Remya Nair is a postdoctoral researcher at Emory University. She studies cancer metabolism as a vulnerability that can be targeted to address drug resistance. In this Postdoc Portrait interview, she shares how metabolites can actively give multiple myeloma a survival advantage and how she plans to use this to improve therapeutic outcomes.
Decoupling Metabolic Pathways in Multiple Myeloma
Q | What drew you to cancer metabolism?
I began my scientific training studying how pathogenic fungi adapt to hostile environments, particularly how iron availability and stress responses drive drug resistance. During my postdoctoral work, I realized that cancer cells face similar pressures and use surprisingly conserved survival strategies. This parallel drew me toward cancer metabolism and hematologic malignancies, where I could apply mechanistic insights from microbiology to clinically relevant questions. That interdisciplinary foundation strongly shapes how I approach problems in cancer biology today.
Q | What scientific problem are you trying to solve?
I study how cancer cells adapt their metabolism to survive therapy. My work focuses on multiple myeloma, a blood cancer that often becomes resistant to treatment. Rather than looking only at mutations or alterations intrinsic to cancer cells, I investigate how external cues—such as nutrients from diet or metabolites in the tumor microenvironment—rewire cancer metabolism and signaling pathways to promote drug resistance. By understanding these interactions, my goal is to identify metabolic vulnerabilities that can be targeted to improve therapeutic outcomes.
The Dynamic Future of Oncology
Q | What’s one thing you learned from studying drug resistance that you didn’t expect?
One thing I didn’t expect was just how profoundly metabolic alterations influence response to therapy. I initially viewed metabolism as a supporting player, but my research revealed that metabolites can actively reprogram signaling and survival pathways in multiple myeloma. Seeing how these physiologically relevant metabolic cues dramatically alter therapeutic sensitivity was both surprising and exciting, and it fundamentally changed how I think about drug resistance in cancer.
Q | If your research succeeds, what could it change for science or society?
This research could fundamentally change how we think about cancer drug resistance. Rather than viewing resistance as driven primarily by genetic changes within tumor cells, it highlights metabolism and the tumor environment as active players in shaping therapeutic response. For science, this reframes metabolism as a targetable vulnerability rather than a passive background process. For society, it could lead to more effective, durable treatments by informing combination therapies that prevent or overcome resistance, ultimately improving outcomes for patients with cancers like multiple myeloma.
Q | What question are you most excited to answer next?
I’m most excited to understand which metabolic pathways consistently shape treatment response across different cancer types and which ones are unique to specific tumors. By mapping both common and cancer-specific metabolic players, I hope to uncover shared vulnerabilities as well as novel targets that could be exploited therapeutically. This broader view could help reveal why certain therapies fail across cancers and guide more universally effective, metabolism-informed treatment strategies.
Responses have been edited for length and clarity.
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