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We’re bringing together leaders in cancer research.

Speaker

Rugang Zhang, PhD
John M. O’Quinn Endowed Chair in Cancer Research
Associate Director for Discovery Science
Department Chair & Professor, Department of Experimental Therapeutics
Faculty, UTHealth Graduate School of Biomedical Sciences
The University of Texas MD Anderson Cancer Center

“Exploiting Epigenetic Vulnerabilities to Enable Senescence-based Therapeutic Strategies in Epithelial Ovarian Cancer”

The past decade has brought unprecedented progress in understanding the genetics of epithelial ovarian cancer (EOC), but cures remain elusive due to the lack of insights into mechanisms that can be leveraged to develop new therapies. EOC is genetically heterogeneous and, therefore, it is imperative that therapeutic strategies become personalized by targeting distinct molecular subsets of EOC. Despite the importance of epigenetic regulators in EOC is increasingly recognized, the mechanism of action for these epigenetic regulators and the associated vulnerabilities exposed by their dysregulations have remained elusive for most of them. In this talk, we will present our recent work elucidating how specific epigenetic mechanisms can be exploited to induce therapy-driven senescence. We will further discuss how senescent tumor states can be exploited through rational combination strategies, including immunotherapy. Together, these integrated approaches offer new opportunities to address unmet clinical needs in genetically defined subsets of EOC.

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Speaker

Alexander Muir, PhD
Assistant Professor
Ben May Department of Cancer Research
Committee on Cancer Biology
Committee on Molecular Metabolism and Nutrition
University of Chicago

“Hangry cancer cells: metabolic stress and tumor biology”

A hallmark of tumors is aberrant angiogenic signaling and dysfunctional vasculature. This results in poor perfusion in the tumor microenvironment (TME). Limited perfusion causes hypoxia and metabolic stress in the TME. Despite the longstanding understanding that tumors are metabolically stressed, we have limited understanding of how this contributes to cancer pathogenesis. I will discuss new tools that expand our understanding of how metabolic stress regulates tumor biology, which led to the findings that metabolic stress limits the efficacy of targeted, immuno- and chemotherapeutics, leading to the current view that metabolic stress is a barrier to successful treatment of cancer. However, while metabolic stress limits the efficacy of standard therapies, it creates novel therapeutic targets, as cellular processes which are non-essential in well-perfused healthy tissues become essential for metabolically stressed tumors. I will discuss work identifying these stress-contingent essential processes and argue these processes represent an entire new class of therapeutic targets, TME-synthetic lethal targets, that leverage the unique TME, rather than being limited by it.

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Speaker

Denis Guttridge, PhD
Professor, Department of Pediatrics
Director, Darby Children’s Research Institute
Associate Director of Translational Science, Hollings Cancer Center
Medical University of South Carolina

“Evolving Insights into Cancer Cachexia: Lessons Learned from the Muscle Microenvironment“

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Speaker

William A. Weiss, MD, PhD
Evelyn and Mattie Anderson Endowed Chair in Cancer Research
Professor, Departments of Neurology, Pediatrics, and Neurological Surgery
UC San Francisco

Co-Leader, Pediatric Malignancies Program
UCSF Helen Diller Family Comprehensive Cancer Center

“Models and vulnerabilities for brain cancers”

Medulloblastoma is the most common tumor of childhood. Glioblastoma is the most common tumor of adulthood. I will present new models of human group 3 medulloblastoma. We differentiate human induced pluripotent stem cells cells to neuroepithelial stem (NES) cells, transduce NES cells with MYC, alone and in combination with other gain of function effectors, and transplant orthotopically into the hindbrain. I will discuss characterization and developmental therapeutics in resulting models. I will also present developmental therapeutic studies in glioblastoma, focusing separately on molecular glues targeting RAS and bi-steric inhibitors of mTORC1. I will discuss screens to identify combination therapies that improve efficacy, as well as separate screens and approaches to enhance delivery to the brain while abrogating peripheral toxicity.