Syeda Warisul Fatima is a postdoctoral researcher at Emory University investigating the non-genetic mechanisms that allow aggressive cancers to adapt and evade treatment. In this Postdoc Portrait interview, she shares what initially drew her to biology and the translatability of her work.
Beyond the Genetic Blueprint
Q | What drew you to cancer biology?
My interest in biology began early during my undergraduate training, when I was first introduced to DNA fingerprinting. What fascinated me was the idea that hidden traits and identities—something not visible at the surface—could be revealed through molecular signatures. It shaped how I began to think, which is that what we observe is often only a fraction of what is there. That curiosity evolved into a more persistent question during my training in cancer biochemistry: Why do cells with the same genetic background behave so differently under similar conditions? In complex diseases like cancer, where variability in progression and treatment response is so pronounced, a purely genetic explanation felt incomplete. This led me to explore how metabolism and epigenetic regulation shape cellular identity and behavior. Aggressive cancers such as breast and brain cancers, known for their heterogeneity and therapeutic resistance, have become especially compelling systems to study these questions. At the same time, my doctoral work in cancer biology and drug development particularly in enzymatic-based bioformulations introduced me to not just understanding disease but intervening with precision. This work led to three international patents (USA, UK, India), reinforcing a translational perspective early in my career. That dual approach—questioning underlying mechanisms while thinking toward clinical application—continues to guide my work. I am particularly drawn to problems where careful observation challenges assumptions, and where deeper understanding can meaningfully inform therapeutic strategy. Since then, my work has been shaped by looking beyond what is visible, resolving what lies beneath, and translating that insight into precise interventions that truly change outcomes!
Q | What scientific problem are you trying to solve?
My research seeks to understand how cancer cells adapt and evade therapy through non-genetic mechanisms, with a focus on how disease evolves from early detection to clinical outcome. While classification into molecular subtypes guides treatment decisions, it often fails to capture the dynamic nature of tumor behavior. This is reflected in the variability of clinical responses and the frequent emergence of therapeutic resistance.
I focus on how systemic and environmental factors such as metabolic health, inflammation, and lifestyle-associated stressors reshape epigenetic landscapes and drive reversible cell-state transitions. These adaptive changes allow tumor cells to persist under therapeutic pressure, challenging the notion of cancer as a static, mutation-driven disease.
Using integrative multiomic approaches, I investigate how these states emerge, evolve, and persist over time. My work bridges patient-centered clinical questions with molecular investigation, aiming to understand not only what drives disease progression, but how it can be redirected.
In parallel, I develop translational strategies, including nano-enabled therapeutic systems and biologically derived interventions, to improve drug delivery and precision targeting. Building on my work as an inventor of three international patents in cancer nanomedicine, I aim to identify actionable vulnerabilities and design interventions that enhance treatment durability.
Ultimately, my goal is to move beyond describing disease toward actively shaping its trajectory by developing therapies that are not only precise, but adaptable to the evolving nature of cancer, with meaningful impact on patient outcomes in real clinical settings.
Targeting Cellular Memory and Resistance
Q | What’s one thing you learned from working with cancer that you didn’t expect?
One of the most unexpected and somewhat unsettling insights has been how readily cancer cells can change their identity without acquiring new genetic mutations. This became particularly evident in aggressive cancers such as triple-negative breast cancer and glioblastoma, where cells can shift between different phenotypic states over relatively short timescales, driven more by changes in gene regulation than by alterations in DNA sequence.
What makes this even more striking is that these changes are not always temporary. Environmental and metabolic stresses can leave lasting imprints, often described as cellular “memory,” that continue to influence how cells behave even after the original conditions are gone.
This challenges the traditional view of cancer as a fixed, mutation-driven disease. Instead, it reveals a system that is highly adaptive, context-dependent, and, in some cases, potentially reversible.
That realization has shifted how I think about treatment moving beyond targeting static markers toward understanding how these dynamic states arise, and whether they can be redirected to improve therapeutic response in some of the most difficult-to-treat cancers.
Q | If your research succeeds, what could it change for science or society?
If this work succeeds, I hope it can help shift how we think about cancer not as a fixed disease defined only by genetic mutations, but as something dynamic that can change, adapt, and, in some cases, be redirected. In that sense, it may contribute to a broader shift in how we approach aggressive cancers, focusing on the evolving nature of tumor cells rather than only static markers. In the clinic, one of the most difficult moments is when a treatment that once worked stops working and options become limited. What motivates me is the possibility that some of these changes may not be permanent because there are underlying, reversible states we have not yet learned how to target. Even the idea that what seems uncertain today could become actionable tomorrow offers a sense of direction and hope. By understanding and intervening in these processes, we may be able to extend the effectiveness of treatments, restore sensitivity, and reduce the cycle of resistance and relapse. At the same time, improving how therapies are delivered through more precise and targeted approaches could help reduce unnecessary toxicity and make treatment more tolerable for patients. If even a part of this leads to more durable responses, more personalized care, or simply gives patients more time with effective therapy, that would feel like a meaningful contribution.
Q | What question are you most excited to answer next?
I am most excited to understand whether the epigenetic changes driven by metabolic stress in cancer can be reversed and whether doing so can meaningfully improve how patients respond to treatment. In the clinic, we often see patients who initially respond well but later develop resistance, with limited options thereafter. What stays with me is the question of whether these outcomes are truly fixed, or whether there are underlying, reversible states we have not yet learned to target effectively. My goal is to explore how these metabolically influenced cell states can be modulated using next-generation therapeutic approaches, including targeted and nano-enabled delivery systems. If we can learn to reset or redirect these states, it may open the possibility of restoring treatment sensitivity and improving long-term outcomes for patients. That possibility of turning resistance into response is what I find most compelling!
Responses have been edited for length and clarity.
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