Elucidating the role of tumor cell-intrinsic hypoxia inducible factor (HIF)-1α and HIF-2α pathway activation in tumor immune evasion

NIH RePORTER · NIH · K08 · $188,592 · view on reporter.nih.gov ↗

Abstract

Project Summary/Abstract This is an application for a K08 Career Development Award for Jonathan Trujillo, MD PhD, who is a clinical instructor in the Section of Hematology/Oncology at the University of Chicago. He is building a career as a physician-scientist focused on identifying immunotherapy resistance mechanisms to improve outcomes for patients with cancer. His proposed project will determine the role of tumor cell-intrinsic hypoxia-inducible factor (HIF)-1α and HIF-2α activation in mediating tumor immune evasion and immunotherapy resistance. Cancer remains the second leading cause of mortality in the United States in spite of intensive treatments. Immune checkpoint inhibitors have shown impressive and durable clinical responses in some patients, yet the majority of patients fail to respond to these immunotherapies. Emerging data indicate that increased hypoxia-induced signaling, which is mediated by the hypoxia inducible factor (HIF)-1α and HIF-2α pathways, within the tumor microenvironment is associated with reduced T cell-based inflammation and resistance to anti-PD-1 blockade. The impact of tumor cell-intrinsic HIF-1α and HIF-2α activation on the anti-tumor T cell response has yet to be determined. The overarching hypothesis of this proposal is that cancer cell-intrinsic HIF-1α or HIF-2α activation leads to defective T cell priming and ineffective T cell infiltration, thereby promoting tumor immune evasion and immunotherapy resistance. Novel genetically engineered mouse models of melanoma with conditional expression of a stabilized variant of HIF-1α or HIF-2α have been generated to determine whether cancer cell- intrinsic HIF-1α or HIF-2α activation limits the degree of T cell accumulation within tumor tissue and reduces tumor sensitivity to immune checkpoint inhibitors. The proposed studies will determine whether HIF-1α or HIF- 2α functions by impairing T cell priming and/or by limiting effector T cell infiltration and function in the tumor microenvironment. Mechanistic studies will be performed to determine whether HIF-1α or HIF-2α pathway activation results in failure to accumulate and activate dendritic cells required to generate T cell responses, failure to upregulate chemokines needed for DC or T cell recruitment, aberrant tumor vasculature which can limit T cell infiltration, or induction of immunosuppressive factors that can impair T cell responses. These data may provide rationale for the combination of novel HIF inhibitors and immune checkpoint blockade therapy. Dr. Trujillo has devised a career development plan to accomplish the following goals during this award: 1) develop expertise in immunologic and genomics techniques and mouse models of anti-tumor immunity; 2) become proficient in bioinformatics; 3) to expand knowledge in renal cell carcinoma with a focus on immunotherapeutics and novel HIF inhibitors. He has developed a strong mentoring committee led by his primary mentor Dr. Thomas Gajewski, an internationally renowned ...

Key facts

NIH application ID
10863982
Project number
5K08CA270394-02
Recipient
UNIVERSITY OF CHICAGO
Principal Investigator
Jonathan A Trujillo
Activity code
K08
Funding institute
NIH
Fiscal year
2024
Award amount
$188,592
Award type
5
Project period
2023-06-12 → 2027-05-31