Presenter Profile: Triparna Sen, PhD
Icahn School of Medicine at Mount Sinai, New York
ILCN: What is your presentation about?
Dr. Sen: The presentation will focus on the preclinical genomics of lung cancer plasticity and metastasis, with an emphasis on small cell lung cancer (SCLC). I will discuss how genomic, transcriptomic, and epigenetic alterations fuel lineage plasticity and drive metastatic spread. My talk will include the striking transformation from non-small cell lung cancer (NSCLC) to SCLC that occurs as a mechanism of therapy resistance. I will also highlight how the tumor-immune microenvironment contributes to these transitions, shaping resistance and immune evasion. Together, these layers of biology reveal why SCLC remains such an aggressive and adaptable disease.
Leveraging Omics to Understand the Biology of Lung Cancer
12:00–13:15 CEST, Monday, September 8 • Room 05
During the session, Triparna Sen, PhD, will share insights on the preclinical genomics of lung cancer plasticity and metastasis. LEARN MORE
ILCN: Why is this topic timely or important in 2025?
Dr. Sen: Plasticity has emerged as one of the biggest barriers to durable responses in lung cancer therapy. NSCLC to SCLC transformation exemplifies how tumors can change identity under treatment pressure, often leading to aggressive relapse and limited options. In 2025, with the expansion of targeted therapies, immunotherapies, and TCEs, it is essential to understand not just static genomic alterations but also dynamic transcriptomic and epigenetic states, as well as the microenvironmental cues that permit these transitions. This knowledge is vital for anticipating resistance and guiding biomarker and therapeutic strategies.
ILCN: How do you see your work in this area benefiting future clinical strategies or patient care?
Dr. Sen: By integrating genomic, transcriptomic, and epigenomic profiling with preclinical models, our work is uncovering how SCLC emerges both de novo and through histological transformation from NSCLC. We are identifying biomarkers that flag these shifts early and vulnerabilities that appear when tumor cells reprogram their lineage. At the same time, by studying the immune microenvironment, we are learning how immune suppression and exclusion enable plasticity and metastasis. These insights will help develop strategies for monitoring transformation, selecting patients for appropriate therapies, and designing rational combinations to prevent or delay lineage plasticity, ultimately improving patient outcomes.
ILCN: What are you most looking forward to at this year’s World Conference?
Dr. Sen: The World Conference on Lung Cancer is a unique opportunity to bring together scientists, translational researchers, and clinicians to collectively tackle the challenges of thoracic malignancies. I am also excited to build new collaborations that accelerate the translation of laboratory discoveries into patient benefit.
ILCN: What do you hope the audience takes away from your presentation?
Dr. Sen: I hope the audience comes away with a clear understanding that lung cancer plasticity—whether in de novo SCLC or in NSCLC that transforms to SCLC—is a dynamic process shaped by genomics, transcriptomics, epigenetics, and the immune microenvironment. These processes explain both the aggressiveness of SCLC and the challenge of therapeutic resistance. Decoding these mechanisms is likely to provide us with new biomarkers, new therapeutic targets, and effective and durable strategies for patients with lung cancer.
