Project Grant R01CA288578

Award Date 5/8/24
Completion Date 4/30/29
Dollars Obligated $525K
Federal Grant Program
93.353
Assistance Type
Project Grant
Place of Performance
South Carolina, USA
Similar Awards
This Project Grant award from the National Cancer Institute (CFDA 93.396 Cancer Biology Research) provides $1,396,152 to the University of Chicago to conduct research on the role of the protein BNIP3 and mitophagy (the breakdown of mitochondria) in muscle atrophy associated with pancreatic cancer cachexia. The 5-year project will use genetically engineered mouse models of pancreatic ductal adenocarcinoma to examine how BNIP3 promotes the atrophy of specific muscle fiber types by reducing...
This Project Grant award from the National Cancer Institute (NCI) under the Cancer Detection and Diagnosis Research program (CFDA 93.394) supports research by The Johns Hopkins University to advance the understanding and treatment of cachexia, a condition of severe muscle wasting, associated with pancreatic ductal adenocarcinoma (PDAC). The $432,889 award spanning from April 2025 to March 2030 will fund studies to: Investigate the role of glutamine metabolism disruption in PDAC-induced...
The National Cancer Institute (NCI) awarded a $102,324 Project Grant under the Cancer Research Manpower (CFDA 93.398) program to The Medical University of South Carolina (MUSC) to investigate the role of peroxisomes in modulating T cell function and anti-tumor immunity. The overarching goal is to elucidate the impact of peroxisome biogenesis on adaptive immune responses, particularly within the tumor microenvironment, and generate exhaustion-resistant anti-tumor T cells. The two-year project...
This Project Grant award, provided by the National Cancer Institute under the Cancer Biology Research program (CFDA 93.396), supports research to determine whether deficiencies in the lymphatic and vascular endothelium of the intestine are an underlying cause of cancer-induced cachexia that can be targeted for treatment. The $502,563 award to Northwestern University, with a project period from July 2024 to June 2029, will fund a two-pronged approach to further understand the molecular mechanisms...
This $646,739 Project Grant awarded by the National Cancer Institute (CFDA 93.396 Cancer Biology Research) to Cedars-Sinai Medical Center supports research to investigate the role of hepatic stellate cells (HSCs) in promoting liver metastasis in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). The project aims to elucidate the mechanisms by which extra-tumoral HSCs produce the pro-tumorigenic chemokine CXCL12, which activates cancer cells, intra-tumoral HSCs, and...
The National Cancer Institute (NCI) awarded a $433,157 Project Grant (CFDA 93.395 - Cancer Treatment Research) to Endeavor Health Clinical Operations, a division of Northshore University HealthSystem Research Institute, for a study titled "Lipid-Rich Macrophages at the Tumor-Adipose Interface: A New Target for Locally-Invasive Prostate Cancer Therapy." The 2-year project, beginning on July 18, 2024, will investigate the role of lipid-rich adipose tissue macrophages in prostate cancer...
The National Cancer Institute (NCI) awarded a $620,820 Project Grant (CFDA 93.396 - Cancer Biology Research) to The General Hospital Corporation, doing business as Massachusetts General Hospital (MGH), to investigate mechanisms of immune therapy resistance. The project aims to understand: The molecular mechanisms governing the transcription factor CREB5, which the researchers found can drive immune evasion in tumors by upregulating extracellular matrix genes including collagen. The...
This Project Grant award from the National Cancer Institute (CFDA 93.395 - Cancer Treatment Research) provides $234,749.00 to The Ohio State University to conduct research aimed at understanding how tumor-associated macrophages (TAMs) within the tumor microenvironment can suppress anti-tumor immune responses in non-small cell lung cancer (NSCLC). The two-year project, running from April 2025 to March 2027, will investigate the role of hedgehog signaling in TAMs and its impact on CD8+ T cell...
This Project Grant from the National Cancer Institute, part of the Department of Health and Human Services, provides $390,000 to Thomas Jefferson University under the Cancer Biology Research program. The grant will fund research from August 2021 to July 2023 to investigate the role of the Toll-like Receptor 4-fibronectin extracellular matrix protein pathway in the malignant microenvironment of early cutaneous T-cell lymphoma. Specifically, the university researchers will determine the impact...
The National Cancer Institute (NCI) awarded a $107,948 Project Grant through the Cancer Research Manpower (CFDA 93.398) program to The Johns Hopkins University. The grant supports a comparative analysis of the effects of the cytokines M-CSF and GM-CSF on human monocyte metabolic reprogramming and differentiation into tumor-associated macrophage-like cells. The research aims to characterize differences in tumor-associated macrophage (TAM) functional attributes between M-CSF and GM-CSF derived...

THE ROLE OF TGFB2 AND MACROPHAGES IN CANCER CACHEXIA - SUMMARY CACHEXIA IS A SIGNIFICANT CONTRIBUTOR TO INCREASED MORTALITY IN VARIOUS CHRONIC DISEASES, INCLUDING CANCER. PATIENTS WITH CANCER CACHEXIA EXPERIENCE UNINTENTIONAL BODY WEIGHT LOSS, WHICH CAN INVOLVE MUSCLE LOSS, WITH OR WITHOUT FAT MASS. THE DECLINE IN MUSCLE MASS NOT ONLY IMPAIRS MUSCLE FUNCTION, BUT ALSO DIMINISHES QUALITY OF LIFE AND RAISES MORTALITY RISK. OUR PRELIMINARY RESEARCH HAS REVEALED AN UPREGULATION OF TRANSFORMING GROWTH FACTOR 2 (TGFB2) PRECEDING THE RECRUITMENT OF M2 MACROPHAGES TO THE SKELETAL MUSCLE IN CACHECTIC MICE. ADDITIONALLY, WE OBSERVED THAT DEPLETING M2 MACROPHAGES INHIBITED THE TRANSITION FROM CACHEXIA TO SEVERE CACHEXIA BY PRESERVING MUSCLE MASS AND REDUCING FIBROSIS. THESE DATA HIGHLIGHT THE INVOLVEMENT OF M2 MACROPHAGE ACTIVATION IN CACHEXIA PROGRESSION WITH THE ASSISTANCE OF TGFB2. IN THIS PROPOSAL, WE WILL INVESTIGATE THE ROLE OF TGFB2 IN INITIATING FIBROSIS AND ACTIVATING M2 MACROPHAGES IN THE SKELETAL MUSCLE OF CANCER CACHECTIC MICE. FURTHERMORE, WE HYPOTHESIZE THAT M2 MACROPHAGES ACT AS A PIVOTAL TRANSITION POINT DRIVING THE ADVANCEMENT OF SEVERE CANCER CACHEXIA. THE OUTCOMES OF THIS STUDY MAY UNCOVER A NOVEL MECHANISM AND INNOVATIVE STRATEGIES FOR THE TREATMENT OF CANCER CACHEXIA.

Posted 5/8/24, 12:00 AM