Samir Zaidi, MD, PhD
Assistant Professor of Internal Medicine (Medical Oncology/Hematology)Cards
About
Research
Publications
2026
Correlative Biomarker Analysis of PSMA Expression on CTCs and PSMA Imaging in a Phase I Study of PSMA Targeted Tubulysin Conjugate EC1169
Zaidi S, Kuo P, Paiva Prudente T, Lacuna K, Babiker H, Aparicio R, Schonhoft J, Fernandez L, Messmann R, Groaning M, Tolcher A, Gordon M, Yoo D, Vaishampayan U, Picus J, Petrylak D, Sartor O, Morris M. Correlative Biomarker Analysis of PSMA Expression on CTCs and PSMA Imaging in a Phase I Study of PSMA Targeted Tubulysin Conjugate EC1169. Clinical Cancer Research 2026, 32: 1766-1776. PMID: 41591990, PMCID: PMC13034684, DOI: 10.1158/1078-0432.ccr-25-2313.Peer-Reviewed Original ResearchThis study investigates PSMA expression heterogeneity in metastatic prostate cancer, showing that reduced PSMA-positive circulating tumor cells correlate with longer progression-free survival despite discordant imaging results.
2025
Patterns of intra- and inter-tumor phenotypic heterogeneity in lethal prostate cancer
Roudier M, Gulati R, Sayar E, Patel R, Tratt M, Richards H, Cejas P, Gomez M, Qiu X, Xie Y, Hanratty B, Zaidi S, Zhao J, Adil M, Mittal C, Zhao Y, Dumpit R, Coleman I, Low J, Persse T, Galipeau P, Lee J, Tretiakova M, Chambers M, Vakar-Lopez F, True L, Perrone M, Lam H, Kollath L, Ding C, Harmon S, Cheng H, Yu E, Montgomery R, Hawley J, Lin D, Corey E, Schweizer M, Setty M, Ha G, Sawyers C, Morrissey C, Long H, Nelson P, Haffner M. Patterns of intra- and inter-tumor phenotypic heterogeneity in lethal prostate cancer. Journal Of Clinical Investigation 2025, 135: e186599. PMID: 40493417, PMCID: PMC12321404, DOI: 10.1172/jci186599.Peer-Reviewed Original ResearchMetastatic prostate cancerLethal prostate cancerProstate cancerPhenotypic heterogeneityMetastatic prostate cancer patientsMolecularly heterogeneous diseaseTumor cell populationIntra-tumor heterogeneityCellular proliferation rateMetastatic sitesSingle-cell sequencing studiesMolecular subtypesClinical featuresTumor heterogeneityTumor phenotypeTumor samplesHeterogeneous diseaseClinical managementAnatomical sitesTherapeutic approachesSubtype heterogeneityPatientsTissue-basedCell populationsProliferation rate
2024
The neuroendocrine transition in prostate cancer is dynamic and dependent on ASCL1
Romero R, Chu T, González Robles T, Smith P, Xie Y, Kaur H, Yoder S, Zhao H, Mao C, Kang W, Pulina M, Lawrence K, Gopalan A, Zaidi S, Yoo K, Choi J, Fan N, Gerstner O, Karthaus W, DeStanchina E, Ruggles K, Westcott P, Chaligné R, Pe’er D, Sawyers C. The neuroendocrine transition in prostate cancer is dynamic and dependent on ASCL1. Nature Cancer 2024, 5: 1641-1659. PMID: 39394434, PMCID: PMC11584404, DOI: 10.1038/s43018-024-00838-6.Peer-Reviewed Original ResearchConceptsNeuroendocrine prostate cancerProstate cancerLineage plasticityAndrogen receptor signaling inhibitorsCancer progressionMouse prostate organoidsProstate cancer progressionRB1 deletionProstate organoidsMultiplex immunofluorescenceIn vivo platformTransient regressionDriver mutationsLuminal cellsSignaling InhibitorsAscl1Neuroendocrine transitionLineage transformationOrganoid culturesCancerTherapy outcomeProstateAdenocarcinomaTherapy timeIn vivo microenvironmentCEACAM5-Targeted Immuno-PET in Androgen Receptor–Negative Prostate Cancer
Imberti C, De Gregorio R, Korsen J, Hoang T, Khitrov S, Kalidindi T, Nandakumar S, Park J, Zaidi S, Pillarsetty N, Lewis J. CEACAM5-Targeted Immuno-PET in Androgen Receptor–Negative Prostate Cancer. Journal Of Nuclear Medicine 2024, 65: 1043-1050. PMID: 38782457, PMCID: PMC11218725, DOI: 10.2967/jnumed.123.267107.Peer-Reviewed Original ResearchConceptsNeuroendocrine prostate cancerCarcinoembryonic antigen-related cell adhesion molecule 5CEACAM5 expressionProstate cancerAggressive neuroendocrine prostate cancerAndrogen receptor (AR)-negativeEx vivo organ distributionXenograft prostate cancer modelsProstate cancer cell linesProstate cancer modelCell line LNCaP.Immuno-PET imagingCell line PC3Prostate cancer hallmarksCancer cell linesCancer modelsRadiolabeled antibodiesImmuno-PETSurface antigensProstatePET imagingCancerCancer hallmarksWestern blottingCell linesUnderstanding osteokine biology
Zaidi M, Zaidi S, Yuen T. Understanding osteokine biology. Cell Metabolism 2024, 36: 888-890. PMID: 38718755, PMCID: PMC11705590, DOI: 10.1016/j.cmet.2024.04.008.Peer-Reviewed Original Research
2023
Exportin 1 inhibition prevents neuroendocrine transformation through SOX2 down-regulation in lung and prostate cancers
Quintanal-Villalonga A, Durani V, Sabet A, Redin E, Kawasaki K, Shafer M, Karthaus W, Zaidi S, Zhan Y, Manoj P, Sridhar H, Shah N, Chow A, Bhanot U, Linkov I, Asher M, Yu H, Qiu J, de Stanchina E, Patel R, Morrissey C, Haffner M, Koche R, Sawyers C, Rudin C. Exportin 1 inhibition prevents neuroendocrine transformation through SOX2 down-regulation in lung and prostate cancers. Science Translational Medicine 2023, 15: eadf7006-eadf7006. PMID: 37531417, PMCID: PMC10777207, DOI: 10.1126/scitranslmed.adf7006.Peer-Reviewed Original ResearchConceptsPatient-derived xenograftsProstatic adenocarcinomaNE transformationXenograft modelExportin 1Associated with poor prognosisProstate adenocarcinoma cell lineInactivation of TP53Adenocarcinoma xenograft modelEctopic SOX2 expressionEGFR inhibitor osimertinibAdenocarcinoma cell lineNE phenotypeNeuroendocrine transformationSelinexor treatmentStandard cytotoxicsProstate cancerLineage plasticityPotential therapeutic targetNE featuresPoor prognosisProstateSOX2 expressionAdenocarcinomaLung
2022
5 Oral Lineage plasticity in prostate cancer depends on FGFR and JAK/STAT inflammatory signaling
Chan J, Zaidi S, Love J, Zhao J, Setty M, Wadosky K, Gopalan A, Choo Z, Persad S, Chaudhary O, Xu T, Masilionis I, Morris M, Mazutis L, Chaligne R, Chen Y, Goodrich D, Karthaus W, Pe’er D, Sawyers C. 5 Oral Lineage plasticity in prostate cancer depends on FGFR and JAK/STAT inflammatory signaling. European Journal Of Cancer 2022, 174: s4-s5. DOI: 10.1016/s0959-8049(22)00818-8.Peer-Reviewed Original ResearchLineage plasticity in prostate cancer depends on JAK/STAT inflammatory signaling
Chan J, Zaidi S, Love J, Zhao J, Setty M, Wadosky K, Gopalan A, Choo Z, Persad S, Choi J, LaClair J, Lawrence K, Chaudhary O, Xu T, Masilionis I, Linkov I, Wang S, Lee C, Barlas A, Morris M, Mazutis L, Chaligne R, Chen Y, Goodrich D, Karthaus W, Pe'er D, Sawyers C. Lineage plasticity in prostate cancer depends on JAK/STAT inflammatory signaling. Science 2022, 377: 1180-1191. PMID: 35981096, PMCID: PMC9653178, DOI: 10.1126/science.abn0478.Peer-Reviewed Original ResearchConceptsFibroblast growth factor receptorProstate cancerLineage plasticityJanus kinaseGenetically engineered mouse modelsCastration-resistant diseaseFibroblast growth factor receptor signalingTumor cell statesGrowth factor receptorSingle-cell analysisMetastatic diseaseStratify patientsIncreased JAK/STATAntiandrogen resistanceEpithelial populationsDrug resistanceFactor receptorClinical trialsInhibitor treatmentMouse modelInflammatory signalingGene expressionCell statesMurine organoidsMolecular mechanisms
2021
Prostate cancer research in the 21st century; report from the 2021 Coffey‐Holden prostate cancer academy meeting
Miyahira A, Zarif J, Coombs C, Flavell R, Russo J, Zaidi S, Zhao D, Zhao S, Pienta K, Soule H. Prostate cancer research in the 21st century; report from the 2021 Coffey‐Holden prostate cancer academy meeting. The Prostate 2021, 82: 169-181. PMID: 34734426, PMCID: PMC8688282, DOI: 10.1002/pros.24262.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCoffey-Holden Prostate Cancer Academy MeetingCoffey-Holden Prostate Cancer AcademyProstate cancer researchProstate cancerMetastatic castration resistant prostate cancerCastration resistant prostate cancerResistant prostate cancerProstate cancer biologyProstate Cancer FoundationCancer researchAntitumor immunityCancer immunotherapyClonal hematopoiesisMediators of plasticityTumor microenvironmentTargeted therapyProstateCell plasticityCancer FoundationCancer biologyCancerSignaling pathwayCancer genomesSignaling biologyAcademy Meeting
2019
Histone H2B monoubiquitination regulates heart development via epigenetic control of cilia motility
Robson A, Makova SZ, Barish S, Zaidi S, Mehta S, Drozd J, Jin SC, Gelb BD, Seidman CE, Chung WK, Lifton RP, Khokha MK, Brueckner M. Histone H2B monoubiquitination regulates heart development via epigenetic control of cilia motility. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 14049-14054. PMID: 31235600, PMCID: PMC6628794, DOI: 10.1073/pnas.1808341116.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell MovementCell ProliferationChromatin Assembly and DisassemblyCiliaDisease Models, AnimalEpigenesis, GeneticGene Expression Regulation, NeoplasticHeartHeart Defects, CongenitalHistonesHumansLoss of Function MutationMiceRegulatory Factor X Transcription FactorsSignal TransductionUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesUbiquitinationXenopusConceptsHistone H2B monoubiquitinationCilia genesH2B monoubiquitinationCilia motilityFunctional gene ontologyHuman congenital heart diseaseUpstream transcriptional regulatorsTissue-specific expressionChromatin remodeling genesChromatin remodelingEpigenetic controlH2Bub1 levelsTranscriptional regulatorsChIP-seqDepletion phenotypeGene OntologyGenomic analysisTranscription factorsKnockdown resultsLeft-right asymmetryCilia functionHeart developmentH2Bub1RNF20Complex consisting
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Center of Molecular and Cellular Oncology
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