Abstract

Abstract Background: It has not been fully understood how we can differentiate a new primary breast cancer from a recurrent tumor, when second tumor arises in ipsilateral breast after the surgery for primary breast cancer. To address this research question, we estimate the usefulness of a method analyzing polymorphism of androgen receptor gene and mitochondrial D-loop somatic mutation. Materials and methods: 1) Select patients: Among the 558 patients who received the breast conservative surgery in Tokai University Hospital (1991∼2004), 9 ipsilateral breast tumors and 11 contralateral breast tumors were submitted for the analysis. 2) Formalin-fixed paraffin-embedded (FFPE) sections of non-neoplastic lymph node were examined whether polymorphism of AR gene present or not. 3) When polymorphism of AR gene in non-neoplastic lymphoid tissue were demonstrated, ipsilateral and contralateral breast cancers were further examined. 4) When AR gene in breast cancers on same allele in primary and secondary tumors, FFPE sections were further analyzed by mutaion analysis of mitochondrial D-loop region. Results: 1) Polymorphism of AR was demonstrated in 8/9 (88.9%) and 9/11 (81.8%) non-neoplastic lymph nodes obtained from the patients who had ipsilateral and contralateral breast tumor, respectively. 2) Only 2 of 8 ipsilateral breast cancers demonstrated AR polymorphism different from primary cancer. In contrast, 6 of 9 contralateral breast cancers had different polymorphism for AR from primary breast cancers. 3) Analysis of mitochondrial D-loop mutation showed that 8 seconary ipsilateral cancers had different mutation in 3/8 (37.5%), identical mutation in 3/8 (37.5%), and no mutation in 2/8 (25.0%). Results of analysis for ipsilateral secondary breast cancers Conclusion: Half of the ipsilateral in breast secondary tumors were estimated as new primary lesions by molecular estimation. Combination analyses of AR gene polymorphism and mitochondrial D-loop somatic mutation unable us to distinguish between true recurrent or new primary cancers. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-08-02.

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