Samir Zaidi, MD, PhD
Assistant Professor of Internal Medicine (Medical Oncology/Hematology)Cards
Contact Info
Yale Medicine
333 Cedar Street
New Haven, CT 06520
United States
Training
Memorial Sloan Kettering Cancer Center (2022)
Massachusetts General Hospital, Harvard (2018)
About
Titles
Assistant Professor of Internal Medicine (Medical Oncology/Hematology)
Biography
Dr. Samir Zaidi, MD, PhD, is an Assistant Professor of Medicine (Medical Oncology) and Stephen Sherwin MD Investigator at the Yale School of Medicine, as well as a member of the Center for Molecular and Cellular Oncology (CMCO) at the Yale Cancer Center. Dr. Zaidi specializes in the treatment of patients with genitourinary cancers.
Dr. Zaidi earned his Bachelor of Science (BS) in Biology from the Massachusetts Institute of Technology (MIT). He then pursued his combined MD and PhD degrees at the Yale School of Medicine and the Graduate School of Arts and Sciences, graduating Cum Laude (MD) and with Distinction (PhD). He completed his internal medicine residency through the Stanbury Physician–Scientist Pathway at Massachusetts General Hospital (MGH) at Harvard Medical School. Following this, Dr. Zaidi joined Memorial Sloan Kettering Cancer Center (MSKCC) for a fellowship in medical oncology, subsequently serving as an Assistant Attending Physician in Genitourinary Oncology and Louis V. Gerstner Physician Scholar.
Returning to Yale from MSKCC, Dr. Zaidi maintains both clinical and research interests in genitourinary cancers, focusing especially on prostate and kidney cancers. His research centers on understanding the tumor-specific and microenvironmental factors contributing to cancer resistance and lineage plasticity. Rooted firmly in basic biology, Dr. Zaidi's scientific approach emphasizes translational research aimed at developing innovative therapeutic strategies. As an integral member of the Yale Cancer Center and CMCO, Dr. Zaidi contributes significantly to initiatives designed to bridge clinical investigation and fundamental cancer biology, ultimately aiming to enhance patient care through improved cancer therapies.
Departments & Organizations
Education & Training
- Medical Oncology Fellow
- Memorial Sloan Kettering Cancer Center (2022)
- Resident
- Massachusetts General Hospital, Harvard (2018)
- MD
- Yale School of Medicine (2016)
- PhD
- Yale School of Medicine, Genetics (2015)
- BS
- Massachusetts Institute of Technology (MIT), Biology (2009)
Board Certifications
Medical Oncology
- Certification Organization
- AB of Internal Medicine
- Original Certification Date
- 2022
Internal Medicine
- Certification Organization
- AB of Internal Medicine
- Original Certification Date
- 2020
Research
Research at a Glance
Yale Co-Authors
Publications Timeline
Arya Mani, MD, FACC, FAHA
Kaya Bilguvar, MD, PhD
Martina Brueckner, MD
Abha Gupta, MD, PhD
Adife Gulhan Ercan-Sencicek, MSc, MS, PhD
Akiko Iwasaki, PhD
Publications
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 ResearchMeSH Keywords and ConceptsConceptsNeuroendocrine 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 microenvironmentEffect of CDC7 inhibition and MYC degradation on neuroendocrine transformation in the lung and prostate cancer.
Quintanal-Villalonga A, Kawasaki K, Redin E, Rakhade S, Durani V, Sabet A, Karthaus W, Zaidi S, Zhan Y, Manoj P, Sridhar H, Zhong H, Mello B, Ciampricotti M, Bhanot U, Haffner M, Socci N, Yu H, Chan J, Rudin C. Effect of CDC7 inhibition and MYC degradation on neuroendocrine transformation in the lung and prostate cancer. Journal Of Clinical Oncology 2024, 42: e20105-e20105. DOI: 10.1200/jco.2024.42.16_suppl.e20105.Peer-Reviewed Original ResearchConceptsRisk of transformationNE transformationProstatic adenocarcinomaTherapeutic vulnerabilitiesMYC degradationPhase II clinical trialLung tumor modelDelays tumor relapseII clinical trialsTherapy in vivoIn vivo prostateMechanisms of resistanceMYC isoformsNE phenotypeTumor relapseUntreated tumorsNeuroendocrine transformationProstate cancerStemness transcription factorsPotential therapeutic targetTargeted therapyPoor prognosisTumor modelProstateTumor populationCEACAM5-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 ResearchMeSH Keywords and ConceptsConceptsNeuroendocrine 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 ResearchMeSH Keywords and Concepts
2023
2233MO CDC7 inhibition constrains lineage plasticity and prevents resistance and neuroendocrine transformation in the lung and prostate
Quintanal-Villalonga Á, Zaidi S, Karthaus W, Zhan Y, Shafer M, Qiu J, de Stanchina E, Haffner M, Sawyers C, Rudin C. 2233MO CDC7 inhibition constrains lineage plasticity and prevents resistance and neuroendocrine transformation in the lung and prostate. Annals Of Oncology 2023, 34: s1150. DOI: 10.1016/j.annonc.2023.09.1261.Peer-Reviewed Original ResearchExportin 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. PMID: 37531417, PMCID: PMC10777207, DOI: 10.1126/scitranslmed.adf7006.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsPatient-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 expressionAdenocarcinomaLungEffect of Janus kinase (JAK) signaling inhibition on lineage plasticity and drug sensitivity in castrate resistant prostate cancer.
Zaidi S, Chan J, Love J, Zhao J, Setty M, Lawrence K, Gopalan A, Goodrich D, Morris M, Chen Y, Karthaus W, Pe'er D, Sawyers C. Effect of Janus kinase (JAK) signaling inhibition on lineage plasticity and drug sensitivity in castrate resistant prostate cancer. Journal Of Clinical Oncology 2023, 41: 227-227. DOI: 10.1200/jco.2023.41.6_suppl.227.Peer-Reviewed Original ResearchConceptsAndrogen receptor signaling inhibitorsFDA-approved inhibitorFibroblast growth factor receptorLineage plasticityProstate cancerAndrogen receptorInhibitors of JAK/STATSuccess of targeted cancer therapyCastration resistant prostate cancerSignaling inhibitorsLoss of tumor suppressor genesCases of prostate cancerFibroblast growth factor receptor signaling pathwayJanus kinaseSingle cell RNA analysisRadiologically guided biopsyResistant prostate cancerEffects of Janus kinaseIncreased androgen receptorTumor-derived organoidsGenetic editing toolsResistance to therapySingle cell RNA sequencingGrowth factor receptorTumor suppressor gene
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 ResearchMeSH Keywords and ConceptsConceptsFibroblast 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 mechanismsGenomic alterations and evolution in patients with prostate cancer with histologic evidence of neuroendocrine differentiation.
Barnett E, Carbone E, Keegan N, Vasselman S, Nweji B, Zaidi S, Scher H. Genomic alterations and evolution in patients with prostate cancer with histologic evidence of neuroendocrine differentiation. Journal Of Clinical Oncology 2022, 40: 5029-5029. DOI: 10.1200/jco.2022.40.16_suppl.5029.Peer-Reviewed Original ResearchConceptsCastration resistant prostate cancerCastrate resistant prostate cancer samplesNeuroendocrine prostate cancerHistological transformationRB1 alterationsProstate cancerDevelopment of neuroendocrine prostate cancerInhibits androgen receptor signalingNeuroendocrine prostate cancer patientsConfidence intervalsEvidence of neuroendocrine differentiationResistant prostate cancerProstate cancer patientsAndrogen receptor signalingIRB-approved protocolFOXA1 mutationsSequencing resultsTP53 alterationsAR alterationsNeuroendocrine differentiationMSK-IMPACTDifferentially altered genesPathology reportsPanel sequencingDisease course
Academic Achievements & Community Involvement
honor Burroughs Wellcome Fund Career Award for Medical Scientists (CAMS)
National AwardBurroughs Wellcome FundDetails06/01/2023United Stateshonor Louis V. Gerstner Scholar
Other AwardMemorial Sloan Kettering Cancer CenterDetails09/01/2022United States
Get In Touch
Contacts
Yale Medicine
333 Cedar Street
New Haven, CT 06520
United States
Center of Molecular and Cellular Oncology
300 George Street
New Haven, CT 06520
United States