It has been recently identified that drug-tolerant persister cells are highly resistant to apoptotic cell death, however, are vulnerable to iron-mediated ferroptosis. This unique pathological condition is accompanied with enrichment of mesenchymal behavior and metastatic aggressiveness, properties which are also intrinsically shared with TNBC tumors together with their sensitivity to ferroptotic cell death.
We are interested to understand the biological role of key mediators of ferroptosis in TNBC subtypes and their relation to persister behavior using cellular, pre-clinical and clinical models. These pathophysiological and mechanistic insights are expected to significantly improve the understanding of how ferroptosis can regulate chemotherapy response in TNBC and if these molecular regulators can be utilized as therapeutic targets together with chemotherapy to enhance response to therapy.