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NIH RePORTER

NIH RePORTER research funding database via the public, keyless api.reporter.nih.gov v2 API: search NIH and other HHS-funded research projects by text, principal investigator, organization, state, fiscal year, agency and activity code; read one project with abstract, investigators, program officers, costs and study section; and list the PubMed IDs of publications linked to a project.

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const result = await firecrawl.scrape({
  alexandria: {
    provider: "reporter-nih-gov",
    capability: "research-grants/project",
    options: {
      appl_id: 11171443,
    },
  },
});

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{
  "abstract": "Abstract (Overall):\nPancreatic Ductal Adenocarcinoma (PDAC) is a deadly disease whose mechanisms of development remain\nincompletely understood. Evidence suggests that pancreatic cancers may arise from acinar cells undergoing a\nprocess called acinar to ductal metaplasia (ADM) or from ductal cells to give rise to Pancreatic Intraepithelial\nNeoplasias (PanINs). How mutations or combinations of mutations promote PDAC development and the role of\ninflammation in the process still remains unclear. Moreover, interactions between immune cells, cancer-\nassociated fibroblasts (CAFs) and cancer cells can promote PDAC development and progression, but much\nremains to be learned about how signaling between cells in the tumor microenvironment (TME) affects the stem\ncell compartment (`stemness') thought to underlie PDAC development and promotes immune evasion. Thus,\nmultiple questions about fundamental mechanisms governing PDAC development persist.\nTo address these challenges, our superb and highly interactive team will identify genetic and stromal (immune\ncells and CAFs) interactions and pathways that regulate the inception and progression of PDAC using innovative\nmouse models and human tissue-based approaches. We propose three Projects to address the following overall\naims:\n1. Identify the originating cell(s) and deconstruct genetic pathways underlying PDAC initiation\n2. Discover immune signals that cross-talk with epithelial cells and CAFs to promote pancreas cancer\ndevelopment and stemness\n3. Investigate the impact of tumor genetics on PDAC immunobiology and response to macrophage-targeted\nimmunotherapy\nEffort on these projects will be organized through an Administrative and Biostatistics Core (A) and empowered\nby two Research Cores, focused on human tissue procurement (Core B), and use of high-dimensional imaging\nto measure cell and signaling interactions in tissues (CODEX; Core C).\nThe participating investigators on this P01 lead teams that have collaborated productively for y… [657 more characters]",
  "activity_code": "P01",
  "agency": {
    "abbreviation": "NCI",
    "code": "CA",
    "name": "National Cancer Institute"
  },
  "agency_code": "NIH",
  "appl_id": 11171443,
  "award_amount": 2023000,
  "award_notice_date": "2025-08-20",
  "contact_pi_name": "KIM, SEUNG K",
  "core_project_num": "P01CA244114",
  "date_added": "2025-08-23",
  "fiscal_year": 2025,
  "funding": {
    "arra_funded": false,
    "award_type": "5",
    "budget_end": "2027-07-31",
    "budget_start": "2025-08-01",
    "cfda_code": "93.396",
    "covid_response": [],
    "direct_cost": 1283733,
    "ic_fundings": [
      {
        "abbreviation": "NCI",
        "code": "CA",
        "direct_cost": 1283733,
        "fiscal_year": 2025,
        "indirect_cost": 739267,
        "name": "National Cancer Institute",
        "total_cost": 2023000
      }
    ],
    "indirect_cost": 739267,
    "is_new": false,
    "opportunity_number": "PAR-20-077"
  },
  "funding_mechanism": "Non-SBIR/STTR",
  "is_active": true,
  "observed_at_ms": 1791417600000,
  "organization": {
    "city": "STANFORD",
    "congressional_district": "CA-16",
    "country": "UNITED STATES",
    "department": "ANATOMY/CELL BIOLOGY",
    "duns": "009214214",
    "ipf_code": "8046501",
    "latitude": 37.426852,
    "longitude": -122.17047,
    "name": "STANFORD UNIVERSITY",
    "state": "CA",
    "type": "SCHOOLS OF MEDICINE",
    "uei": "HJD6G4D6TJY5",
    "zipcode": "943052004"
  },
  "principal_investigators": [
    {
      "first_name": "LAURA",
      "full_name": "LAURA D ATTARDI",
      "is_contact_pi": false,
      "last_name": "ATTARDI",
      "middle_name": "D",
      "profile_id": 1885021,
      "title": "PROFESSOR"
    },
    {
      "first_name": "Seung",
      "full_name": "Seung K Kim",
      "is_contact_pi": true,
      "last_name": "Kim",
      "middle_name": "K",
      "profile_id": 1927492,
      "title": "PROFESSOR"
    }
  ],
  "program_officers": [
    {
      "first_name": "NATALIA",
      "full_name": "NATALIA MERCER",
      "last_name": "MERCER"
    }
  ],
  "project_end_date": "2027-07-31",
  "project_num": "5P01CA244114-05",
  "project_start_date": "2021-08-01",
  "public_health_relevance": "Project Narrative (Overall):\nThis P01 application from investigators at Stanford University seeks to discover, apply, and translate science\nabout pancreatic cancer (PDAC), with the ultimate goal of improving care for patients with this disease. To\naddress fundamental, persistent questions about the biology of PDAC, we have assembled a superb,\ninteractive team of productive collaborators to lead our Projects and Research Cores that will identify genetic,\nimmune cell, and cancer-associated fibroblasts based interactions and pathways that regulate the inception\nand progression of PDAC. Advances from studies proposed here could broadly impact pancreas cancer\nbiology and drive translational efforts in PDAC.",
  "spending_categories": [],
  "study_section": {
    "code": "ZCA1",
    "name": "ZCA1-RPRB-H(J1)P"
  },
  "subproject_id": null,
  "terms": [
    "Acceleration",
    "Acinar Cell",
    "Address",
    "Affect",
    "Amplifiers",
    "Biology",
    "Biostatistics Core",
    "Cancer Biology",
    "Carcinoma",
    "Cell Compartmentation",
    "Cell Ontogeny",
    "Cells",
    "Chronic",
    "Collaborations",
    "Conceptions",
    "Data",
    "Data Analyses",
    "Data Set",
    "Dedications",
    "Dependence",
    "Detection",
    "Development",
    "Disease",
    "Duct (organ) structure",
    "Ductal Epithelial Cell",
    "Epithelial Cells",
    "Epithelium",
    "Evolution",
    "Fibroblasts",
    "Frustration",
    "Generations",
    "Genetic",
    "Genetically Engineered Mouse",
    "Genotype",
    "Goals",
    "Human",
    "Image",
    "Imaging technology",
    "Immune",
    "Immune Evasion",
    "Immune response",
    "Immune signaling",
    "Immunobiology",
    "Immunotherapeutic agent",
    "Immunotherapy",
    "Infiltration",
    "Inflammation",
    "Inflammatory",
    "Investigation",
    "KRAS2 gene",
    "… [69 more items]"
  ],
  "title": "Pancreatic Cancer Development: Genetic and Immune Regulation",
  "url": "https://reporter.nih.gov/project-details/11171443"
}

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NIH RePORTER

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