Identification of MAML1-induced molecular mechanisms underlying chemoresistance processes

Triple-negative breast cancer (TNBC) is a highly aggressive tumor subtype, characterized by early onset, high metastatic capacity, and a high recurrence rate, representing a significant clinical challenge. Currently, platinum-based chemotherapy and PARP inhibitors (indicated in tumors with BRCA1/2 gene mutations) are the mainstay of systemic treatment aimed at inducing DNA damage and replicative stress. However, a significant proportion of patients show primary or acquired resistance to such treatments. In this context, the MAML1 protein emerges as a potential key regulator of tumor progression. Preliminary data indicate that MAML1 may support cell survival and proliferation under conditions of carboplatin- or olaparib-induced therapeutic stress, promoting DNA damage repair mechanisms.