Postdoctoral Researcher Remya Nair Explores Cancer Metabolism and Therapeutic Resistance

Remya Nair investigates metabolic reprogramming in hematologic malignancies.

Image credit:
Murali Das, © iStock.com, Design Cells

Remya Nair is a postdoctoral researcher at Emory University. Her work focuses on cancer metabolism as a potential therapeutic vulnerability that can counteract drug resistance. In this postdoctoral portrait interview, she discusses how metabolites can actively confer survival advantages to multiple myeloma and outlines her strategy to leverage these insights for improved treatment outcomes.

Decoupling Metabolic Pathways in Multiple Myeloma

Q | What drew you to cancer metabolism?

My training focused on pathogenic fungi adapting to harsh environments, particularly how iron availability and stress responses drive drug resistance. During my postdoctoral work, I observed that cancer cells encounter similar pressures and employ conserved survival strategies. This parallel led me to cancer metabolism and hematologic malignancies, allowing me to apply mechanistic insights from microbiology to clinically relevant questions. This interdisciplinary foundation continues to shape my approach to cancer biology today.

Q | What scientific problem are you trying to solve?

I examine how cancer cells remodel their metabolism to survive therapy. My research centers on multiple myeloma, a hematologic malignancy that frequently develops resistance to treatment. Rather than focusing solely on intrinsic genetic alterations, I investigate how external cues—such as dietary nutrients or tumor‑microenvironment metabolites—reprogram cancer metabolism and signaling to promote drug resistance. Ultimately, I aim to identify metabolic vulnerabilities that can be targeted to enhance therapeutic outcomes.

Q | What’s one thing you learned from studying drug resistance that you didn’t expect?

I was surprised by how profoundly metabolic alterations influence therapeutic response. Initially viewing metabolism as a supportive player, I discovered that metabolites can actively reprogram signaling and survival pathways in multiple myeloma. Recognizing how physiologically relevant metabolic cues dramatically affect drug sensitivity has been both surprising and transformative for my perspective on cancer drug resistance.

Q | If your research succeeds, what could it change for science or society?

This research has the potential to fundamentally reshape our understanding of cancer drug resistance. Instead of attributing resistance mainly to genetic changes within tumor cells, it highlights metabolism and the tumor microenvironment as active contributors to therapeutic response. Scientifically, it reframes metabolism as a targetable vulnerability rather than a passive background process. Societally, it may foster more effective, durable treatments through combination strategies that prevent or overcome resistance, improving outcomes for patients with cancers such as multiple myeloma.

Q | What question are you most excited to answer next?

I am most excited to identify which metabolic pathways consistently influence treatment response across various cancers and which are unique to particular tumors. By mapping both common and cancer‑specific metabolic players, I aim to uncover shared vulnerabilities and novel targets that can be exploited therapeutically. This broader perspective may illuminate why some therapies fail across cancers and guide the development of universally effective, metabolism‑informed treatment strategies.

The Dynamic Future of Oncology

Q | What’s one thing you learned from studying drug resistance that you didn’t expect?

I was surprised by how profoundly metabolic alterations influence therapeutic response. Initially viewing metabolism as a supporting player, I discovered that metabolites can actively reprogram signaling and survival pathways in multiple myeloma. Recognizing how physiologically relevant metabolic cues dramatically affect drug sensitivity has been both surprising and transformative for my perspective on cancer drug resistance.

Q | If your research succeeds, what could it change for science or society?

This research has the potential to fundamentally reshape our understanding of cancer drug resistance. Instead of attributing resistance mainly to genetic changes within tumor cells, it highlights metabolism and the tumor microenvironment as active contributors to therapeutic response. Scientifically, it reframes metabolism as a targetable vulnerability rather than a passive background process. Societally, it may foster more effective, durable treatments through combination strategies that prevent or overcome resistance, improving outcomes for patients with cancers such as multiple myeloma.

Q | What question are you most excited to answer next?

I am most excited to identify which metabolic pathways consistently influence treatment response across various cancers and which are unique to particular tumors. By mapping both common and cancer‑specific metabolic players, I aim to uncover shared vulnerabilities and novel targets that can be exploited therapeutically. This broader perspective may illuminate why some therapies fail across cancers and guide the development of universally effective, metabolism‑informed treatment strategies.

Responses have been edited for length and clarity.

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