of the fastest-reproducing cancer cells; “O” for overgrowth of cells; “M” for metastasis, when cancer cells migrate to other tissues, where cancer can kill; “I” refers to involution, and “T” for transition, both dormant states that may occur in cancer and potentially be driven by replacing vitamin D.

“The DINOMIT model provides new avenues for preventing and improving the success of cancer treatment,” he added. (ANI)

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Beef, chicken, fish may help treat stomach ulcers

May 16, 2009 By 1 Comment

Washington, May 16 (ANI): Beef, chicken, fish, eggs, dairy products and some fruits and vegetables could help keep stomach ulcers at bay, says a new study.

Bacteria known as Helicobacter pylori are known to cause such ulcers, and thus antibiotics are used a primary therapy for such infection. But today the bacteria are growing increasingly resistant to antibiotics.

And now, the study by scientists at Beth Israel Deaconess Medical Center (BIDMC) and the Massachusetts Institute of Technology, has shown that the amino acid glutamine, found in many foods as well as in dietary supplements, may prove beneficial in offsetting gastric damage caused by H. pylori infection.

The findings offer the possibility of an alternative to antibiotics for the treatment of stomach ulcers.

“Our findings suggest that extra glutamine in the diet could protect against gastric damage caused by H. pylori. Gastric damage develops when the bacteria weakens the stomach’s protective mucous coating, damages cells and elicits a robust immune response that is ineffective at ridding the infection,” says senior author Dr. Susan Hagen, Associate Director of Research.

She noted that eventually, years of infection result in a combination of persistent gastritis, cell damage and an environment conducive to cancer development.

Glutamine is a nonessential amino acid naturally found in certain foods, including beef, chicken, fish, eggs, dairy products and some fruits and vegetables. L-glutamine – the biologically active isomer of glutamine – is widely used as a dietary supplement by body builders to increase muscle mass.

In earlier studies, researchers had shown that glutamine protects against cell death from H. pylori-produced ammonia.

“Our work demonstrated that the damaging effects of ammonia on gastric cells could be reversed completely by the administration of L-glutamine. The amino acid stimulated ammonia detoxification in the stomach – as it does in the liver – so that the effective concentration of ammonia was reduced, thereby blocking cell damage,” explained Hagen.

Thus, they hypothesized that a similar mechanism might be at work in the intact stomach infected with H. pylori.

After testing the hypothesis on mice, researchers found that at six-weeks-post infection, the animals exhibited increased expression of three cytokines – interleukin 4, interleukin 10 and transforming growth factor-alpha mRNA.

“These all play an important role in the stomach’s ability to protect against damaging effects resulting from other responses to H. pylori infection,” explained Hagen.

The study results showed that in 20 weeks, H. pylori-infected mice, that were fed the L-glutamine diet exhibited lower levels of inflammation than did the mice that received the standard control diet.

“Because many of the stomach pathologies during H. pylori infection [including cancer progression] are linked to high levels of inflammation, this result provides us with preliminary evidence that glutamine supplementation may be an alternative therapy for reducing the severity of infection,” explained Hagen.

She added that studies in human subjects would be the next step to determine the relevance of this finding in the clinical setting.

The study was published in the latest issue of the Journal of Nutrition. (ANI)

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Red Sea Coral extract may help fight skin cancer

May 16, 2009 By Leave a Comment

Washington, May 16 (ANI): A research team led by an Indian-origin scientist at South Dakota State University has found that a substance derived from Red Sea Coral can help treat skin cancer.

The team led by SDSU distinguished professor Chandradhar Dwivedi looked at the chemopreventive effects of sarcophine-diol, made from a substance called sarcophine that can be isolated from soft coral found in the Red Sea.

They found that sarcophine-diol has the potential to inhibit cell growth of cancers, and induce orderly, programmed cell death of skin cancer cells.

“We are finding that sarcophine-diol could be used both for chemoprevention and as a chemotherapeutic agent,” said Dwivedi.

The study showed that treating human skin cancer cells with different concentrations of sarcophine-diol for different lengths of time reduced the viability of cancer cells in each case.

Sarcophine-diol also inhibited the proliferation or uncontrolled growth of cancer cells. It also induced apoptosis, or programmed cell death, in cancer cells.

Dwivedi said that the extent of apoptosis observed in different treatments in the study was correlated to the level of sarcophine-diol used.

The study found that treatments with higher concentrations of sarcophine-diol induced higher level of so-called “executioner” proteins that have a role in apoptosis, or programmed cell death compared to a control group.

“Further investigations of sarcophine-diol in experimental models and in cell culture studies are needed to explore its mechanisms of action,” Dwivedi said.

“Sarcophine-diol has excellent potential to be a potent chemotherapeutic agent that can be further investigated for use against nonmelanoma skin cancer development,” he added.

The study is published in the academic journal Translational Oncology. (ANI)

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Bone density may help predict prostate cancer risk

May 2, 2009 By Leave a Comment

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Washington, April 27 (ANI): A new study by Johns Hopkins researchers has found that men with denser bones may be more likely to develop prostate cancer./pp
Recent research at other institutions has suggested that women with high bone mineral density are at an increased risk of aggressive breast cancer. /pp
For the study, Stacy Loeb, M.D., in the Department of Urology at the Johns Hopkins University School of Medicine, and colleagues gathered data from the BLSA, a long-term study that has tracked health-related information for hundreds of Baltimore-area men and women since 1958. /pp
The researchers collected data on the bone mineral density of 519 men, measured from 1973 to 1984. They then looked at BLSA data again to see which men were eventually diagnosed with prostate cancer. /pp
When they analyzed their results, researchers found that the 76 men who went on to develop prostate cancer had bone density that remained significantly higher as they aged compared to those who remained cancer free./pp
Although the reasons for this phenomenon are unclear, Loeb speculates that growth factors in bone may contribute to prostate cancer growth. /pp
Additionally, bone density may reflect sex hormone levels in men, which can also affect prostate cancer development./pp
We don’t have an explanation yet, but we’re hoping that these findings stimulate further study, said Loeb. /pp
The study has presented at the American Urological Association Annual Meeting 2009. (ANI)/p

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Herbal extract inhibits pancreatic cancer development

April 20, 2009 By Leave a Comment

Washington, Apr 20 (ANI): A herb used in traditional medicine by many Middle Eastern and Asian countries not only kill pancreatic cancer cells but also appears to inhibit development of pancreatic cancer as a result of its anti-inflammatory properties, researchers from the Kimmel Cancer Center at Jefferson found.

Hwyda Arafat, M.D., Ph.D., associate professor of Surgery at the Jefferson Medical College of Thomas Jefferson University, said that thymoquinone, the major constituent of the oil extract from a Middle Eastern herbal seed called Nigella sativa, exhibited anti-inflammatory properties that reduced the release of inflammatory mediators in pancreatic cancer cells.

Dr. Arafat said that Nigella sativa seeds and oil, used in traditional medicine by many Middle Eastern and Asian countries, helps treat a broad array of diseases, including some immune and inflammatory disorders.

Previous studies have also shown it to have anti-cancer effects on prostate and colon cancers.

Based upon their previously published findings that thymoquinone inhibits histone deacetylases (HDACs), Dr. Arafat and her colleagues compared the anti-inflammatory properties of thymoquinone and trichostatin A, an HDAC inhibitor that has previously shown to ameliorate inflammation-associated cancers.

The researchers used pancreatic ductal adenocarcinoma (PDA) cells, some of which were pretreated with the cytokine TNF-alpha to induce inflammation.

Thymoquinone almost completely abolished the expression of several inflammatory cytokines, including TNF-alpha, interleukin-1beta, interleukin-8, Cox-2 and MCP-1, an effect that was more superior to the effect of trichostatin A.

The herb also inhibited the activation and synthesis of NF-kappaB, a transcription factor that has been implicated in inflammation-associated cancer.

Activation of NF-kappaB has been observed in pancreatic cancer and may be a factor in pancreatic cancer’s resistance to chemotherapeutic agents.

When animal models of pancreatic cancer were treated with thymoquinone, 67 percent of the tumours were significantly shrunken, and the levels of proinflammatory cytokines in the tumours were significantly reduced.

Inflammation has been implicated in the development of several solid tumour malignancies. Chronic pancreatitis, both hereditary and sporadic, is associated with the risk of developing pancreatic cancer.

“Not only patients with chronic pancreatitis could benefit from this, but also several other groups with risk of development or recurrence of pancreatic cancer, such as high-risk family members and post-surgical patients. These potent effects show promise for the herb as a potential preventive and therapeutic strategy for pancreatic cancer. More importantly, the herb and oil are safe when used moderately, and have been used for thousands of years without reported toxic effects.” Dr. Arafat said

The study was presented at the AACR 100th Annual Meeting 2009 in Denver. (ANI)

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Lung cancer susceptibility gene identified

April 16, 2009 By Leave a Comment

Washington, Apr 16 (ANI): A gene, known as RGS17, has been identified as a distinct gene linked to increased lung cancer susceptibility and development in a new study.

Cancer cell biologists at the University of Cincinnati (UC) say that this gene can predispose people with a strong family history of lung cancer towards developing the disease.

They say that further research may make the gene a marker to identify high-risk patients who may benefit from earlier, more aggressive lung cancer screening.

“Understanding how the RGS17 gene impacts cancer development could change clinical diagnosis and treatment as radically as discovery of the breast cancer genes (BRCA1 and BRCA2) did. A proven genetic test could help us identify people at risk before the disease progresses,” said Dr. Marshall Anderson, who has led the multi-institutional Genetic Epidemiology of Lung Cancer Consortium (GELCC).

Lung cancer is the leading cause of cancer related disease and death, which is primarily caused by tobacco smoke. However, science has shown that there is also a strong genetic component to the disease.

“This study represents a significant contribution to our understanding of lung cancer susceptibility and is another step toward to the goal of preventive medicine. The authors undertook a daunting challenge of performing a family-based study of lung cancer in an effort to identify specific causal genes,” said David Christiani at the Harvard School of Public Health.

For the study, the researchers collected biological samples from numerous multigenerational families with five or more members who were affected by lung cancer.

By a combination of what is known as “fine mapping”-where genetic information is dissected and analysed-and genetic association studies, they identified RGS17 as a major candidate susceptibility gene for familial lung cancers.

The researchers used a genetically altered mouse model, and found lung tumours to shrink when RGS17 was suppressed, which indicated that the gene was involved in cancer development and must be present for cancer growth.

“What was most interesting is that this same gene was over-expressed in 60 percent of the samples from non-hereditary lung tumours. This suggests that perhaps epigenetic factors may be contributing to abnormal genetic development,” said Anderson.

Additional research is underway to find out how environmental factors may influence familial cancer development.

The study has been published in a recent issue of the journal Clinical Cancer Research. (ANI)

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