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  • Title: Apoptosis as a possible candidate mechanism for removal of tamoxifen-related endometrial cells with KRAS mutations.
    Author: Tsujioka H, Hachisuga T, Hikita S, Ueda T, Yotsumoto F, Shirota K, Yoshizato T, Kawarabayashi T, Kuroki M, Miyamoto S.
    Journal: Anticancer Res; 2010 Aug; 30(8):3119-23. PubMed ID: 20871029.
    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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