Cancer Watch

 

THE FAT TO CANCER

Obesity proves to be an important risk for many cancer types

 

 


New virus linked to rare skin cancer

WASHINGTON

Researchers have discovered a new virus they believe may be linked to a rare but extremely lethal type of skin cancer. In a study published in Science, a research team from the University of Pittsburgh Cancer Institute said it found a strong link between the rare cancer and a new virus they called Merkel cell polyomavirus (MCV).

    "This is the first polyomavirus to be strongly associated with a particular type of human tumor," said Patrick Moore, a member of the research team.

    While the researchers emphasized that more study was needed to confirm the link, they said the discovery could lead to new cancer treatments. The scientists identified the virus's DNA sequence in 80 percent of Merkel cell tumors. The virus penetrates tumor cells in a pattern indicating that the infection precedes the cells' growth into a cancer, they said.

    Merkel cell carcinoma mostly afflicts the elderly and people with weaker immune systems, including AIDS and transplant patients. Cases have tripled over the past 20 years to about 1,500 a year, and about half the patients with advanced stages of the cancer live only nine months. Two-thirds die within five years.

    The researchers believe the new virus produces a carcinogenic protein and blocks a gene that stops the growth of cancer cells.

    "Information that we gain could possibly lead to a blood test or vaccine that improves disease management and aids in prevention," Moore said.

    The researchers noted that a vaccine now exists to prevent cervical cancer, which is caused by another virus known as human papillomavirus. "MCV is another model that may increase our understanding of how cancers arise, with possibly important implications for nonviral cancers like prostate or breast cancer," said pathology professor Yuan Chang.


RNAs impede spread of breast cancer

PARIS

Scientists have isolated bits of genetic code whose disappearance in breast-cancer patients allows the disease to spread to bones and lungs. When present, the three types of small ribonucleic acid, or microRNA, suppress metastasis, said a study in Nature.

    Metastasis is the overwhelming cause of death in patients with solid tumors. Less than 10 percent of women with metastatic breast cancer survive beyond a decade.

    Based on experiments with mice and research on cancer patients conducted at the Memorial Sloan-Kettering Cancer Center in New York, the findings could pave the way to drugs that could prevent or treat metastasis not just in breast cancer, but other forms of the disease as well. More immediately, they will help doctors gauge the possibility that a given patient's cancer will migrate or relapse.

    "The gene signature we have identified could offer another tool for assessing the likelihood that cancer will progress," said the study's senior author Joan Massague, a researcher at Sloan-Kettering's Howard Hughes Medical Institute.

    Earlier studies reported that certain tumors, including breast cancer, had decreased levels of microRNA. Massague and his colleagues wanted to find out if these tiny molecules that regulate gene activity might play a role in spreading the disease.

    The first step-comparing the genetic profile of nonmetastatic and metastatic human breast cancer cells-showed highly reduced numbers of three kinds of microRNA in the latter, both in the laboratory and in patients. When the researchers restored the microRNA to normal levels, it greatly reduced the human cancer cells' ability to spread to the lungs or bones of mice. Further analysis showed that one of these absent microRNA, called miR-126, boosted the proliferation rate of metastatic cells, while the other two-miR-335 and miR-206-helped the cancer cells to infect the lungs or bone.

    MicroRNAs are tiny strings of nucleotides, the basic building blocks of DNA. They regulate gene activity by repressing or enhancing the work of messenger RNAs (mRNA), another type of molecule that ferries the blueprint for constructing proteins from DNA genes to the cell's ribosomes, the factories where proteins are made.

    The first set of experiments showed an unmistakable link between the microRNA and metastasis. But what precise mechanism caused the cancer to spread? To find out, the researchers looked to see which genes were regulated by the trio of microRNA they had identified.

    Six genes, they discovered, became hyperactive with the loss of miR-335, including two-SOX4 and TNC-that were known to control the kind of cell migration that enables cancer to invade other tissues. When the scientists "knocked down" the activity of these genes, they also reduced the cancer cells' ability to spread.

    The final step confirmed the laboratory findings: data from 368 patients with breast cancer showed that tumors in which these miR-335-regulated genes were especially active were much more likely to metastasize.

    Scientists are now in a position to develop drugs targeting the genes that contribute to metastasis, said Massague. His findings also hold promise for other types of cancer as well. "We have basically opened a window into a major future inquiry into such genes," he said.


Obesity boosts cancer risk

PARIS

Being obese boosts the risk of half a dozen types of cancer, and the odds strengthen as one's waistline thickens, according to a major review published by The Lancet in February.

    Doctors at the University of Manchester, northwestern England, trawled through 141 studies that monitored the health of 282,000 people who gained weight. Their benchmark of fat was the body-mass index (BMI), in which the individual's weight in kilos is divided by the square of the person's height in meters. Individuals with a BMI of 25 to 29.9 are considered overweight, while those with a BMI of 30 or more are obese.

    The investigators found that every gain of five points in BMI among men raised the risk of gullet cancer by 52 percent, of thyroid cancer by 33 percent and of colon and kidney cancers by 24 percent. Among women, a BMI increase of five points hiked the risk of cancer of the uterus lining by 59 percent, of the gallbladder by 59 percent, of the gullet by 51 percent and of the kidney by nine percent.

    Smaller but still significant associations were seen between BMI increase and cancer of the rectum, colon and skin among men, and of the breast, pancreas, thyroid, and colon among women. In both sexes, there was an increased risk of leukemia, non-Hodgkin's lymphoma, and multiple myeloma.

    Obesity has long been linked to deaths from cardiovascular disease and to diabetes in industrialized countries, a phenomenon that is now extending to cities in developing economies. According to some estimates, deaths from obesity in the United States outstripped those from smoking in 2005. But only recently has strong evidence emerged of an association between excess body fat and cancer.

    A ground-breaking report issued last year by the World Cancer Research Fund and the American Institute for Cancer Research found a link with cancers of the throat, colon, rectum, kidney and, among postmenopausal women, the breast.

    In an accompanying commentary, Swedish nutritionists Susanna Larsson and Alicja Wolk of the Karolinska Institute in Stockholm speculated that excess body fat may cause changes in levels of insulin, sex steroids, and other hormones. This could have an impact on apoptosis, the mechanism by which a flawed cell commits suicide. Cancerous cells are able to bypass apoptosis and proliferate unchecked. Localized accumulation of fat cells could also contribute significantly to specific tumors, such as cancers of the liver and throat, suggested Larsson and Wolk.


Ten new genetic clues for prostate cancer

PARIS

Gene sleuths announced they had identified more than 10 new genetic links to prostate cancer, two of which would be included in a new diagnostic test aimed at spotting men at risk from this disease. Working separately, scientists gathered in three international consortia crunched through genetic data garnered from blood samples provided by thousands of volunteers.

    Men with prostate cancer had a strong tendency to have telltale variants in locations on chromosomes 2, 3, 6, 7, 10, 11, and 19 and the X chromosome for gender, they reported in the latest issue of Nature Genetics.

    One of the group of investigators worked in Iceland, trawling over a local DNA treasure trove. Two of the genetic variants, on the X chromosome and chromosome 2, would be included in a new lab test for prostate cancer, they said.

    The new diagnostic tool, called deCODE PrCa, would look for a total of eight such signatures, said deCODE genetics, a biopharmaceutical company that is looking through the Icelandic DNA data in the search for new medical products.

    Researcher Gilles Thomas, who took part in a study by the United States National Institutes of Health, said that, individually, the genetic variants "play a low-key part" in prostate cancer, but became more dangerous when they accumulated. "It's being able to spot several variants at one time that we can start helping people who are at high risk," he said.

    Prostate cancer is the commonest cancer afflicting men in developed countries and heredity is known to play a key but poorly understood role in it. Men with close relatives who have had prostate cancer are twice as likely to develop the disease as counterparts with no recent family history of this ailment. But, until now, only a few genes have been associated with the disease, and they account for only a small percentage of potential cases.


US cancer deaths continue to drop

WASHINGTON

Cancer death rates in the United States dropped by a yearly average of 2.1 percent from 2002 to 2004, nearly double the rate of the preceding decade. A study by top US cancer-research groups found fewer deaths from colorectal cancer in men and women, prostate and lung cancer in men, and breast cancer in women. Lung cancer deaths fell two percent for men, and rose 0.2 percent for women, a rate increase researchers said was still lower than in 1993-2002.

    "The significant decline in cancer death rates demonstrates important progress in the fight against cancer that has been achieved through effective tobacco control, screening, early detection and appropriate treatment," said director Julie Gerberding of the US Centers for Disease Control and Prevention (CDC). "The evidence is unmistakable: we are truly turning the tide in the cancer battle," said American Cancer Society (ACS) chair John Seffrin. "The gains could be even greater if everyone in the US had access to essential health care, including primary care and prevention services," he added.

    The ACS said 1.4 million Americans would have been diagnosed with cancer this year, with 560,000 expected to die also in 2007.

    The study was carried out jointly by the National Cancer Institute, CDC, and ACS.

    The nearly five-percent drop in colorectal-cancer deaths for both sexes is likely explained by the early detection of precancerous polyps among people above 50, thanks to widespread endoscopic examination or colonoscopy, the study said. Colorectal cancer death rates dropped 4.9 percent for men, and 4.5 percent for women each year between 2002 and 2004. The decline in lung cancer in both men and women was attributed to fewer people smoking.

    "Incidence rates for female breast cancer dropped substantially from 2001 through 2004 ... possibly related to declining use of hormone-replacement therapy as well as the recently reported decline in use of screening mammography," the report said. M

 

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