Project Grant F31CA306130
- This federal Project Grant award in the amount of $159,540.00 was provided by the National Cancer Institute (CFDA 93.398 Cancer Research Manpower) to the University of North Carolina at Chapel Hill to conduct research aimed at characterizing and overcoming MHC-I-mediated immune evasion in triple-negative breast cancer. The key products and services to be delivered under this 2.5-year award include: 1) Functionally and molecularly characterizing MHC-I-low breast tumors to determine how MHC-I loss...
- The U.S. National Cancer Institute (NCI) awarded a $151,040 Project Grant under the Cancer Research Manpower program (CFDA 93.398) to the Dana-Farber Cancer Institute, Inc. (DFCI) in Boston, Massachusetts. The grant supports research to investigate the role of interferon gamma (IFNγ) in promoting metastasis and immune evasion of triple negative breast cancer (TNBC). Specifically, the project aims to 1) elucidate the role of IFNγ in immune evasion during TNBC dissemination and metastatic...
- This Project Grant award of $124,134 from the National Cancer Institute (CFDA 93.398 - Cancer Research Manpower) supports research to investigate the mechanisms of pathogenesis and treatment response in immune checkpoint inhibitor-induced colitis. The research aims to define the role of specific T cell subsets recruited from circulation in promoting inflammation and mediating therapeutic response in this condition, which can occur in up to 40% of cancer patients receiving immune checkpoint...
- This Project Grant award from the National Cancer Institute (CFDA 93.398 - Cancer Research Manpower) to the University of Pittsburgh provides $165,486.00 to investigate how the intracellular protein MALT1 promotes immunosuppression in the tumor immune microenvironment of triple-negative breast cancer (TNBC). The award aims to analyze MALT1 regulation of the TNBC tumor immune microenvironment by characterizing MALT1 protease-dependent secretion of immunosuppressive cytokines from TNBC cells. This...
- This Project Grant award, totaling $102,984, was provided by the National Cancer Institute (CFDA 93.398 Cancer Research Manpower) to support research conducted by The Trustees of Columbia University in the City of New York. The research aims to dissect the novel role of Focal Adhesion Kinase (FAK) in modulating immunity during metastatic reactivation and progression of cancer. The key objectives are to investigate how FAK suppresses the STING innate immunity pathway, thereby enabling immune...
- The National Cancer Institute (CFDA 93.398 Cancer Research Manpower) awarded a $147,486 Project Grant to the Sloan-Kettering Institute for Cancer Research to support a 3-year research training program in cellular immunology and mechanobiology. The program aims to examine how the mechanical properties of the tumor microenvironment influence metastatic site preference and immune system response. Key research activities include in vivo modeling, biophysical measurements, and single-cell analysis to...
- This Project Grant award from the National Cancer Institute (CFDA 93.395 - Cancer Treatment Research) provides $400,000 in funding to Promilead, LLC to activate the TFEB protein and enhance the efficacy of immunotherapy for triple negative breast cancer (TNBC). The key objectives are to: Determine how TFEB expression and activation in TNBC cells can favorably modulate tumor-associated macrophages to suppress tumor growth. Prior research has shown that TFEB has tumor suppressive roles in breast...
- This federal Project Grant award of $144,768 from the National Cancer Institute (CFDA 93.398 Cancer Research Manpower program) supports research into PIK3C2A as a potential immunotherapeutic target for triple-negative breast cancer (TNBC). The researchers at the Trustees of Indiana University, Indianapolis hypothesize that inhibiting the PIK3C2A protein can enhance tumor antigen presentation, thereby potentiating the anti-tumor effects of immune checkpoint blockade therapy for TNBC. The research...
- This $284,201.82 Project Grant from the National Cancer Institute, a division of the Department of Health and Human Services, will fund research into malignant cell engagement in immune circuits of human colorectal cancer. The Broad Institute, Inc. will utilize single cell RNA sequencing data from over 700,000 malignant, immune, and stromal cells from colorectal cancer patients to test the hypothesis that malignant cells expressing interferon-stimulated genes acutely promote anti-tumor immunity,...
- This $135,993 Project Grant award from the National Cancer Institute's Cancer Research Manpower program (CFDA 93.398) supports research at Duke University to investigate the role of the ABL kinase-regulated HIF-1α-TAZ signaling pathway in promoting brain metastasis in triple-negative breast cancer (TNBC). The goal is to evaluate whether ABL-dependent activation of HIF-1 and TAZ leads to enhanced expression of unique transcriptional targets that promote brain metastasis in TNBC, and whether...
PFN1'S ROLE IN GENOMIC STABILITY AND IMMUNE RESPONSE IN BREAST CANCER - PROJECT SUMMARY BREAST CANCER IS THE SECOND LEADING CAUSE OF CANCER RELATED DEATHS IN WOMEN IN THE UNITED STATES IMMUNE CHECKPOINT BLOCKADE IMMUNOTHERAPY IS AN EMERGING TREATMENT FOR BREAST CANCER, PARTICULARLY FOR TRIPLE-NEGATIVE BREAST CANCER WHICH LACKS TARGETED THERAPIES. IMMUNE CHECKPOINT BLOCKADE FAILURE IS OFTEN DUE TO IMMUNE- EXCLUDED TUMOR MICROENVIRONMENTS, SPECIFICALLY THE ABSENCE OF CD8+ T CELL INFILTRATION. CURRENTLY IMMUNE CHECKPOINT BLOCKADE AGENTS ARE USED IN COMBINATION WITH CONVENTIONAL CHEMOTHERAPIES WHICH ENHANCE THE FUNCTION OF IMMUNOTHERAPY BY INDUCING DNA DAMAGE A TRIGGER FOR AN ANTI-TUMOR IMMUNOLOGICAL RESPONSE. HOWEVER, TUMORS ARE KNOWN TO BECOME RESISTANT TO CHEMOTHERAPIES, THEREFORE IDENTIFICATION OF NOVEL MECHANISMS TO INDUCE DNA DAMAGE AND THUS CD8+ T CELL INFILTRATION IS KEY FOR IMPROVING IMMUNE CHECKPOINT BLOCKADE IMMUNOTHERAPY SUCCESS. PROFILIN-1 (PFN1) IS AN ACTIN-BINDING PROTEIN THAT HAS BEEN REPORTED TO HAVE CONTEXT DEPENDENT TUMOR INTRINSIC ROLES IN BREAST CANCER. WHILE OVEREXPRESSION OF PFN1 HAS BEEN SHOWN TO SUPPRESS TUMORIGENESIS, KNOCKDOWN OF PFN1 HAS BEEN DEMONSTRATED TO LIMIT METASTATIC OUTGROWTH. HOWEVER, THE IMPACT OF PFN1 MODULATION ON THE TUMOR IMMUNE MICROENVIRONMENT IN BREAST CANCER REMAINS UNINVESTIGATED. MY PRELIMINARY DATA SUGGESTS GENETIC DISRUPTION OF THE PFN1 GENE LEADS TO AN INCREASE IN CD8+ T CELL INFILTRATION AND SIGNIFICANT TUMOR REGRESSION. THE GOAL OF THIS PROJECT IS TO INVESTIGATE WHETHER AND HOW LOSS OF PFN1 CAUSES A PRO-INFLAMMATORY, ANTI-TUMOR MICROENVIRONMENT THEREBY INCREASING IMMUNOTHERAPY EFFICACY. THE PROPOSED RESEARCH WILL BE COMPLEMENTED BY A TRAINING PLAN I DESIGNED TO ACHIEVE THE AIMS OF THIS PROJECT AND PREPARE MYSELF FOR THE NEXT PHASE OF MY RESEARCH CAREER. MY UNDERGRADUATE AND EARLY GRADUATE SCHOOL RESEARCH FOCUSED ON MOLECULAR MECHANISMS OF CANCER CELL MIGRATION AND TUMOR BIOLOGY. DURING THE F31 FELLOWSHIP PERIOD I WILL EXTEND MY UNDERSTANDING OF CANCER TO THE TUMOR IMMUNE MICROENVIRONMENT AND IMMUNOTHERAPY TREATMENT. I WILL LEARN TECHNICAL SKILLS INCLUDING HOW TO PERFORM FLOW CYTOMETRY ANALYSIS, IMMUNOTHERAPY ADMINISTRATION, AND MICROFLUIDIC DEVICE FABRICATION. I WILL BUILD UPON MY SKILLS IN THE DESIGN OF RIGOROUS SCIENTIFIC APPROACHES, MENTORSHIP, AND OUTREACH.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $49.5k | 7/16/25 |