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Study On The Relationship Between Centrosomal Regulator-Skp2, Stk15 And Precancerous Lesions And Canceration Of Breast

Posted on:2007-10-06Degree:MasterType:Thesis
Country:ChinaCandidate:L WeiFull Text:PDF
GTID:2144360182991930Subject:Pathology and pathophysiology
Abstract/Summary:PDF Full Text Request
PURPOSE:To explore the roles of centrosomal-regulators skp2 and stk15 in the progressionof breast tumor ,offer clues to investigate the mechanism of tumorigenesis and find new molecular marker for diagnosis and therapy ,Gene copy alteration and the mRNA expression levels are detected in different breast tissues: normal tissue, precursor lesions, DCIS and invasive duct carcinoma. Methods:1 The mRNA expression levels of skp2 and stkl5 in different breast tissues;normal tissues, precursor lesions, DCIS, invasive duct carcinoma (30 samples per group)were detected by In Situ Hybridization2 The gene copy number of skp2 and stk15 in different breast tissues;normal, precursor lesions, DCIS, invasive duct carcinoma (20 samples per group) were examined by Fluorescence Quantitative PCRResults:Compared to normal tissues, skp2 mRNA was over-expressed in precursor lesions, DCIS and invasive duct carcinoma, there was no difference between precursor lesions and DCIS;Skp2 DNA copy increased in precursor lesions, DCIS and invasive duct carcinoma and Correlated with tumor development.Compared to normal tissues, stk15 mRNA was over-expressed in precursor lesions, DCIS and invasive duct carcinoma, there was no difference between DCIS and invasive duct carcinoma;Stk15 DNA copy increased in DCIS and invasive duct carcinoma, no copy alteration was detected in precursor lesions.Conclusion:Consistent alterations of skp2 and stkl5 DNA and mRNA levels imply the DNA copy abnormality leads to the increase of mRNA expression, and skp2 and stkl5 are linked to tumor development and progression and may serve as early markers in tumorigenesis.
Keywords/Search Tags:skp2, stk15, Centrosomal-regulators, breast carcinogenesis, Breast Pre-cancerous lesion
PDF Full Text Request
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