Elucidation of the Mechanism of c-Myc Expression in Invasive Ductal Breast Cancer Using Fluorescence in situ Hybridization

Abstract

Certain breast cancer treatments are ineffective and develop drug resistance in some cases. In various cancers, the c-Myc protein plays a critical role in cell proliferation regulation and cell cycle control, promoting carcinogenesis and treatment resistance. High c-Myc protein expression is in 30—50% of high-grade breast tumors. This study focused on examining the relationship between c-Myc protein expression and c-myc gene amplification in triple-negative breast cancer (TNBC) compared with other invasive ductal carcinomas. We performed c-Myc immunohistochemistry and c-myc fluorescence in situ hybridization on 108 invasive ductal carcinoma cases, which had not received preoperative treatment and were resected between January 2019 and December 2021. The proportion of TNBC increased in the group with high c-Myc expression within invasive ductal carcinoma. Fluorescence in situ hybridization divided cases with high c-Myc protein expression into those with and without c-myc gene amplification, suggesting that c-Myc protein expression in breast cancer is induced by c-myc gene amplification. Additionally, cases of high c-Myc protein expression might result from tumor cell polyploidization and epigenomic factors. Given that c-Myc protein is associated with breast cancer malignancy and treatment resistance, determining gene amplification presence or absence can be crucial in developing breast cancer prognostic and treatment strategies.