By Jasmin Twiggs
We are proud to feature Keystone Symposia Fellow Charalampos (Harris) A. Lazaris, MBA, PhD, a Senior Expert in Oncology Data Science at Novartis Biomedical Research in Cambridge, Massachusetts. Dr. Lazaris studies how cancer cells rewire which genes are switched on and off, and how those rewired programs create dependencies, or “addictions,” that can be turned against the disease.
Growing up in Greece, Harris watched close family members struggle with serious illness, and he wanted to help people get better. For years that meant becoming a medical doctor, until he sat the national university entrance exams and did not get into medical school.
"That door closing turned out to be one of the best things that ever happened to me.”
He studied biology instead, at the University of Ioannina, and something clicked almost immediately: “I realized this was medicine — just at a different resolution.” Rather than treating patients one at a time, he could work to understand the mechanisms driving disease and change outcomes for many. What captivated him was gene regulation: how a single genome, identical in every cell, gives rise to neurons, muscle, and liver alike. As he puts it, an embryo goes from a single fertilized egg to hundreds of specialized cell types, each arriving “at precisely the right place at precisely the right time” — a puzzle he considers one of the most profound in science.
Alongside his love of biology, Harris had a long-held affinity for computers, and a Master’s in Bioinformatics at the University of Edinburgh finally brought the two together. That intersection, he says, is where he “found my place in science.” It gave him the tools to study gene regulation, and how it breaks down in cancer, at a scale biology alone couldn’t reach. Cancer, as he sees it, is “a disease of disrupted gene regulation.”
Most cancer research focuses on mutations and other changes to the DNA sequence itself. Harris works on a less-examined layer: transcriptional and epigenetic control, or how the genome’s physical organization and regulatory switches keep cancer-driving programs turned on.
Within that framework, he studies two forms of dependency that often turn out to be intertwined. In oncogenic addiction, cancer cells become hooked on one or more overactive cancer genes, or the pathways they drive. In non-oncogenic addiction, they instead lean on stress-response or survival pathways that are not themselves genetically altered, but that the cancer has co-opted for its own benefit. Much of Harris’s work asks how the genome’s three-dimensional architecture is linked to these dependencies. The genome is partitioned into structural neighborhoods whose boundaries act as insulation, and in Nature Communications, he showed that the strongest of these boundaries preferentially wall off super-enhancers, large clusters of regulatory elements that act as especially potent control hubs for gene expression. That finding carried a clear corollary: if strong boundaries keep these potent enhancers in check, losing that insulation should let them run loose. A study in Nature Genetics showed exactly that, finding that the loss of insulating chromatin boundaries in T-cell acute lymphoblastic leukemia lets a super-enhancer upregulate c-MYC, one of the most commonly activated genes in cancer — a direct link between disrupted genome architecture and oncogene activation.
Harris was a co-first author on a study in Nature Medicine, where the two forms of dependency meet. There, his team showed that the oncogenic driver NOTCH1 sustains leukemia by hijacking the cell’s own stress-response machinery — an otherwise ordinary, non-oncogenic survival program. An oncogenic addiction, in other words, is enforced through a non-oncogenic one, making the interplay between them a potential vulnerability.
"Cancer cells can become ‘hooked’ on gene-expression programs that drive their growth and survival — and those dependencies are precisely the vulnerabilities we can target.”
Today, in his role at Novartis, Harris focuses on transcriptional dependencies in solid tumors, integrating three complementary views of the cell: genomics, epigenomics, and transcriptomics. The aim is practical: understanding these dependencies could sharpen which patients are chosen for a given therapy and lead to longer-lasting responses for people living with cancer.
For Harris, a defining moment of the Fellows Program came at the Scientific Advisory Board (SAB) meeting in Boulder, Colorado, in January 2026. It was his first time in the room where Board members decide which symposia to renew and which topics to elevate, and the first time he could offer his own perspective rather than only listen.
He does not pretend it was easy at first. “The first few hours were a little overwhelming,” he recalls: his first time in Colorado, his first SAB meeting, a room full of scientists with decades of experience. What changed things was the tone of the room, welcoming and without hierarchy.
"When I finally spoke up, something had shifted.”
The value of being there, he realized, was not in listening but in contributing — and that his contribution was “expected and respected, regardless of career stage.” The discussions ranged well beyond gene regulation and cancer, into science advocacy, outreach, and how Keystone can best support research communities worldwide. Meeting past Fellows and hearing the range of paths they had taken clarified something he had not fully named before: he wanted not only to do rigorous research but to help decide which questions the community takes on.
Mentorship, in Harris’s view, is one of the most powerful forces in science: a way to develop not only exceptional research but resilient scientists.
"A good mentor does not simply show you how to do experiments or analyses; they also help you navigate complex work environments, professional relationships, and career choices in a way that aligns with your values.”
He credits a lineage of mentors: his New York University (NYU) doctoral advisors Iannis Aifantis and Aristotelis Tsirigos; Richard Young, in whose Whitehead Institute lab he saw “how powerful it is to do rigorous, curiosity-driven basic research while keeping in mind how those discoveries might eventually reach patients”; and collaborators including Charles B. Epstein at the Broad Institute and Mariateresa Fulciniti and Nikhil Munshi at the Dana-Farber Cancer Institute, who shaped how he thinks about moving mechanistic discoveries toward the clinic.
Within the Fellows Program, his mentor Chryssa Kanellopoulou and the “Fellows Fridays” sessions have filled gaps rarely covered in formal training: funding, team dynamics, conflict resolution, and work–life balance.
"I often find myself wishing that this kind of structured mentorship and skills training were a standard part of graduate and postdoctoral training.”
His advice to earlier-career scientists is hard-won, and the lesson he returns to is personal: “Don’t let shyness hold you back.” Approach the speaker after the talk; send the cold email. “The worst anyone can say is no,” he notes, admitting he “spent too long hesitating, worried about seeming too eager.” He wishes he had understood earlier that even the most established scientists enjoy connecting with curious early-career researchers. He now puts that conviction into practice, mentoring students in molecular and computational biology and serving as President of the NYU Graduate School of Arts and Science Doctoral Alumni Association. He has also volunteered through the STEM Mentoring Fellowship at the New York Academy of Sciences and the open-science non-profit ASAPbio.
"I want not only to continue doing rigorous research, but also to play an active role in deciding which questions we tackle as a community — and helping bring the right people together to tackle them.”
It is a fitting ambition for someone whose own path crossed five universities across three countries. Six degrees in all — from Greece to Edinburgh to New York — each move, he says, “a leap into the unknown” that shaped how he thinks and works. Having stood in one scientific community after another, he has come to believe that “science looks different depending on where you’re standing.”