AI in Cancer Care, Targeted Therapies Among Cancer Conference Talks

Sunday, April 27, from 9:30 a.m. to 11:30 a.m.

Opening Plenary Session PL02 - Opening Plenary: Unifying Cancer Science and Medicine – A Continuum of Innovation for Impact from 9:40 a.m. to 10:07 a.m.

Kevan M. Shokat, PhD, UCSF professor of Cellular and Molecular Pharmacology and AACR Academy Fellow, presents “Overcoming The Undruggable Nature Of The Most Common Human Oncogene, K-Ras.” Somatic mutations in the small GTPase K-Ras are responsible for approximately 30% of human cancers and are generally associated with poor response to standard therapies. The mutations in K-Ras were identified in the early 1980’s but it took almost four decades for the first drugs targeting the protein to be approved. The long delay was a result of the apparent lack of a drug binding pocket on K-Ras despite detailed structural and biochemical characterization of the protein, leading to it being referred to as “undruggable.” While progress has been made with new medicines, such as sotorasib and adagrasib, being approved for patients with K-Ras (G12C) lung cancer, drug development of agents to inhibit the more frequent K-Ras (G12D) and K-Ras (G12V) versions found in colon and pancreatic cancer, still remains a challenge. Another challenge is drug resistance which is faced by all targeted cancer therapies including the new K-Ras (G12C) directed drugs. In this lecture Shokat will provide a perspective on challenges and opportunities of newly developed K-Ras targeting drugs.

Sunday, April 27, from 1:00 p.m. to 2:30 p.m.

Major Symposium - SY42 - Tissue Mechanics and Physical Forces in Cancer

Valerie M. Weaver, PhD, director of the UCSF Center for Bioengineering & Tissue Regeneration and professor of Surgery in Division of Surgical Oncology, presents “Forcing Cancer Initiation And Progression Through Myeloid Lipid Peroxidation-Mediated DNA Damage” from 1:30 p.m. to 1:50 p.m. Weaver discusses cancer as a physical disease and how the interplay between connective tissue, physical forces and immune response plays a role in cancer risk, cancer aggression and therapy response. She will discuss how the immune system spurs the fibrosis and mechanical changes in tissues that drive cancer and how the immune cells respond to the altered physical properties of that connective tissue, corrupting their anti-tumor response and metabolism. In addition to changing the metabolism, the extracellular matrix and anti-tumor function, myeloid cells produce lipid aldehydes that cause DNA damage and mutations in the cancer tissue. She will examine ways to correct the behavior of corrupted myeloid cells including development of novel treatments.

Sunday, April 27, from 3:00 p.m. to 5:00 p.m.

Mini-symposium MS.CL01.01 - Liquid Biopsy: Circulating Tumor Cells

Laura Huppert, MD, a breast oncologist and assistant professor in the UCSF Division of Hematology/Oncology, presents “Development Of A Novel Assay To Detect Circulating Tumor Cells (CTC) In The Cerebrospinal Fluid Of Patients With Leptomeningeal Disease” (#1147) from 3:50 p.m. to 4:05 p.m. Approximately 5-15% of patients with metastatic breast cancer (MBC) will develop leptomeningeal disease (LMD), characterized by the spread of tumor cells to the lining of the brain and spinal cord. Diagnosis can be limited by the availability to detect tumor cells in the cerebrospinal fluid (CSF) and prognosis of LMD is poor – on the order of less than six months – with limited treatment options. Given the poor prognosis after diagnosis of LMD, improving methods to detect rare CTCs in the CSF could lead to earlier intervention and improved patient outcomes. To address this unmet clinical need, the researchers developed a novel process for detecting and characterizing CTCs in the CSF of patients with LMD and report on the results intended to improve LMD diagnosis and potentially have a positive impact on patient outcomes.

Sunday, April 27, from 6:30 p.m. to 8:30 p.m.

Town Meeting: Session TM07 – Charting the Trajectory for Advancements in Pediatric Cancer Research- A Pediatric Cancer Working Group Town Hall

Alejandro Sweet-Cordero, MD, UCSF chief of Pediatric Oncology and chair of the AACR Pediatric Cancer Working Group, hosts the 2025 PCWG Town Hall which will feature presentations from experts in the pediatric cancer community on the theme of "Charting the Trajectory for Advancements in Pediatric Cancer Research" followed by a panel discussion. The Town Hall also includes a Networking Reception at the beginning of the session.

He also serves as chairperson and presenter for the Major Symposium DC07 - Molecular Tumor Profiling for Pediatric Oncology on Monday, April 28, 2025 from 3:00 p.m. to 4:30 p.m.

Monday, April 28, from 10:15 a.m. to 11:45 a.m.

Major Symposium SY26 - Metabolism and Organelle Biology in Cancer

Rushika Perera, PhD, vice chair of the UCSF Department of Anatomy and chief scientific officer of the UCSF Pancreas Center, is chairperson for the session and presenter of “Decoding Novel Lysosome Functions In Pancreatic Cancer” from 11:20 a.m. to 11:35 a.m. Pancreatic ductal adenocarcinoma (PDAC) is the most common and aggressive cancer of the pancreas. PDAC tumors are highly reliant on nutrient scavenging pathways such as autophagy, and the lysosome to sustain metabolic homeostasis and cellular quality control. To fully understand the functions of the lysosome in PDAC progression, Perera’s lab uses biochemical approaches to isolate intact lysosomes from PDAC cells, followed by mass spectrometry-based proteomics. Using this strategy, the research team has uncovered unique features and functions of PDAC lysosomes that promote cellular adaptation to stress and tumor growth. They have developed techniques to profile lysosome content and composition during different stages of tumor evolution including metastasis to the liver and lungs – the two major sites of secondary tumor growth in PDAC patients. This research highlights how dynamic changes in lysosome composition in vivo, enables PDAC cells to rapidly adapt to growth at different organ sites and may inform the development of therapeutic strategies focused on lysosome inhibition in cancer.

Monday, April 28, from 12:30 p.m. to 2:00 p.m.

Major Symposium SY08 - Developments in RAS Signaling Inhibition: Bench to Bedside

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 session and also presents “The End of KRAS cancers?” from 12:35 p.m. to 12:55 p.m. McCormick will provide an overview of some of the approaches that he and others are taking to attack cancers driven by mutant KRAS, and review some of the drugs developed which use different mechanisms to attack this protein. He will also talk about new approaches being employed to further increase the chances of treating these cancers.

Tuesday, April 29, from 8:00 a.m. to 10:00 a.m.

Plenary Session PL04 - Targeting the Cancer Ecosystem

Max F. Krummel, PhD, Robert E. Smith Endowed Chair in Experimental Pathology at UCSF, presents “Leveraging Tumor Immune Archetypes In Treating Cancer” from 8:32 a.m. to 8:59 a.m. This plenary session will address co-evolution of tumor and host at the tissue and systems levels and explore how complexity of the cancer ecosystem presents both challenges and opportunities for therapy. There will be a discussion of therapeutic means to target the complex tumor micro- or macroenvironment and promote new states phenotypically similar to healthy tissues. The session will illustrate the importance of considering the heterocellular tumor ecosystem in efforts to understand and treat cancer and highlight mechanisms of cellular and anatomic crosstalk that may represent therapeutic targets.

Tuesday, April 29, from 10:15 a.m. to 11:45 a.m.

Major Symposium SY05 - Cardio-Oncology: A Novel Platform for Investigation

Javid Moslehi, MD, William Grossman Distinguished Professor in Cardiology and chief of the UCSF Cardio-Oncology & Immunology Program, is chairperson of the session, presenting the symposium introduction as well as the talk “Immune Checkpoint Inhibitors And Cardiac Toxicity: From Mice To Humans” from 11:10 a.m. to 11:30 a.m. In the past 20 years, cardio-oncology has emerged as a new cardiovascular subspecialty in part because of the success that has been attained in oncology. Patients now live longer with the cancer, making cardiovascular health more relevant. Although these therapies have changed the natural course of many cancers, several may also lead to cardiovascular complications. Many new anticancer drugs approved over the past decade are “targeted” therapies that interfere with intracellular signaling contributing to tumor progression. Unexpected cardiovascular and cardiometabolic effects of patient treatment with these inhibitors have provided unique insights into the role of these targets in human cardiovascular biology. The session will address these topics and propose that numerous ongoing oncology clinical trials are an opportunity for closer collaboration between cardiologists and oncologists to study the cardiovascular and cardiometabolic changes caused by the modulation of these pathways in patients and can serve as a potential avenue for optimization of anti-cancer therapies and for cardiovascular research and drug discovery.

Tuesday, April 29, from 10:15 a.m. to 11:45 a.m.

Major Symposium SY16 - Novel Classes of Human Cancer Rejection Antigens: Beyond Point Mutations

Hideho Okada, MD, PhD, director of the UCSF Brain Tumor Immunotherapy Center and UCSF professor of Neurological Surgery, Surgery and Immunology, presents “Tumor-Wide RNA Splicing Aberrations Generate Therapeutically Actionable Public Neoantigens” from 10:45 a.m. to 11:05 a.m. T cell-based immunotherapies hold promise in treating cancer by leveraging the immune system's recognition of cancer-specific antigens. However, their efficacy is limited in tumors with few somatic mutations and substantial intratumoral heterogeneity. In this presentation, Okada discusses novel sources of antigens for cancer immunotherapy, including a previously uncharacterized class of tumor-wide public neoantigens originating from RNA splicing aberrations in diverse cancer types. He and his team identified T cell receptor clones capable of recognizing and targeting neoantigens derived from aberrant splicing in GNAS and RPL22. In cases with multi-site biopsies, they detected the tumor-wide expression of the GNAS neojunction in glioma, mesothelioma, prostate cancer and liver cancer. Their study highlights a role for dysregulated splicing factor expression in specific cancer types and their findings establish a molecular basis for T cell-based immunotherapies addressing the challenges of intratumoral heterogeneity.

Tuesday, April 29, from 10:15 a.m. to 11:45 a.m.

Major Symposium SY49 - Minorities in Cancer Research Scientific Symposium: Using Self-identified Race/Ethnic Categories in Cancer Disparities Research in the Era of Precision Medicine

Scarlett Lin Gomez, MPH, PhD, co-leader of the UCSF Cancer Control Program and professor in the UCSF Department of Epidemiology and Biostatistics, will present her research from 11:00 a.m. to 11:20 a.m. Over the past 25-years, the science of cancer health disparities research has evolved from first-generation studies that focused on describing population group differences in cancer incidence and mortality to transdisciplinary translational studies that investigate the contribution of biological, behavioral, clinical, and social drivers to cancer care outcomes. While comparisons of racial and ethnic group differences using self-identified categories have been instrumental in identifying populations that are at risk for poor outcomes following diagnosis and treatment, concerns have been raised about using self-identified race/ethnicity in biomedical research. The objective of this session is to review the advantages and disadvantages of using self-identified race/ethnic categories in cancer disparities research and identify best practices for monitoring and addressing the burden of cancer risk across different populations in light of methodologies and instruments that potentially have greater precision in basic, clinical, and population-based research studies.

Gomez also presents “Prevention, Early Detection, Population Sciences, And Disparities Research” from 12:39 p.m. to 1:04 p.m. during Plenary Session PL06 - AACR Annual Meeting 2025 Highlights: Vision for the Future, on Wednesday, April 30, from 12:10 a.m. to 1:30 p.m.

Tuesday, April 29, from 2:30 p.m. to 4:00 p.m.

Mini-symposium MS.ET02.01 - Novel Cancer Therapeutic Targets

Tadashi Manabe, MD, PhD, UCSF post-doctoral scholar, presents “Unveiling The Potent Anti-Tumor Activity And Underlying Mechanism Of Action Of The Novel Pan-RAF Inhibitor Exarafenib In BRAF-Mutated NSCLC” (#6389) from 2:50 p.m. to 3:05 p.m. Manabe will present research on Exarafenib, a novel therapeutic approach that addresses a critical unmet need in lung cancer treatment. Somatic BRAF driver alterations play a crucial role in various cancers, including melanoma and non-small cell lung cancer (NSCLC). These BRAF alterations are classified into three distinct classes based on their oncogenic mechanisms. To determine the frequency of Class 2 and Class 3 mutations in lung cancer, which currently lack treatment options, the researchers collaborated with Guardant Health to analyze a comprehensive database of liquid biopsies from cancer patients. Manabe will report on their clinical findings that include promising responses in two cases with Class 2 BRAF alterations, potentially offering new treatment strategies for patients with BRAF mutations.

Wednesday, April 30, from 10:15 a.m. to 11:45 a.m.

Major Symposium SY29 - Biomolecular Condensates in Cancer: Mechanisms and Therapeutic Opportunities

Xiaokun Shu, PhD, professor in the UCSF Department of Pharmaceutical Chemistry, presents “New Physical Biology Of Oncoprotein Condensates: Differential Regulation Of The Transcriptome By Phase Separation” from 10:45 a.m. to 11:05 a.m. Shu will present his research on Myc, which is an oncoprotein transcription factor that is dysregulated in over half of all human cancers. Dysregulation results in unbalanced Myc activity and leads to tumor development. The molecular mechanism of how mixed dysregulation results in tumorigenesis is still unclear despite more than three decades of research, and there is still no FDA-approved drug against Myc. The goal of the researchers is to develop a therapy to Myc-induced cancer that results from dysregulation and unbalanced power of Myc. Shu reports on the development of a protein-protein interaction reporter to screen a large number of small molecules, identifying potent molecules that are now be testing them in animal models.