Loss of Aurora A/STK15/BTAK overexpression correlates with transition of in situ to invasive ductal carcinoma of the breast.

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/4638

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題名:	Loss of Aurora A/STK15/BTAK overexpression correlates with transition of in situ to invasive ductal carcinoma of the breast.
作者:	Hoque, A.;Carter, J.;Xia, W.;Mien-Chie Hung;Sahin, A. A.;Sen, S.;Lippman, S. M.
日期:	2003-12
上傳時間:	2009-11-27 05:57:10 (UTC+0)
出版者:	Asia University
摘要:	The biological mechanisms involved in the progression of ductal carcinoma in situ (DCIS) to invasive breast cancer are not fully understood. We previously have shown that the putative oncogene Aurora-A/STK15/BTAK, encoding a centrosome-associated kinase that regulates centrosomes and chromosome segregation, is amplified in human breast cancer. In this study, 37 archival breast tissue specimens of histologically confirmed DCIS lesions with adjacent invasive carcinoma and morphologically nonmalignant mammary ducts were analyzed immunohistochemically for expression of STK15. Statistically significant differences in overexpression of STK15 was found between invasive cancer and either nonmalignant mammary ducts (P < 0.0001) or DCIS lesions (P < 0.0005). Abnormalities in centrosome size and number was detected in the samples analyzed and 56% (14 of 25) of the cases also showed aneuploidy reflected in >2 signals of chromosome 3 and 17. Our data demonstrate that STK15 overexpression correlates with centrosome anomaly and aneuploidy in DCIS, and loss of STK15 overexpression is associated with progression of in situ to ductal invasive breast carcinoma
關聯:	CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION 12(-):1518-1522
顯示於類別:	[生物科技學系] 期刊論文

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