Localization of PS6K to chromosomal region 17q23 and determination of its amplification in breast cancer.
نویسندگان
چکیده
The application of comparative genomic hybridization to the analysis of genetic abnormalities in breast carcinoma has consistently revealed that chromosome region 17q22-24 is a frequent site of gene amplification in this type of cancer. As part of an examination of expressed sequence tags for novel amplified genes in this region, we identified PS6K amplifications in both breast tumor tissues and cell lines. PS6K was localized to 17q23 and encodes a serine-threonine kinase whose activation is thought to regulate a wide array of cellular processes involved in the mitogenic response including protein synthesis, translation of specific mRNA species, and cell cycle progression from G1 to S phase. Northern and Western analyses revealed that amplification of this gene was accompanied by corresponding increases in mRNA and protein expression, respectively. These data represent the first determination of a gene amplification within 17q22-24 in breast cancer and suggest an oncogenic activity for PS6K.
منابع مشابه
Determination of Its Amplification in Breast Cancer to Chromosomal Region
The application of comparative genomic hybridization to the analysis of genetic abnormalities in breast carcinoma has consistently revealed that chromosome region 17q22–24 is a frequent site of gene amplification in this type of cancer. As part of an examination of expressed sequence tags for novel amplified genes in this region, we identified PS6K amplifications in both breast tumor tissues an...
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BACKGROUND Gene amplification leading to overexpression is a common event in breast tumors that is linked to tumor development and progression. The 17q23 region is amplified in >40% of breast tumors and contains several candidate oncogenes. Because common genetic variation in several oncogenes has been associated with cancer risk, we assessed the relevance of common variants in the 17q23 candid...
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عنوان ژورنال:
- Cancer research
دوره 59 7 شماره
صفحات -
تاریخ انتشار 1999