The effects of transferring tumor suppressor gene p16INK4A to p16INK4A - deleted cancer cells
نویسندگان
چکیده
منابع مشابه
The effects of transferring tumor suppressor gene p16INK4A to p16INK4A-deleted cancer cells*
OBJECTIVES p16 is known to be an important tumor suppressor gene and is also called MTS1 (multiple tumor suppressive gene 1). Especially in the case of non-small cell lung cancer, it was not expressed in more than 70% of cell lines examined. To determine changes in cell-cycle related proteins and the tumorigenic effect, we, therefore, transfected p16INK4A gene into lung cancer cell lines. MET...
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BACKGROUND Cell cycle inhibitor and tumor suppressor gene p16/MTS-1 has been reported to be altered in a variety of human tumors. The purpose of the study was to evaluate primary pancreatic ductal adenocarcinomas for potentially inactivating p16 alterations. METHODS We investigated the status of p16 gene by polymerase chain reaction (PCR), nonradioisotopic single strand conformation polymorph...
متن کاملMutational effects on the p16INK4a tumor suppressor protein.
Several point mutations of p16INK4a were studied by site-specific mutagenesis and functional analysis to assess the effects of these mutations on the function of the protein. These mutations were reported in several malignancies. Three deletional mutants of p16INK4a were also analyzed to reveal the relationship between p16INK4a and p15INK4b and to test the importance of the ankyrin repeats obse...
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The tumor suppressor gene p16(INK4a) inhibits the kinase activity of the cyclin-dependent kinase 4-6/cyclin D complexes and subsequent phosphorylation of critical substrates necessary for transit through the G1 phase of the cell cycle. Recent studies suggested that control of the G1/S boundary might not be the sole biological function of p16(INK4a). We hypothesized that p16(INK4a) might influen...
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BACKGROUND The p16(INK4a) gene methylation has been reported to be a major tumorigenic mechanism. METHODS We evaluated the methylation status of the p16(INK4a) genes in 231 invasive breast cancer and 90 intraductal carcinoma specimens using a methylation-specific polymerase chain reaction and p16 protein expression using immunohistochemistry. The quantity of cell-free methylated p16(INK4a) DN...
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ژورنال
عنوان ژورنال: The Korean Journal of Internal Medicine
سال: 1999
ISSN: 1226-3303,2005-6648
DOI: 10.3904/kjim.1999.14.1.53