Loss of Aurora A / STK 15 / BTAK Overexpression Correlates with Transition of in Situ to Invasive Ductal Carcinoma of the Breast
Loss of Aurora A / STK 15 / BTAK Overexpression Correlates with Transition of in Situ to Invasive Ductal Carcinoma of the Breast
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发表时间：
2003
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通讯作者：
A. Hoque;J. Carter;W. Xia;M. Hung;A. Sahin;S. Sen;S. Lippman
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作者：
A. Hoque;J. Carter;W. Xia;M. Hung;A. Sahin;S. Sen;S. Lippman
导管原位癌（DCIS）进展为浸润性乳腺癌的生物学机制尚未完全了解。我们以前已经表明，推定的癌基因Aurora-A/STK 15/BTAK，编码一个中心体相关激酶，调节中心体和染色体分离，在人类乳腺癌中扩增。在这项研究中，37档案乳腺组织标本的组织学证实的DCIS病变与相邻的浸润性癌和形态学上的非恶性乳腺导管进行了化学分析STK 15的表达。STK 15的过度表达在浸润性乳腺癌和非恶性乳腺导管之间存在统计学显著差异（3号和17号染色体的P2信号）。我们的数据表明，STK 15过表达与DCIS中的中心体异常和非整倍体相关，STK 15过表达的缺失与原位浸润性乳腺癌的进展相关。
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 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.