Postdoc Spotlight: Ishwaree Datta Explores How Cancer Cells Evade Immune Attack

Ishwaree Datta examines how solid tumor cells endure immune pressure during macrophage-mediated trogocytosis.

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Ishwaree Datta is a postdoctoral researcher at the University of California, Santa Barbara, investigating how solid tumors adapt to evade immune system attacks. In this Postdoc Portrait interview, she discusses how cancer cells resist host immune responses and how she aims to exploit those stress responses to uncover therapeutic vulnerabilities.

Decoding Immune Attacks and Cancer Cell Adaptation

Q | What drew you to cancer and the immune system?

My scientific journey began in a microbiology lab, where I studied how bacteria acquire iron in nutrient‑poor conditions. I was fascinated by how a single‑cell organism solves the problem of survival under scarcity. The underlying question—how something small and vulnerable persists in a hostile environment—has guided my work across different systems. In graduate school I used fruit flies to explore tumor growth and treatment resistance. Now, as a postdoctoral fellow, I study human cancer cells and immune cells in ovarian cancer models. The experimental systems have changed, but the central question remains the same.

When I first observed trogocytosis—the process whereby macrophages repeatedly bite into tumor cells—I noticed that the cancer cells survived and continued to divide. This highlighted a clinically devastating gap: we still do not fully understand how a cancer cell can withstand an immune attack and live to fight another day. Elucidating this mechanism and finding ways to disrupt it have become the focus of my research, with the goal of developing more effective immunotherapies.

Q | What scientific problem are you trying to solve?

Cancer immunotherapy has transformed care for many patients, yet most solid tumors eventually find a way to survive. We still lack a clear understanding of how cancer cells evade immune‑mediated death. My work asks a simple but critical question: What happens to a cancer cell that is attacked by the immune system but does not die? To answer this, I examine the molecular changes in cancer cells that survive macrophage trogocytosis. These surviving cells appear to activate stress‑response pathways that may help them endure future immune assaults, potentially driving relapse and therapy resistance. By deciphering how cancer cells persist after immune injury, I hope to identify druggable vulnerabilities that could be targeted with existing agents or combination strategies, converting incomplete immune responses into durable cures.

Overcoming Resistance to Immunotherapy in Solid Tumors

Q | What’s one thing you learned from cancer cell survival that you didn’t expect?

Initially, I assumed that the outcome of macrophage‑tumor interactions would be dictated primarily by immune cell efficiency—how well macrophages engage, how much tumor membrane they remove via trogocytosis, and how many bites are needed to trigger cell death. The data, however, revealed a surprising degree of agency on the part of the cancer cells.

When I examined tumor cells that had survived trogocytosis, I found they were not passive victims awaiting a lethal blow. Instead, the attacked cancer cells rapidly mounted stress responses, rewired their metabolism, and upregulated survival signals within minutes of the attack.

This discovery shifted my research focus from merely enhancing macrophage killing power to blocking the adaptive pathways that tumor cells use to evade immunotherapy. Identifying those targetable mechanisms now drives my work.

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

Understanding why solid tumors recur after immunotherapy could lead to combination treatments that prevent cancer cells from adapting to immune attack in the first place, thereby improving long‑term outcomes for patients.

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

I aim to determine whether the cancer cells that survive immunotherapy are the same ones that seed relapse. If they are, elucidating the targetable survival mechanisms they employ would become a leading avenue for therapeutic intervention.

Responses have been edited for length and clarity.

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