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    Modulating Human Microbiome Function to Enhance Immune Responses Against Cancer (R01 Clinical Trial Not Allowed)

    This grant funds research exploring how the human microbiome affects anti-tumor immunity, seeking targets for cancer prevention by modulating microbe-immune interactions.

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    Cancer Research Grants 2026

    This grant is no longer accepting proposals

    National Institutes of Health has archived this opportunity.

    Funder: [National Institutes of Health - https://www.nih.gov]

    Due Dates: February 5, 2024 | June 5, 2024 | October 5, 2024 (Standard NIH R01 due dates)

    Funding Amounts: Application budgets are not limited but must reflect project needs; maximum project period is 5 years.

    Summary: Supports basic research to elucidate how the human microbiome modulates anti-tumor immune responses and to identify novel molecular targets for cancer prevention.

    Key Information: Clinical trials are not allowed; applications must rigorously address parameters like concentration, timing, and duration of beneficial microbes; foreign institutions are eligible.


    Description

    This NIH funding opportunity (PAR-22-061) aims to support basic research focused on understanding the mechanisms by which the human microbiome influences anti-tumor immune responses. The goal is to identify novel molecular targets that can be leveraged for cancer prevention strategies. Research should specifically explore how host interactions with particular microbes or microbial consortia, or their metabolites, modulate immune responses that either enhance or prevent tumor formation, especially inflammation-associated or sporadic cancers.

    The FOA emphasizes the importance of rigorously investigating factors such as the concentration, timing, and duration of administered beneficial microbes, as these parameters may significantly impact their effectiveness. The research should employ state-of-the-art techniques including metabolomics, molecular immunology, bioinformatics, and relevant animal or human models to elucidate host-microbe signaling pathways that modulate tumor immunity.

    Examples of appropriate research topics include, but are not limited to:

    • Investigating how Lactobacilli species inhibit colon cancer and the role of T-cell-dependent IgAs.
    • Examining the influence of commensal microbiota on differentiation of naïve T cells into Th17 subsets affecting tumor formation.
    • Evaluating the role of colonic Foxp3+RORγt+ regulatory T cells in mediating anti-inflammatory effects of commensal microbes.
    • Studying how modulation of microbial hydrogen sulfide (H2S) production affects host immunosurveillance.
    • Assessing the impact of short-chain fatty acid (SCFA) production on tumor-associated macrophage functions.
    • Exploring how microbial bile acid metabolism influences immune responses in liver and colon tumors.

    Applications that merely establish associations without mechanistic insights, focus on non-immune tumor stroma signaling, or microbial mechanisms unrelated to tumor immunity will be considered non-responsive.

    This FOA does not allow clinical trials; it is intended for well-developed projects supported by preliminary data. A companion FOA (PAR-22-062) supports exploratory or pilot projects with similar scientific scope.

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