Cancer arises when cells acquire genetic alterations that allow them to survive, adapt, and evolve under conditions that would normally eliminate damaged cells. Our laboratory seeks to understand how these alterations reshape fundamental cellular processes and create opportunities for therapeutic intervention.
The de Cubas Laboratory studies the molecular mechanisms that drive kidney cancer progression, therapeutic resistance, and tumor-immune interactions. Our research focuses on chromatin remodeling genes that are among the most frequently mutated in clear cell renal cell carcinoma (ccRCC), particularly SETD2. We investigate how the loss of these critical regulators alters mitochondrial function, cellular metabolism, stress signaling, and the immune landscape of tumors.
A major goal of our work is to uncover the vulnerabilities that emerge when cancer cells adapt to genetic and metabolic stress. By combining molecular biology, cancer genetics, immunology, functional genomics, and preclinical models, we seek to identify mechanisms that can be translated into new therapeutic strategies. Our studies have revealed previously unrecognized links between chromatin dysregulation, mitochondrial stress, innate immune activation, and apoptotic control, leading to the discovery of novel drug sensitivities in aggressive kidney cancers.
Our research spans basic, translational, and preclinical investigation. We utilize patient-derived samples, advanced cellular models, genomic technologies, and animal systems to understand how tumors evolve and respond to treatment. Ultimately, our mission is to translate fundamental biological discoveries into therapies that improve outcomes for patients with kidney cancer and other solid tumors.