Literature DB >> 20871029

Apoptosis as a possible candidate mechanism for removal of tamoxifen-related endometrial cells with KRAS mutations.

Hiroshi Tsujioka1, Toru Hachisuga, Shoko Hikita, Taeko Ueda, Fusanori Yotsumoto, Kyoko Shirota, Toshiyuki Yoshizato, Tatsuhiko Kawarabayashi, Masahide Kuroki, Shingo Miyamoto.   

Abstract

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.

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Year:  2010        PMID: 20871029

Source DB:  PubMed          Journal:  Anticancer Res        ISSN: 0250-7005            Impact factor:   2.480


  1 in total

1.  Mutations of RAS genes in endometrial polyps.

Authors:  Takashi Takeda; Kouji Banno; Yusuke Kobayashi; Masataka Adachi; Megumi Yanokura; Eiichiro Tominaga; Kenjiro Kosaki; Daisuke Aoki
Journal:  Oncol Rep       Date:  2019-10-04       Impact factor: 3.906

  1 in total

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