Leading cancer researchers from UC San Francisco will present talks on environmental and genetic determinants in cancer development, precision cancer treatment with radiotheranostics, overcoming drug resistance, and other cancer research topics at this year’s annual meeting of the American Association for Cancer Research (AACR) conference, which will be held April 17-22 in San Diego.
The theme of this year’s conference, “Precision, Partnership, Purpose: Advancing Cancer Science to Save Lives Globally,” celebrates the collective effort of the cancer community at the heart of cancer research, and highlights advances in the biology, prevention, detection, diagnosis, and treatment of cancer, as well as state-of-the-art concepts and technologies shaping cancer research.
This year’s program featured innovative research and discussions by experts from the UCSF Helen Diller Family Comprehensive Cancer Center.
Featured Presentations
Major Symposia (all times Pacific)
Monday, April 20, 10:15 a.m. to 11:45 a.m.
Valerie M. Weaver, PhD, director of the UCSF Center for Bioengineering & Tissue Regeneration and professor of Surgery in Division of Surgical Oncology, is chair for the major symposium “SY07 - Understanding the Impact of Mechanobiology on Tumor Evolution.” She also presents “Forcing Inflammation to Drive Tumor Initiation and Progression” from 10:20 a.m. to 10:40 a.m. with a discussion from 10:40 a.m. to 10:45 a.m. Fibrosis-induced tissue tension compromises vasculature to induce hypoxia and impede drug delivery, stimulates inflammation and compromises anti-tumor immunity to drive tumor progression and metastasis. Recent evidence suggests fibrosis-induced tissue tension may also induce mutations to initiate tumorigenesis and promote cancer progression and could promote genomic instability to drive tumor heterogeneity. Weaver and other presenters will describe this tumor-associated tension and clarify how it can contribute to malignant transformation and progression.
Monday, April 20, 11:10 a.m. to 11:30 a.m.
Pamela N. Munster, MD, co-leader of the UCSF Center for BRCA Research and Molecular Oncology Program, presents “Synthetic Lethality Beyond BRCA” during the major symposium “SY19 - DNA Damage Response and Synthetic Lethality in Cancer” with a discussion to follow from 11:30 a.m. to 11:35 a.m. Homologous recombination deficient tumors, including tumors with mutations in BRCA1 and BRCA2, are sensitive to PARP inhibitors via the mechanism of synthetic lethality. New drug combinations, described by Munster, including PARP inhibitors and chemotherapeutic agents, can be used to target homologous recombination-deficient solid tumors. For example, a combination of the PARP inhibitor rucaparib, plus irinotecan, was well tolerated for up to eighteen months with durable responses in BRCA-, PALB2-, and ATM-mutated cancers, despite progression on previous platinum.
Tuesday, April 21, 10:20 a.m. to 10:40 a.m.
Rushika Perera, PhD, vice chair of the UCSF Department of Anatomy and chief scientific officer of the UCSF Pancreas Center, presents “Identifying Selective Dependencies of Liver Metastatic Pancreatic Cancer Cells” during the major symposium “SY37 - Tumor-secreted Factors: The Next Hallmark of Cancer?” with a discussion following her presentation from 10:40 a.m. to 10:45 a.m. In the emerging landscape of cancer research, the role of tumor-secreted factors is gaining prominence as a critical area of investigation, illuminating their influence on cancer progression and metastasis. This session brings together cutting-edge insights into how tumors interact with their microenvironments, showcasing their impact on selective vulnerabilities in cancer cells. Perera will discuss how the remodeling of the autophagy-lysosome system in liver metastatic pancreatic cancer reveals specific targets that could disrupt supportive metastatic niches. These findings underscore the critical importance of tumor-secreted factors as a cohesive and transformative aspect of cancer biology, opening new avenues for innovative therapeutic strategies.
Tuesday, April 21, 10:45 a.m. to 11:05 a.m.
Natalia Jura, PhD, a professor at the UCSF Cardiovascular Research Institute, presents “Mechanisms of PI3Kα Activation by RTKs, Ras, and Cancer-associated Mutations” during the major symposium “SY09 - Structural Insights to Cancer Biology and Therapy” with a discussion following her presentation from 11:05 a.m. to 11:10 a.m. Structural biology has become a central driver of discovery in cancer research, enabling direct visualization of oncogenic signaling mechanisms and informing new therapeutic strategies. The presentations will highlight how proteins central to cancer signaling populate complex conformational landscapes, including transient or invisible states that are essential for regulation and signaling but are not captured by classical static structures. Jura will discuss the structural mechanisms of protein kinase regulation.
Wednesday, April 22, 10:40 a.m. to 11:00 a.m.
Michael J. Evans, PhD, professor in residence in the UCSF Department of Radiology and Biomedical Imaging, presents “Getting a ‘GRIP’ on Anti-tumor Immunity with Granzyme-targeted PET” during the major symposium “SY33 - Radioligand Therapy: Immunity and Biological Mechanisms.” With significant effort and interest in radioligand therapy by academia, industry, and government, paradigm-changing studies have demonstrated that RLT has the possibility to dramatically impact cancer treatment. Yet a major limitation for the further development of this field is a lack of fundamental knowledge of the mechanism(s) of action of systemic therapeutic isotopes with tumors, the tumor microenvironment, and the immune system. Evans and his fellow presenters discuss the state-of-the-art in radiotheranostics as related to cancer biology, clinical oncology, and immunology to understand how RLT approaches work and how to overcome their limitations to drive the development of next generation therapies.
Wednesday, April 22, 11:10 a.m. to 11:30 a.m.
Davide Ruggero, PhD, the Helen Diller Family Chair in Basic Cancer Research at UCSF, presents “Decoding Drug Tolerance in Cancer: The Impact of Translation Specificity” during the major symposium “SY24 - The Role of mRNA Translation Reprogramming in Cancer” with a discussion following his presentation from 11:30 a.m. to 11:35 a.m. Translation is a fundamental biological process during which the translational apparatus decodes information carried in the messenger RNAs (mRNAs) to synthesize proteins. Stress-induced perturbations in mRNA translation play a major role in homeostatic adaptation. In turn, dysregulated mRNA translation plays a major role across a broad spectrum of neoplasia, wherein the growing body of data suggest that perturbations in translational programs drive metastatic cancer progression and therapeutic resistance. In this session, Ruggero and others will discuss recent results that illuminate the mechanisms whereby translational reprogramming leads to cancer dissemination and attenuation of anti-neoplastic effects of drugs.
Special Sessions
Monday, April 20, 5:25 p.m. to 5:40 p.m.
Allan Balmain, PhD, Barbara Bass Bakar Distinguished Professorship in Cancer Genetics at UCSF, presents “How tissue environments and tumor promoters conspire with mutations to drive carcinogenesis” during the special session “SS07 – The Making of Cancer: From Cellular Events to Systemic Disease – Breakthrough Discoveries from Cancer Grand Challenges. Balmain’s talk will discuss the role of the environment in cancer and describe how the concept of environmental tumor promoters shifts the focus away from a purely genetic view of how cancers develop. He will discuss his new study in Nature, which proposes a synthesis between ideas put forward almost a century ago based on seminal experiments on carcinogen-induced tumors in mice, observations made by cancer epidemiologists over several decades, and the recent revelation that normal human tissues are a patchwork of mutant clones. The repeated interplay between variation and selection — the first principles of Darwinian evolution —underlies the clonal selection leading to tumorigenesis. A deeper understanding of these processes can enhance prospects for cancer prevention by eliminating or mitigating the effects of environmental or endogenous tumor promoters.
Balmain also presents “Genetic and environmental effects on cell-cell competition and clonal selection during mouse skin tumor development” during the major symposium “SY18 - Genetic and Environmental Determinants of Cancer” on April 22 from 10:36 a.m. to 10:51 a.m. with discussion following his presentation from 10:51 a.m. to 10:56 a.m. Cancer risk and tumor evolution are determined by a multitude of factors, including genetic and environmental influences. These factors also alter tissue microenvironments and the selective pressures within normal tissues, promoting the expansion of cells harboring specific mutations into clones with tumorigenic potential. Balmain will detail the role of different kinds of inflammation in causing mutated cells to grow and progress to cancers.
NCI-NIH Selected Session
April 20, 4:00 p.m. to 5:00 p.m.
Iona Cheng, MD, MPH, MD, a cancer and genetic epidemiologist and UCSF professor of Epidemiology & Biostatistics, is co-chair and panelist for the NCI-NIH session “NIH06 - Leveraging NCI-supported Cancer Epidemiology Cohorts to Advance Cancer Prevention and Control.” Cancer epidemiology cohorts play a critical role in advancing cancer control and prevention, generating transformative insights that inform interventions and strategies to reduce cancer incidence, morbidity, and mortality in humans. These cohorts provide invaluable resources —including exposure data, biospecimens, and longitudinal follow-up across populations — that drive impactful research. Cheng will lead a panel discussion on the advancement of cancer prevention and control through cancer epidemiology cohorts, data sharing and harmonization, recruitment and retention of newly funded cohorts, and leveraging current cohorts to address scientific gaps.
Cheng is also a presenter for “The Impact of Structural and Social Drivers of Health on Cancer Risk and Survival” during the “advances in population sciences” session “APS02 - Advances in the Use of Geospatial and Neighborhood Data for Cancer Population Sciences Research and Translation” on April 19, from 1:45 p.m. to 2:05 p.m. Cheng will be presenting on contemporary examples of the role of structural and social drivers in relation to cancer incidence and mortality as well as advancements in the field, evaluating SSDH in relation to biological pathways, translation and community impact of SSDH, and future directions in this field.
Tuesday, April 21, 12:30 p.m. to 2:00 p.m.
Jennifer R. Grandis, MD, associate vice chancellor for clinical and translational research at UCSF, is chair for the “advances in prevention research” session “APRV02 - Cancer Predisposition Syndromes” and she presents “Solid tumors in Fanconi Anemia” from 1:25 p.m. to 1:45 p.m. Most cancers are sporadic, afflicting individuals who have no known genetic predispositions. However, people with cancer predisposition syndromes experience extraordinarily high rates of cancer, often >700-fold higher than the general population. These conditions provide unique opportunities to unravel the genetic and molecular underpinnings of carcinogenesis. In addition, the lethality of many of these cancers arising in cancer predisposition syndromes represents an urgent need for more effective screening, preventive and therapeutic interventions. In this session, Grandis will present recent data on cancer in Fanconi Anemia.
Tuesday, April 21, 1:00 p.m. to 1:20 p.m.
Jonathan Chou, MD, PhD, a genitourinary medical oncologist and researcher at UCSF, presents “Tumor cell intrinsic and extrinsic mechanisms of ADC resistance” during the “advances in diagnostics and therapeutics” session “ADT01 - Resistance to Antibody Drug Conjugates” with a discussion following his presentation from 1:20 p.m. to 1:25 p.m. Antibody drug conjugates (ADCs) have rapidly moved from novel therapeutic modality to entrenched standard of care in many solid tumor cancer types. However, the optimal use of these agents requires a molecular understanding of the heterogenous responses to these drugs that span from complete and durable response to rapid disease progression. In this session, Chou and fellow presenters will present unpublished and recently published data on recurrent mechanisms that underlie clinical resistance to ADCs featuring studies in breast, lung, colon, and bladder cancer.
Wednesday, April 22, 10:15 a.m. to 11:45 a.m.
Michelle R. Arkin, PhD, UCSF professor of Pharmaceutical Chemistry, is the chair for the “advances in diagnostics and therapeutics” session “ADT02 - Induced Proximity Pharmacology: Degraders and Beyond” and presents “Gluing Native Protein-protein Interactions to Augment Anticancer Pathways” from 11:16 a.m. to 11:31 a.m. with a discussion following her presentation from 11:31 a.m. to 11:36 a.m. The concept of induced proximity – pulling together two biomolecules to effect novel pharmacology – is changing the way chemical biologists and drug investigators approach cancer targets. Many potential cancer targets are currently undruggable. Inducing proximity between target proteins and the protein-degradation machinery has proven very effective in degrading cancer-driving proteins, while newer proximity-based approaches can stabilize anticancer proteins, rewire cancer processes, or increase tissue selectivity. Arkin and her fellow presenters will showcase preclinical and clinical progress in drugging the heretofore undruggable.
Minisymposium
Sunday, April 19, 3:35 p.m. to 3:50 p.m.
Adam Blaisdell, MD, PhD, a UCSF gastroenterologist, presents “1340 - The Zinc Finger 7 Motif of TNFAIP3/A20 Enforces a Critical Block in Exhausted CD8 T Cell Degranulation and Represents a Potent Target for Enhancing Adoptive Cellular Therapies for Cancer” during minisymposium “MS.IM01.03 - Combating T Cell Checkpoints.” CD8 T cells eliminate tumors through effector cytokines (IFNgamma, TNF) and cytotoxic granule protein release (perforin, granzymes). CD8 T cell exhaustion limits the efficacy of cancer immunotherapy and adoptive cellular therapies (ACTs). Blaisdell and his colleagues performed a genome‑wide CRISPR screen in repeatedly stimulated human TCR‑T cells, identifying A20/ZF7 (a protein and zinc finger domain) as a key suppressor of T cell persistence and cytotoxicity in the face of exhaustive stress. Germline and targeted ZF7 perturbations (Cas9 or base editing) increased CAR‑T and TCR‑T efficacy in solid and liquid tumor models. These results demonstrate that selective targeting of central suppressors such as A20 can not only reverse CD8 T cell exhaustion but also engage alternative signaling programs to unleash cytotoxicity and address critical gaps in the understanding of the biological networks that restrain perforin-dependent cytotoxicity in CD8 T cell exhaustion and provide a foundation for enhancing the potency and durability of ACTs.
Educational Sessions
Friday, April 17, from 3:00 p.m. to 4:30 p.m.
Hunter Shain, PhD, UCSF associate professor in the UCSF Department of Dermatology, is chair for the educational session “Decoding Tumor Evolution through the Human Tumor Atlas Network: An Ecological and Evolutionary Perspective and presents “Evolution of Cutaneous Squamous Cell Carcinoma.” Shain is involved in the work of the Human Tumor Atlas Network (HTAN), where he leads the Pre-Cancer Atlas of Skin Cancer Project. During this session, Shain will walk the audience through the journey from a normal skin cell, known as a keratinocyte, to a common form of skin cancer, known as cutaneous squamous cell carcinoma. He will cover the key non-genetic and genetic events driving the transitions from normal skin cells to pre-cancerous lesions, to fully-evolved life-threatening cancers.
Friday, April 17, from 4:45 p.m. to 6:15 p.m.
Kevan M. Shokat, PhD, UCSF professor of Cellular and Molecular Pharmacology and AACR Academy Fellow, is chair for the educational session “ED07. Mechanisms of Resistance to Targeted and IO Therapies and Strategies for Overcoming Resistance” and presents
“Mechanisms of Resistance to Direct Ras inhibitors and Approaches for Overcoming Resistance” from 4:46 p.m. to 5:06 p.m. with a discussion to follow from 5:06 p.m. to 5:15 p.m. Shokat is a renowned molecular bioscientist whose breakthrough research in targeting the once undruggable K-Ras protein has opened a new therapeutic option, offering hope for treating cancers with poor survival rates. In this session, Shokat will discuss his recent research uncovering how Ras-driven tumors develop drug resistance and considers strategies to counteract it.
Friday, April 18, from 12:30 p.m. to 2:00 p.m.
Javid Moslehi, MD, William Grossman Distinguished Professor in Cardiology and chief of the UCSF Cardio-Oncology & Immunology Program, is chairperson of the educational session, “Beyond Cardiotoxicity: How Cardiovascular Disease and Systemic Risk Factors Drive Tumorigenesis” and presents “Cardio-oncology: Beyond Toxicology” from 12:31 p.m. to 12:41 p.m. Moslehi and his colleagues have been investigating why a subset of patients receiving immune checkpoint inhibitors can develop myocarditis. He will discuss the mechanisms of myocarditis as well as ways to identify which patients are at risk so treatments can be tailor treatments appropriately.
Friday, April 18, from 2:30 p.m. to 4:00 p.m.
Frank McCormick, PhD, FRS, the David A. Wood Chair of Tumor Biology and Cancer Research and professor in the UCSF Department of Cellular and Molecular Pharmacology, is chairperson for the educational session “How KRAS Inhibitors Got to the Clinic: From Discovery to Patient Benefit” and also presents and discusses “Targeting Active KRAS and Its Effectors” from 2:31 p.m. to 3 p.m. Over the last decade, a remarkable number of KRAS inhibitors have been discovered and developed into clinical candidates. These inhibitors fall into two major structural classes: (1) small molecules that bind directly to KRAS and (2) small molecules that form a ternary complex between cyclophilin A and KRAS. KRAS exists in an inactive, GDP-bound state, or an active GTP-bound state. Drugs that target each of these states, or both states, have been developed. The relative merits of targeting each state will also be discussed.
Please visit AACR 2026 website for complete meeting abstract and session information.