Nicholas Brady, Ph.D.
Assistant Professor of Pathology and Laboratory Medicine
Dr. Nicholas Brady leads the Brady Lab in Weill Cornell Medicine’s Pathology and Laboratory Medicine department, where his team studies how changes in chromatin states drive the progression of neuroendocrine prostate cancer and seeks new ways to stop or reverse this deadly disease. We spoke with him about his unconventional career path, his passion for teaching, and why mentorship matters as much as discovery.
Q: First, can you introduce yourself and your lab’s focus?
A: My name is Nicholas Brady, but I go by Nick. My lab studies how changes in chromatin—the way DNA is packaged—drive neuroendocrine prostate cancer. We’re interested in identifying novel transcriptional regulators that work with epigenetic changes to promote lineage plasticity—essentially how these tumors “shape-shift” into more aggressive forms.
Q: What drew you to this field of research?
A: I’ve always been fascinated by cancer biology. In graduate school I focused on the tumor microenvironment, then in my postdoc training I added epigenetics and computational biology. My lab is a hybrid of wet lab and computational work, which lets us tackle both sides of the problem.
What motivates me is that neuroendocrine prostate cancer is a very aggressive disease made worse by the very treatments we have. These men often run out of therapeutic options. We’re trying to understand what triggers the switch that makes these tumors so aggressive and whether we can block, prevent, or even reverse that transformation.
Q: Why is this disease so hard to treat?
A: Two main reasons. First, these patients have usually been heavily pretreated. Prostate cancer is driven by androgens, so men are treated with castration therapies and next-generation androgen receptor inhibitors. Over time, some tumors find ways to escape. They either upregulate androgen signaling in new ways or undergo “lineage plasticity”—they stop looking like prostate tumors and start looking like neuroendocrine tumors. Our current drugs don’t work on these “shape-shifted” tumors.
Second, after years of therapy these tumors become very resilient. They’ve adapted to many changes and are good at finding new escape routes. And a lot of this is driven not by mutations but by epigenetic changes—alterations to DNA packaging that control which genes are accessible. Most treatments don’t yet target those changes, though new therapies are emerging.
Q: Your background is unusual for a cancer biologist. Can you tell us about it?
A: My undergraduate degree is in physics. I had an amazing high school physics teacher who made me love the subject. In college I took tons of math and physics and actually very little biology or chemistry. Afterward, I realized I didn’t want to do theoretical physics – I preferred something with more of a real-world application. I also had a strong background in computing from my dad, who’s a computer engineer.
I started working as a technician in a biology lab running a micro-CT imaging facility with very few biology skills. Postdocs and PhD students spent their own time to teach me molecular biology techniques at the bench. Within a couple of years, I was hooked and decided to pursue a PhD in cancer biology. In my postdoc I pivoted again to focus on epigenetics and computational biology. Now, with my own lab, I’m tying all of that together.
Q: You’ve mentioned the importance of mentors. Who influenced you, and how do you mentor today?
A: My high school physics teacher Mr. Brehmer had a huge impact on me. On the first day of class, he calculated the trajectory of a spring-loaded ball to knock over a G.I. Joe figure—and it worked. To a teenager, that was magic. It made me see science as fun and predictable.
Throughout my career many people patiently taught me basic skills. I try to pay that forward. I am a course director in the computational biology master’s program, and I teach cellular and molecular biology. I bring computationally minded students into the wet lab, teach them to pipette, and share real-world data and techniques with them. It’s come full circle.
Q: What do you enjoy about teaching?
A: Being back in the classroom forces me to think outside my narrow field of expertise. Teaching topics I haven’t visited in years deepens my own understanding. I also get ideas for my own research from papers I assign my students to read. And I love sparking that “aha” moment for students—showing them how textbook data look in real life.
Q: How do you explain your research to non-scientists?
A: My family isn’t scientific, so I use analogies. I say we have drugs that work on prostate cancer, but some tumors “shape-shift” into something that looks more like a brain tumor. Our drugs don’t work on that form. We’re trying to understand and block this shape-shifting or shift the tumors back so treatments work again.
Q: What did your postdoctoral training with our colleague Dr. David Rickman mean for your career?
A: It was a perfect match. His lab had developed a great mouse model of neuroendocrine prostate cancer and had begun generating interesting computational data. I had wet lab and mouse experience but was looking for a supportive environment to develop my own computational skills. Receiving mentorship from Dr. Rickman, collaborating with pathologists like our colleague Dr. Brian Robinson, and leveraging the institution’s resources laid the groundwork for my own independent lab.
Q: How do you see artificial intelligence affecting your field?
A: In the near term, AI will help more molecular biologists write code and do computational work. There’s also interest in using AI to analyze pathology images or classify tumor regions. But AI can’t yet replace the conversation and reasoning you get from a human pathologist. It’s a tool, not a substitute for expertise.
Q: How would you characterize the culture at Weill Cornell Medicine and within our department?
A: Moving to New York was intimidating, but once I arrived at Cornell I never felt alone. The research community here is collaborative, not cutthroat. Core facilities like the Genomics Core and the Center for Translational Pathology are outstanding. And there’s a strong sense of support across postdocs, technicians, students, and faculty.
Q: What might people be surprised to learn about you?
A: I used to play ice hockey. I didn’t start until I was an adult in graduate school. It was the best stress reliever—an incredible workout. I played left defense because it turned out that I was good at skating backwards. When I moved here, I played on a Tri-I graduate student team at Central Park’s outdoor rink for a few years. Also, I’m a Boston Bruins fan; my cat is named Zdeno after Zdeno Chara.
Q: If you had unlimited resources, what’s the one experiment you’d do?
A: I’d run large CRISPR screens and develop lineage tracing mouse models of prostate cancer to pinpoint the earliest events that drive resistance and lineage plasticity. If we can stop that switch before it starts, we could have the biggest therapeutic impact.
Q: Finally, what do you hope readers take away from your story?
A: That mentorship matters. Great mentors shaped my career, and I’m trying to pay that forward. I also hope more scientists engage with the public to improve scientific literacy. The discoveries we make today lead to treatments a decade from now.