Ueda Taeko
   Department   School of Medicine  Obstetrics and Gynecology, Clinical Medical Sciences
   Position  
Article types journal article
Language English
Peer review Peer reviewed
Title Apoptosis as a possible candidate mechanism for removal of tamoxifen-related endometrial cells with KRAS mutations.
Journal Formal name:Anticancer research
Abbreviation:Anticancer Res
ISSN code:17917530/02507005
Domestic / ForeginForegin
Volume, Issue, Page 30(8),3119-3123頁
Author and coauthor Tsujioka Hiroshi, Hachisuga Toru, Hikita Shoko, Ueda Taeko, Yotsumoto Fusanori, Shirota Kyoko, Yoshizato Toshiyuki, Kawarabayashi Tatsuhiko, Kuroki Masahide, Miyamoto Shingo
Publication date 2010/08
Summary BACKGROUND:Endometrial cell KRAS mutations are frequent in tamoxifen (TAM)-treated breast cancer patients. We previously demonstrated that most KRAS mutations disappeared after TAM cessation, suggesting the existence of a removal mechanism for endometrial cells with KRAS mutation. Here, the role of apoptosis in this mechanism was investigated.PATIENTS AND METHODS:DNA was extracted from frozen endometrial polyps of 31 TAM-treated breast cancer patients. Codon 12 mutations in KRAS were detected by enriched polymerase chain reaction enzyme-linked minisequence assay. Apoptosis was detected by the TdT-mediated dUTP-biotin nick end-labeling (TUNEL) method and Ki-67 expression by immunohistochemistry. Relationships between KRAS mutations, the apoptosis index, and the Ki-67 index were determined.RESULTS:KRAS mutations were observed in 9 of these patients. There was no significant relationship between the Ki-67 index and KRAS mutation. However, the apoptosis index was significantly higher in polyps with KRAS mutation (p=0.002).CONCLUSION:Apoptosis may play an important role in removing TAM treatment-related endometrial cells with KRAS mutations.
PMID 20871029