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Study demonstrates how gene variant may contribute to cancer development
October 05, 2005A relatively common cancer susceptibility gene appears to be frequently acquired in metastatic lesions from colorectal cancer, and give cancer cells a growth advantage, according to a study in the October 5 issue of JAMA.
Transforming growth factor beta (TGF-beta) is a potent naturally occurring inhibitor of cell growth, according to background information in the article. It exerts its action by binding to type I (TGFBR1) and type II (TGFBR2) receptors located on the cell membrane. Increased cell growth due to decreased TGF-beta growth inhibition may contribute to cancer development. TGFBR16A is a common polymorphism (variation) of TGFBR1. Previous studies have shown that TGFBR16A is one of the first candidate tumor susceptibility alleles (DNA codings of the same gene) that is found in a large proportion of the general population (13.7 percent) and significantly increases cancer risk by approximately 24 percent. How TGFBR16A contributes to cancer development is largely unknown.
Boris Pasche, M.D., Ph.D., of Northwestern University Feinberg School of Medicine, Chicago, and colleagues conducted a study that included 531 patients with a diagnosis of head and neck cancer, colorectal cancer, or breast cancer recruited from 3 centers in the United States and from 1 center in Spain from June 1, 1994, through June 30, 2004. Multiple genetic testing of the cancer cells was conducted.
The researchers found that TGFBR1 mutated into TGFBR16A, i.e. was somatically acquired, in 13 of 44 (29.5 percent) colorectal cancer metastases, in 4 of 157 (2.5 percent) of colorectal tumors, in 4 of 226 (1.8 percent) head and neck primary tumors, and in none of the 104 patients with breast cancer.
While TGF-beta inhibits the growth of normal cells, cancer cells secrete larger amounts of TGF-beta than their normal counterparts. The researchers showed that, in the presence of TGF-beta, the growth of cancer cells that carry the TGFBR16A gene is 55 percent greater than cancer cells that do not carry this gene, indicating that TGFBR16A give cancer cells a selective advantage. This, together with the findings that TGFBR16A is acquired by tumors, may explain why half of all liver metastases from colorectal cancer carried the TGFBR16A gene while it is only found in 14 percent of the general population.
" individuals who carry the 6A allele, either in the germline or somatically acquired by the tumor, may have a greater likelihood of developing metastases than individuals who do not carry this allele. 6A may therefore serve as a useful biomarker in cancer." The authors add that TGFBR16A may bestow cancer cells with a growth advantage in the presence of TGF-beta.
"Since 13.7 percent of the general population and 17.1 percent of patients with a diagnosis of cancer carry at least 1 copy of the 6A allele, our findings may have substantial public health importance. The high frequency of 6A carriers in the general population and the moderately increased risk of breast, colon, and ovarian cancer that it confers implies that the dominant effects of 6A have an incomplete penetrance. Additional studies are needed to determine which environmental and genetic factors may modify the penetrance of 6A in these tumor types," the researchers write.
"The results highlight a new facet of TGF-beta signaling in cancer and suggest that TGFBR16A may represent a potential therapeutic target in cancer."
JAMA and Archives Journals
The researchers found that TGFBR1 mutated into TGFBR16A, i.e. was somatically acquired, in 13 of 44 (29.5 percent) colorectal cancer metastases, in 4 of 157 (2.5 percent) of colorectal tumors, in 4 of 226 (1.8 percent) head and neck primary tumors, and in none of the 104 patients with breast cancer.
While TGF-beta inhibits the growth of normal cells, cancer cells secrete larger amounts of TGF-beta than their normal counterparts. The researchers showed that, in the presence of TGF-beta, the growth of cancer cells that carry the TGFBR16A gene is 55 percent greater than cancer cells that do not carry this gene, indicating that TGFBR16A give cancer cells a selective advantage. This, together with the findings that TGFBR16A is acquired by tumors, may explain why half of all liver metastases from colorectal cancer carried the TGFBR16A gene while it is only found in 14 percent of the general population.
" individuals who carry the 6A allele, either in the germline or somatically acquired by the tumor, may have a greater likelihood of developing metastases than individuals who do not carry this allele. 6A may therefore serve as a useful biomarker in cancer." The authors add that TGFBR16A may bestow cancer cells with a growth advantage in the presence of TGF-beta.
"Since 13.7 percent of the general population and 17.1 percent of patients with a diagnosis of cancer carry at least 1 copy of the 6A allele, our findings may have substantial public health importance. The high frequency of 6A carriers in the general population and the moderately increased risk of breast, colon, and ovarian cancer that it confers implies that the dominant effects of 6A have an incomplete penetrance. Additional studies are needed to determine which environmental and genetic factors may modify the penetrance of 6A in these tumor types," the researchers write.
"The results highlight a new facet of TGF-beta signaling in cancer and suggest that TGFBR16A may represent a potential therapeutic target in cancer."
JAMA and Archives Journals
Cancer Development Current Events and Cancer Development News RSSResearchers Identify Role of Gene in Tumor Development, Growth and Progression
Virginia Commonwealth University Massey Cancer Center and VCU Institute of Molecular Medicine researchers have identified a gene that may play a pivotal role in two processes that are essential for tumor development, growth and progression to metastasis.
Coffee break: Compound brewing new research in colon, breast cancer
A compound in coffee has been found to be estrogenic in studies by Texas AgriLife Research scientists.
Does green tea prevent cancer? Evidence continues to brew, but questions remain
Although scientists are reluctant to officially endorse green tea as a cancer prevention method, evidence continues to grow about its protective effects, including results of a new study published in Cancer Prevention Research, a journal of the American Association for Cancer Research, which suggests some reduction in oral cancer.
Green tea shows promise as chemoprevention agent for oral cancer, M. D. Anderson study finds
Green tea extract has shown promise as cancer prevention agent for oral cancer in patients with a pre-malignant condition known as oral leukoplakia, according to researchers at The University of Texas M. D. Anderson Cancer Center.
Switching immunosuppressants reduces cancer risk in kidney
Switching to a newer type of immunosuppressant drug may reduce the high rate of skin cancer after kidney transplantation, according to research being presented at the American Society of Nephrology's 42nd Annual Meeting and Scientific Exposition in San Diego, CA.
Texas A&M researchers find new mechanism for circadian rhythm
Molecules that may hold the key to new ways to fight cancer and other diseases have been found to play an important role in regulating circadian rhythm, says Liheng Shi, a researcher in Texas A&M's Department of Veterinary Integrative Biosciences.
NEDD9 Protein Supports Growth of Aggressive Breast Cancer
Researchers at Fox Chase Cancer Center have demonstrated that a protein called NEDD9 may be required for some of the most aggressive forms of breast cancer to grow. Their findings, based on the study of a mouse model of breast cancer, are presented in a recent issue of Cancer Research, available on-line now.
University of Hawaii at Manoa CRCH scientists report adulthood body size associated with cancer risk
A team of scientists led by researcher Brenda Hernandez, Ph.D., M.P.H.-an assistant professor at the University of Hawai'i at Mānoa's Cancer Research Center of Hawai'i-has reported that body mass in younger and older adulthood, and weight gain between these life periods, may influence a man's risk for prostate cancer.
Mayo Clinic Researchers Find That Protein Believed to Protect Against Cancer Has a Mr. Hyde Side
In a biological rendition of fiction's Strange Case of Dr. Jekyll and Mr. Hyde, researchers from the Mayo Clinic campus in Florida and Harvard Medical School have found that a protein thought to protect against cancer development can actually spur the spread of tumors.
Researchers identify new, cancer-causing role for protein
The mainstay immune system protein TRAF6 plays an unexpected, key role activating a cell signaling molecule that in mutant form is associated with cancer growth, researchers at The University of Texas M. D. Anderson Cancer Center report in the Aug. 28 edition of Science.
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