期刊
GYNECOLOGIC ONCOLOGY
卷 111, 期 2, 页码 350-355出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ygyno.2008.07.011
关键词
KIT; Mutations; Amplification; Activation; SCF; Cervix adenosquamous carcinoma
资金
- Fundacao para a Ciencia e a Tecnologia (FCT) [SFRH/BD/36463/2007]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/36463/2007] Funding Source: FCT
Objectives. Uterine adenosquamous carcinoma (ASC) is an uncommon, yet, one of the most aggressive cervical cancer subtype. The successful treatment of some tumors, such as gastrointestinal stromal tumors (GISTs), by anti-KIT inhibitors fosters the study of this receptor tyrosine kinase in other malignancies. In the present study, we intended to molecularly characterize KIT in ASC. Methods. In a series of 30 cases, we studied KIT (CD117), KIT phosphorylated/activated form, as well as KIT ligand, stem cell factor (SCF), by immunohistochemistry. We further screened for KIT hotspot mutations (exon 9, 11, 13 and 17) by PCR-SSCP and for KIT gene amplification by Quantitative real-time PCR in CD117 positive cases. Results. We observed CD117 expression in similar to 13% of cases, with similar to 7% co-expressing SCF, which resulted in KIT phosphorylation/activation. No KIT activating mutations or gene amplification were found, despite the presence of 4q aneuploidy in one case. Conclusions. This is the first study assessing KIT activation and molecular alterations in a large series of rare ASC. Our findings showed the absence of KIT molecular alterations and suggested the presence of KIT activation in a small proportion of cases through KIT/SCF co-expression. (C) 2008 Elsevier Inc. All rights reserved.
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