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INFORMATION FOR

    Christian Felipe Ruiz, PhD

    Associate Research Scientist in Genetics
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    About

    Titles

    Associate Research Scientist in Genetics

    Appointments

    • Genetics

      Associate Research Scientist
      Primary

    Other Departments & Organizations

    Education & Training

    PhD
    Stony Brook University, Genetics (2019)
    BE
    The City College of New York, Biomedical Engineering (2013)

    Research

    Overview

    I am an Associate Research Scientist in the Department of Genetics and the Cancer Biology Institute at Yale University. I trained in quantitative mass spectrometry–based studies of metabolism as a Ph.D. student and, as a postdoc, applied genetically engineered mouse models and dietary interventions to uncover metabolic programs that shape host physiology and disease. With this combination of skills, my long-term goal is to establish a mechanistic bridge between environmental metabolites – derived from diet or the gut microbiome – and tissue metabolism, adaptation, and disease initiation, revealing how nutrient composition shapes disease risk and outcome. My training enables me to integrate systems-level and mechanistic analyses with in vivo studies, linking molecular and physiological scales. I am equally committed to fostering an inclusive, rigorous environment that supports the growth of trainees from diverse and underrepresented backgrounds

    Research at a Glance

    Yale Co-Authors

    Frequent collaborators of Christian Felipe Ruiz's published research.

    Publications

    2026

    • PI3K Regulates Wild-type RAS Signaling to Confer Resistance to KRAS Inhibition.
      Ge X, Singh J, Li W, Markham CS, Ruiz CF, Stites EC, Bhattacharyya M, Liu Y, Muzumdar MD. PI3K Regulates Wild-type RAS Signaling to Confer Resistance to KRAS Inhibition. Cancer Res 2026 PMID: 42095550, DOI: 10.1158/0008-5472.CAN-25-3625.
      Peer-Reviewed Original Research
      This study investigates how PI3K enables pancreatic cancer cells to resist KRAS inhibitors by activating wild-type RAS signaling, suggesting combined PI3K-KRAS targeting as a therapeutic strategy.
    • Diet-induced phospholipid remodeling dictates ferroptosis sensitivity and tumorigenesis in the pancreas.
      Ruiz CF, Ge X, McDonnell R, Agabiti SS, McQuaid DC, Tang A, Kharwa M, Goodell J, Saavedra-Pena RDM, Wing A, Li G, Medici NP, Robert ME, Varshney RR, Rudolph MC, Gorelick FS, Wysolmerski J, Canals D, Haley JD, Rodeheffer MS, Muzumdar MD. Diet-induced phospholipid remodeling dictates ferroptosis sensitivity and tumorigenesis in the pancreas. Cancer Discov 2026 PMID: 42053430, DOI: 10.1158/2159-8290.CD-25-0734.
      Peer-Reviewed Original Research
      This study investigates how dietary fat composition influences pancreatic cancer, showing that monounsaturated fats promote tumor growth while polyunsaturated fats reduce risk by enhancing ferroptosis sensitivity.
    • Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development
      Garcia CC, Venkat A, McQuaid DC, Agabiti SS, Tong A, Mathew B, Cardone RL, Starble R, Ruiz CF, Zheng C, Sogunro A, Jacox JB, Loh KH, Kibbey RG, Krishnaswamy S, Muzumdar MD. Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development. Nature Communications 2026 DOI: 10.1038/s41467-026-69821-2.
      Peer-Reviewed Original Research
      This study investigates how beta cell-derived cholecystokinin drives obesity-associated pancreatic cancer development, showing that targeting endocrine signaling could prevent tumor progression in obesity-related contexts.

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