Christian Felipe Ruiz, PhD
Associate Research Scientist in GeneticsCards
Appointments
Contact Info
About
Copy Link
Titles
Associate Research Scientist in Genetics
Appointments
Genetics
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- PhD
- Stony Brook University, Genetics (2019)
- BE
- The City College of New York, Biomedical Engineering (2013)
Research
Copy Link
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
ORCID
0000-0003-1470-8061
Research at a Glance
Yale Co-Authors
Publications Timeline
Mandar Deepak Muzumdar, MD
Daniel McQuaid
Jeremy B. Jacox, MD, PhD
Boby Mathew
Ken Huaijin Loh, PhD, BSc
Richard Kibbey, MD, PhD
Publications
2026
PI3K Regulates Wild-type RAS Signaling to Confer Resistance to KRAS Inhibition
Ge X, Singh J, Li W, Markham C, Ruiz C, Stites E, Bhattacharyya M, Liu Y, Muzumdar M. PI3K Regulates Wild-type RAS Signaling to Confer Resistance to KRAS Inhibition. Cancer Research 2026, 10.1158/0008-5472.can-25-3625. PMID: 42095550, PMCID: PMC13237827, DOI: 10.1158/0008-5472.can-25-3625.Peer-Reviewed Original ResearchThis 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 C, Ge X, McDonnell R, Agabiti S, McQuaid D, Tang A, Kharwa M, Goodell J, del M. Saavedra-Peña R, Wing A, Li G, Medici N, Robert M, Varshney R, Rudolph M, Gorelick F, Wysolmerski J, Canals D, Haley J, Rodeheffer M, Muzumdar M. Diet-induced phospholipid remodeling dictates ferroptosis sensitivity and tumorigenesis in the pancreas. Cancer Discovery 2026, 10.1158/2159-8290.cd-25-0734. PMID: 42053430, PMCID: PMC13227558, DOI: 10.1158/2159-8290.cd-25-0734.Peer-Reviewed Original ResearchThis 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 ResearchThis 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.Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development
Garcia C, Venkat A, McQuaid D, Agabiti S, Tong A, Mathew B, Cardone R, Starble R, Ruiz C, Zheng C, Sogunro A, Jacox J, Loh K, Kibbey R, Krishnaswamy S, Muzumdar M. Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development. Nature Communications 2026, 17: 3292. PMID: 41760660, PMCID: PMC13066563, DOI: 10.1038/s41467-026-69821-2.Peer-Reviewed Original ResearchThis study investigates how obesity-induced cholecystokinin (CCK) expression in pancreatic beta cells drives pancreatic cancer development by altering cellular signaling within the environment of arising tumors, suggesting potential therapeutic targets.
2025
Tracing the evolution of single-cell 3D genomes in Kras-driven cancers
Liu M, Jin S, Agabiti S, Jensen T, Yang T, Radda J, Ruiz C, Baldissera G, Rajaei M, Li F, Townsend J, Muzumdar M, Wang S. Tracing the evolution of single-cell 3D genomes in Kras-driven cancers. Nature Genetics 2025, 57: 3075-3087. PMID: 40825871, PMCID: PMC12695640, DOI: 10.1038/s41588-025-02297-w.Peer-Reviewed Original ResearchThis study investigates 3D genome changes in Kras-driven cancers, identifying structural bottlenecks in early progression and potential diagnostic and therapeutic biomarkers.
2023
Decoding the obesity–cancer connection: lessons from preclinical models of pancreatic adenocarcinoma
Ruiz C, Garcia C, Jacox J, Lawres L, Muzumdar M. Decoding the obesity–cancer connection: lessons from preclinical models of pancreatic adenocarcinoma. Life Science Alliance 2023, 6: e202302228. PMID: 37648285, PMCID: PMC10474221, DOI: 10.26508/lsa.202302228.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsPancreatic adenocarcinomaPreclinical modelsObesity-cancer connectionObesity-associated cancersMicrobial dysbiosisHormone dysregulationEarly progressionRisk factorsWorldwide prevalencePancreatic tumorigenesisObesityPreclinical modelingCancer typesCancer developmentTumor cellsAdenocarcinomaTumor initiationCancerMetabolic stateCellular metabolismNovel strategyDysbiosisInflammationTherapyPrevalence
2021
1-Deoxysphinganine initiates adaptive responses to serine and glycine starvation in cancer cells via proteolysis of sphingosine kinase
Truman J, Ruiz C, Montal E, Garcia-Barros M, Mileva I, Snider A, Hannun Y, Obeid L, Mao C. 1-Deoxysphinganine initiates adaptive responses to serine and glycine starvation in cancer cells via proteolysis of sphingosine kinase. Journal Of Lipid Research 2021, 63: 100154. PMID: 34838542, PMCID: PMC8953655, DOI: 10.1016/j.jlr.2021.100154.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSphingosine kinase 1Sph levelsLoss of sphingosine kinase 1Cancer cellsAbsence of serineInitial sensorResponse to serineSerine palmitoyl transferaseAvailability of serineIntracellular reactive oxygen speciesSerine synthesisExogenous serinePalmitoyl-CoAAdaptive metabolic changesCondensation of alaninePKM2 activityGlycine starvationDownstream effectorsAdaptive biological responsesLipid substratesReactive oxygen speciesSignaling moleculesPalmitoyl transferaseKinase 1Sphingosine kinaseSphingosine kinase 1 downregulation is required for adaptation to serine deprivation
Truman J, Ruiz C, Trayssac M, Mao C, Hannun Y, Obeid L. Sphingosine kinase 1 downregulation is required for adaptation to serine deprivation. The FASEB Journal 2021, 35: e21284-e21284. PMID: 33484475, PMCID: PMC8272629, DOI: 10.1096/fj.202001814rr.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsSerine starvationSerine deprivationReactive oxygen speciesCell growthDetrimental to cell growthTumor suppressor p53Synthesis of sphingolipidsCancer cellsIntracellular reactive oxygen speciesSuppression of reactive oxygen speciesTumor-promoting pathwaysSubstrate sphingosineMitochondrial oxygen consumptionSphingolipid synthesisSerine palmitoyltransferasePro-survivalSphingosine accumulationNutrient integrationMitochondrial functionMetabolic roleD-erythro-sphingosineBioactive sphingolipidsSphingosine-1-PhosphateSerineMetabolic adaptation
2020
SREBP1 regulates mitochondrial metabolism in oncogenic KRAS expressing NSCLC
Ruiz C, Montal E, Haley J, Bott A, Haley J. SREBP1 regulates mitochondrial metabolism in oncogenic KRAS expressing NSCLC. The FASEB Journal 2020, 34: 10574-10589. PMID: 32568455, PMCID: PMC8335704, DOI: 10.1096/fj.202000052r.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsA549 CellsCarcinoma, Non-Small-Cell LungCell LineCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHEK293 CellsHumansLipogenesisLung NeoplasmsMitochondriaMutationOncogenesOxidative PhosphorylationProto-Oncogene Proteins p21(ras)Signal TransductionSterol Regulatory Element Binding Protein 1Up-RegulationConceptsElectron transport chainGene expression programsNon-small cell lung cancerGenetic knockdownMutant Kras non-small cell lung cancerRNA-seq dataLipogenic transcription factor SREBP1Transcription factor SREBP1PI3K signaling pathwayCell proliferationOncogenic KrasRNA-seqMitochondrial metabolismTransport chainOxidative phosphorylationSREBP1 expressionMetabolic reprogrammingAnabolic metabolismMitochondrial functionSREBP1Malignant phenotypeCancer cellsMacromolecular precursorsMutant KRASLipogenesis
2019
Decoupling of Nrf2 Expression Promotes Mesenchymal State Maintenance in Non-Small Cell Lung Cancer
Haley J, Ruiz C, Montal E, Wang D, Haley J, Girnun G. Decoupling of Nrf2 Expression Promotes Mesenchymal State Maintenance in Non-Small Cell Lung Cancer. Cancers 2019, 11: 1488. PMID: 31581742, PMCID: PMC6826656, DOI: 10.3390/cancers11101488.Peer-Reviewed Original ResearchCitationsAltmetricConceptsNon-small cell lung cancerCell lung cancerEpithelial mesenchymal transitionNon-smallLung cancerExpression of redox regulatorsTherapeutic inhibitionNon-small cell lung cancer patient samplesMesenchymal transitionMesenchymal epithelial transitionNrf2 knockout miceCancer cell statesInhibition of Nrf2Cell statesIsogenic cell modelsOverexpression of Nrf2Multiple in vitroMesenchymal cell stateMetastatic disseminationKnockdown of Nrf2Knockout miceEpithelial phenotypeCellular redox homeostasisMetabolic alterationsMesenchymal phenotype
News
Copy Link
News
Get In Touch
Copy Link