Francesc Lopez-Giraldez, PhD
Research Scientist in GeneticsCards
About
Titles
Research Scientist in Genetics
YCGA Associate Director of Bioinformatics, Genetics
Appointments
Genetics
Research ScientistPrimary
Other Departments & Organizations
- Genetics
- Genomics, Genetics, and Epigenetics
- Yale Cancer Center
- Yale Center for Genome Analysis (YCGA)
- Yale-BI Biomedical Data Science Fellowship
Education & Training
- Post-Doctoral fellowship Beatriu de Pinós
- Generalitat de Catalunya (2009)
- PhD
- Autonomous University of Barcelona, Evolutionary Genetics (2006)
- Graduate student fellowship
- Generalitat de Catalunya (2004)
- MSc
- Pompeu Fabra University, Health and Life Sciences (2004)
- BS
- University of Girona, Biology (2000)
- Undergraduate student fellowship to develop a project on the Phylogeny of the genus Merluccius
- Gobierno de España (2000)
Research
Publications
2026
Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes.
Heer CD, Elia JL, Menon V, Johnson SS, Arbelaez SR, Friedman S, Lopez-Giraldez F, Sundaram RK, Herzon SB, Bindra RS, Gueble SE. Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes. NAR Cancer 2026, 8: zcaf052. PMID: 41522810, DOI: 10.1093/narcan/zcaf052.Peer-Reviewed Original Research
2025
1014 Agonism of VISTA immune checkpoint as a potential treatment therapy for hidradenitis suppurativa
Kidacki M, Cho C, Jaiswal A, Lopez-Giraldez F, Breidbart R, Damsky W, Hsia H, Eisenstein A, Vesely M, Chen L. 1014 Agonism of VISTA immune checkpoint as a potential treatment therapy for hidradenitis suppurativa. Journal Of Investigative Dermatology 2025, 145: s176. DOI: 10.1016/j.jid.2025.06.1031.Peer-Reviewed Original ResearchCorrection to: mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis
Min W, Qin L, Zhang H, López-Giráldez F, Jiang N, Kim Y, Mohan V, Su M, Murray K, Grutzendler J, Zhou J. Correction to: mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis. Circulation Research 2025, 137: e16-e17. PMID: 40536942, DOI: 10.1161/res.0000000000000718.Peer-Reviewed Original ResearchSystemic in utero gene editing as a treatment for cystic fibrosis
Ricciardi A, Barone C, Putman R, Quijano E, Gupta A, Nguyen R, Mandl H, Piotrowski-Daspit A, Lopez-Giraldez F, Luks V, Freedman-Weiss M, Farrelly J, Ahle S, Lynn A, Glazer P, Saltzman W, Stitelman D, Egan M. Systemic in utero gene editing as a treatment for cystic fibrosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2418731122. PMID: 40493185, PMCID: PMC12184489, DOI: 10.1073/pnas.2418731122.Peer-Reviewed Original ResearchConceptsUtero gene editingCystic fibrosisCF transmembrane conductance regulatorTreat CF patientsTransmembrane conductance regulatorWild-type miceIrreversible organ damageNormal organ developmentTreat monogenic diseasesCFTR activityCF patientsConductance regulatorDisease-causing genesMultiorgan diseaseDisease improvementOrgan damageGene editingMonogenic diseasesMutation correctionPolymeric nanoparticlesGastrointestinal tissuesDiseaseBirthFibrosisReproductive systemRates of Evolution of Developmental Changes in Gene Expression in Sordariomycetes
Wang Y, Wang F, Meng G, Lopez-Giraldez F, Dong C, Wang Z, Townsend J. Rates of Evolution of Developmental Changes in Gene Expression in Sordariomycetes. Molecular Biology And Evolution 2025, 42: msaf131. PMID: 40452442, PMCID: PMC12203517, DOI: 10.1093/molbev/msaf131.Peer-Reviewed Original ResearchConceptsRate of gene expression evolutionGene expression evolutionExpression evolutionGene expressionPhenotypic evolutionHeterogeneous rates of evolutionNonsynonymous to synonymous substitution ratesRates of phenotypic evolutionDevelopmental stagesSingle-copy orthologsGene sequence evolutionSynonymous substitution ratesRate of evolutionExpression of genesFunctional pathway analysisCarbon metabolismEvolutionary forcesConsequent phenotypesSexual reproductionSequence evolutionConserved pathwaysMeiosis pathwaysSubstitution ratesCell cyclePathway analysisGenomic analysis of 11,555 probands identifies 60 dominant congenital heart disease genes
Sierant M, Jin S, Bilguvar K, Morton S, Dong W, Jiang W, Lu Z, Li B, López-Giráldez F, Tikhonova I, Zeng X, Lu Q, Choi J, Zhang J, Nelson-Williams C, Knight J, Zhao H, Cao J, Mane S, Sedore S, Gruber P, Lek M, Goldmuntz E, Deanfield J, Giardini A, Mital S, Russell M, Gaynor J, King E, Wagner M, Srivastava D, Shen Y, Bernstein D, Porter G, Newburger J, Seidman J, Roberts A, Yandell M, Yost H, Tristani-Firouzi M, Kim R, Chung W, Gelb B, Seidman C, Brueckner M, Lifton R. Genomic analysis of 11,555 probands identifies 60 dominant congenital heart disease genes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2420343122. PMID: 40127276, PMCID: PMC12002227, DOI: 10.1073/pnas.2420343122.Peer-Reviewed Original ResearchConceptsCongenital heart disease genesCongenital heart diseaseDamaging variantsMissense variantsAnalyzing de novo mutationsCHD probandsEpidermal growth factor (EGF)-like domainsNeurodevelopmental delayLoss of function variantsParent-offspring triosSyndromic congenital heart diseaseHeart disease genesDisease genesGenomic analysisCongenital heart disease subtypesAssociated with neurodevelopmental delayTetralogy of FallotFunctional variantsIncomplete penetranceCHD phenotypesGenesAssociated with developmentGenetic testingMolecular diagnosticsExtracardiac abnormalitiesSpatial Transcriptomics Reveals Differential Inflammatory Pathways in Discoid Lupus Erythematosus and Lichen Planus
Kidacki M, Cho C, Lopez-Giraldez F, Breidbart R, Jaiswal A, Lee M, Chowdhury S, Damsky W, Chen L, Vesely M. Spatial Transcriptomics Reveals Differential Inflammatory Pathways in Discoid Lupus Erythematosus and Lichen Planus. Journal Of Investigative Dermatology 2025, 145: 2344-2348.e7. PMID: 40113031, PMCID: PMC12353771, DOI: 10.1016/j.jid.2025.02.148.Peer-Reviewed Original ResearchRecessive genetic contribution to congenital heart disease in 5,424 probands
Dong W, Jin S, Sierant M, Lu Z, Li B, Lu Q, Morton S, Zhang J, López-Giráldez F, Nelson-Williams C, Knight J, Zhao H, Cao J, Mane S, Gruber P, Lek M, Goldmuntz E, Deanfield J, Giardini A, Mital S, Russell M, Gaynor J, Cnota J, Wagner M, Srivastava D, Bernstein D, Porter G, Newburger J, Roberts A, Yandell M, Yost H, Tristani-Firouzi M, Kim R, Seidman J, Chung W, Gelb B, Seidman C, Lifton R, Brueckner M. Recessive genetic contribution to congenital heart disease in 5,424 probands. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2419992122. PMID: 40030011, PMCID: PMC11912448, DOI: 10.1073/pnas.2419992122.Peer-Reviewed Original ResearchConceptsRecessive genotypeCHD probandsCongenital heart diseaseAssociated with laterality defectsGene-based analysisAnalyzed whole-exome sequencingLeft-sided congenital heart diseaseWhole-exome sequencingCongenital heart disease phenotypeAshkenazi Jewish probandsOffspring of consanguineous unionsSingle-cell transcriptomicsCHD geneExome sequencingMouse notochordSecreted proteinsConsanguineous familyFounder variantGenesSignificant enrichmentLaterality phenotypesHeart diseaseProbandsAbnormal contractile functionConsanguineous unionsPD-1H (VISTA) Expression in Cutaneous Squamous Cell Carcinoma Is Correlated with T-Cell Infiltration and Activation
Kidacki M, Cho C, Lopez-Giraldez F, Huang B, He J, Gaule P, Chen L, Vesely M. PD-1H (VISTA) Expression in Cutaneous Squamous Cell Carcinoma Is Correlated with T-Cell Infiltration and Activation. Journal Of Investigative Dermatology 2025, 145: 2313-2324.e6. PMID: 39983979, PMCID: PMC12353361, DOI: 10.1016/j.jid.2025.01.030.Peer-Reviewed Original ResearchCutaneous squamous cell carcinomaPD-L1 expressionT cell infiltrationPD-L1Squamous cell carcinomaVISTA expressionPD-1HCell carcinomaT cellsBlockade of PD-1Proliferation marker Ki-67Multiplexed quantitative immunofluorescencePD-L1 coexpressionTreatment of cutaneous squamous cell carcinomaControl T cellsPreclinical cancer studiesMyeloid cell functionImmunosuppressive microenvironmentPD-1Receptor antagonismKi-67Individual tumorsGranzyme B.Clinical trialsCancer clinical trialsDMEM and EMEM are suitable surrogate media to mimic host environment and expand leptospiral pathogenesis studies using in vitro tools.
Garcia LE, Lin Z, Culos S, Catherine Muenker M, Johnson EE, Wang Z, Lopez-Giraldez F, Giraud-Gatineau A, Jackson A, Picardeau M, Goodlett DR, Townsend JP, Pětrošová H, Wunder EA Jr. DMEM and EMEM are suitable surrogate media to mimic host environment and expand leptospiral pathogenesis studies using in vitro tools. BioRxiv 2025 PMID: 39896660, DOI: 10.1101/2025.01.22.634353.Peer-Reviewed Original Research
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New Haven, CT 06519
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203.737.6864