Z. Ping Lin, PhD
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Biography
Dr Z Ping Lin, PhD is a research scientist in the Department of Obstetrics, Gynecology, and Reproductive Sciences. His research interests include DNA repair, cell cycle regulation, apoptosis, metastasis, immune evasion, high throughput screening, drug discovery, targeted therapy, and immunotherapy in ovarian cancer.
Last Updated on October 07, 2024.
Appointments
Obstetrics, Gynecology & Reproductive Sciences
Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Postdoctoral Fellow/Associate
- Yale University School of Medicine (2003)
- PhD
- George Washington University Medical Center (1999)
- BS
- Taipei Medical College (1991)
Research
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Overview
Ovarian cancer is the most lethal gynecologic malignancy in the US. Frequent recurrence, therapeutic resistance, and immune evasion underlie the dismal outcome of ovarian cancer. Our laboratory research is aimed at identifying molecular mechanisms by which ovarian cancer cells resort to alternative DNA repair pathways, dysregulate apoptosis, and evade immune response to promote malignant progression. As such we can design synthetic lethal or targeted approaches to augment therapeutic efficacy and improve the survival outcome of ovarian cancer patients.
Medical Research Interests
Apoptosis; Carcinoma, Ovarian Epithelial; Chemicals and Drugs; Diseases; DNA Repair; Drug Discovery; Immune Evasion; Immunotherapy; Molecular Targeted Therapy; Neoplastic Stem Cells
Public Health Interests
Cancer
ORCID
0000-0003-2783-725X
Research at a Glance
Yale Co-Authors
Frequent collaborators of Z. Ping Lin's published research.
Publications Timeline
A big-picture view of Z. Ping Lin's research output by year.
Research Interests
Research topics Z. Ping Lin is interested in exploring.
Elena Ratner, MD, MBA
Peining Li, PhD
Timothy Nottoli, PhD
Yang Yang, PhD
Yong-Lian Zhu, MD
22Publications
846Citations
Carcinoma, Ovarian Epithelial
Apoptosis
DNA Repair
Publications
Featured Publications
Poly (ADP-ribose) polymerase inhibitors
Ratner ES, Sartorelli AC, Lin ZP. Poly (ADP-ribose) polymerase inhibitors. Current Opinion In Oncology 2012, 24: 564-571. PMID: 22759740, PMCID: PMC3799945, DOI: 10.1097/cco.0b013e3283564230.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEpithelial ovarian cancerOvarian cancerOverall survivalEOC patientsPARP inhibitorsBRCA mutationsHereditary epithelial ovarian cancerLower chemotherapy response rateDNA repair defectsDeleterious BRCA1/2 mutationsPlatinum-based chemotherapyRecurrence-free survivalChemotherapy response rateRecent clinical trialsPoor overall survivalNew treatment optionsShorter survival timeSporadic epithelial ovarian cancerPoly (ADP-ribose) polymerasePoly (ADP-ribose) polymerase (PARP) inhibitorsEffect of cisplatinPARP inhibitor olaparibRecurrent diseaseClinical outcomesTherapeutic challengeIn silico screening identifies a novel small molecule inhibitor that counteracts PARP inhibitor resistance in ovarian cancer
Lin ZP, Al Zouabi NN, Xu ML, Bowen NE, Wu TL, Lavi ES, Huang PH, Zhu YL, Kim B, Ratner ES. In silico screening identifies a novel small molecule inhibitor that counteracts PARP inhibitor resistance in ovarian cancer. Scientific Reports 2021, 11: 8042. PMID: 33850183, PMCID: PMC8044145, DOI: 10.1038/s41598-021-87325-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEpithelial ovarian cancerSmall molecule inhibitorsPARP inhibitor resistancePARP inhibitorsBRCA mutationsOvarian cancerEOC cellsPoly ADP-ribose polymerase inhibitorsMolecule inhibitorsInhibitor resistanceADP-ribose polymerase inhibitorsTumor-bearing miceNovel small molecule inhibitorPARP inhibitor olaparibDefective homologous recombination (HR) repairEOC xenograftsClinical efficacySurvival timePutative small molecule inhibitorsInhibitor olaparibPolymerase inhibitorsHR repairInhibitorsCancerHomologous recombination repairTriapine Disrupts CtIP-Mediated Homologous Recombination Repair and Sensitizes Ovarian Cancer Cells to PARP and Topoisomerase Inhibitors
Lin ZP, Ratner ES, Whicker ME, Lee Y, Sartorelli AC. Triapine Disrupts CtIP-Mediated Homologous Recombination Repair and Sensitizes Ovarian Cancer Cells to PARP and Topoisomerase Inhibitors. Molecular Cancer Research 2014, 12: 381-393. PMID: 24413181, PMCID: PMC3962722, DOI: 10.1158/1541-7786.mcr-13-0480.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsCarcinoma, Ovarian EpithelialCarrier ProteinsCell Line, TumorDrug SynergismFemaleHumansNeoplasms, Glandular and EpithelialOvarian NeoplasmsPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesPyridinesRecombination, GeneticRecombinational DNA RepairThiosemicarbazonesTopoisomerase InhibitorsTransfectionConceptsHomologous recombination repairEOC cellsCtIP phosphorylationRecombination repairDNA double-strand break resectionCyclin-dependent kinase activityTopoisomerase II inhibitor etoposidePhosphorylation of CtIPDouble-strand break resectionSmall molecule inhibitorsRPA32 phosphorylationBRCA1 interactionBRCA1 fociNbs1 complexMre11-Rad50Chk1 activationDSB resectionKinase activitySynthetic lethalityRAD51 fociOvarian cancer cellsInhibitor etoposideCell cycleRibonucleotide reductaseCtIPCombination of triapine, olaparib, and cediranib suppresses progression of BRCA-wild type and PARP inhibitor-resistant epithelial ovarian cancer
Lin ZP, Zhu YL, Lo YC, Moscarelli J, Xiong A, Korayem Y, Huang PH, Giri S, LoRusso P, Ratner ES. Combination of triapine, olaparib, and cediranib suppresses progression of BRCA-wild type and PARP inhibitor-resistant epithelial ovarian cancer. PLOS ONE 2018, 13: e0207399. PMID: 30444904, PMCID: PMC6239325, DOI: 10.1371/journal.pone.0207399.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBRCA1 ProteinBreast NeoplasmsCell Line, TumorDrug Resistance, NeoplasmFemaleHumansMice, NudeMice, SCIDPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsPyridinesQuinazolinesThiosemicarbazonesXenograft Model Antitumor AssaysConceptsEpithelial ovarian cancerBRCA wild typeSCID-beige miceXenograft mouse modelOvarian cancerMouse modelSurvival timeNude micePARP inhibitorsEOC cell linesPARP inhibitor olaparibHomologous recombination repairCombination regimentsDefective homologous recombination (HR) repairEOC growthC tumorsSignificant prolongationBRCA mutationsAbdominal circumferenceEOC cellsSingle drugCediranibMarked suppressionTriple combinationTumor growthTargeting Cyclin-Dependent Kinases for Treatment of Gynecologic Cancers
Lin ZP, Zhu YL, Ratner ES. Targeting Cyclin-Dependent Kinases for Treatment of Gynecologic Cancers. Frontiers In Oncology 2018, 8: 303. PMID: 30135856, PMCID: PMC6092490, DOI: 10.3389/fonc.2018.00303.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCDK activityCell cycleDefective cell cycle regulationCyclin-dependent kinase activityCell cycle phase transitionCell cycle regulationCyclin-dependent kinasesNormal cell cycleHomologous recombination repairHallmarks of cancerTargeting Cyclin-Dependent KinasesSynthetic lethal approachCell cycle phasesSmall molecule inhibitorsGynecologic cancerCheckpoint activationPARP inhibitorsCycle regulationHR repairKinase activityRecombination repairDNA damaging modalitiesProtein targetsCDKMajor gynecologic malignanciesPredictive modeling of gene mutations for the survival outcomes of epithelial ovarian cancer patients
C. M, Lavi E, Altwerger G, Lin Z, Ratner E. Predictive modeling of gene mutations for the survival outcomes of epithelial ovarian cancer patients. PLOS ONE 2024, 19: e0305273. PMID: 38976671, PMCID: PMC11230535, DOI: 10.1371/journal.pone.0305273.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEpithelial ovarian cancerEpithelial ovarian cancer patientsEpithelial ovarian cancer casesGene mutation signaturesPlatinum-based chemotherapyThe Cancer Genome AtlasResponse to treatmentOverall survivalGene mutationsMutational signaturesHomologous recombinationSurvival outcomesIncreased sensitivity to platinum-based chemotherapySensitivity to platinum-based chemotherapyAssociated with increased chemoresistanceResistance to platinum-based chemotherapySurvival timeSurvival rateFavorable response to treatmentPlatinum-induced DNA damageKaplan-Meier survival analysisPrediction of survival outcomesOvarian cancer patientsOverall survival ratePrediction of treatment outcomeStable Suppression of the R2 Subunit of Ribonucleotide Reductase by R2-targeted Short Interference RNA Sensitizes p53(–/–) HCT-116 Colon Cancer Cells to DNA-damaging Agents and Ribonucleotide Reductase Inhibitors*
Lin ZP, Belcourt MF, Cory JG, Sartorelli AC. Stable Suppression of the R2 Subunit of Ribonucleotide Reductase by R2-targeted Short Interference RNA Sensitizes p53(–/–) HCT-116 Colon Cancer Cells to DNA-damaging Agents and Ribonucleotide Reductase Inhibitors*. Journal Of Biological Chemistry 2004, 279: 27030-27038. PMID: 15096505, DOI: 10.1074/jbc.m402056200.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAntineoplastic AgentsCell Line, TumorCell SurvivalCisplatinColonic NeoplasmsDeoxyribonucleotidesDNA DamageDown-RegulationDoxorubicinEnzyme InhibitorsEtoposideGene Expression Regulation, NeoplasticGene SilencingHumansHydroxyureaIntracellular Signaling Peptides and ProteinsProtein SubunitsProto-Oncogene ProteinsPyridinesRecombinant ProteinsRibonucleotide ReductasesRNA, Small InterferingThiosemicarbazonesTumor Suppressor Protein p53VincristineConceptsShort interference RNAR2 proteinRibonucleotide reductaseInterference RNADNA damageRNR inhibitorsHCT-116 cellsMammalian ribonucleotide reductaseDNA-damaging agent cisplatinCellular growth rateHCT-116 colon cancer cellsDNA-damaging agentsP53-dependent inductionColon cancer cellsHCT-116 human colon carcinoma cellsHuman colon carcinoma cellsDNA replicationEctopic expressionKnockdown cellsColon carcinoma cellsExpression vectorDeoxyribonucleoside diphosphatesStable expressionR2 subunitRibonucleotide reductase inhibitorAtaxia-telangiectasia mutated kinase regulates ribonucleotide reductase and mitochondrial homeostasis
Eaton JS, Lin ZP, Sartorelli AC, Bonawitz ND, Shadel GS. Ataxia-telangiectasia mutated kinase regulates ribonucleotide reductase and mitochondrial homeostasis. Journal Of Clinical Investigation 2007, 117: 2723-2734. PMID: 17786248, PMCID: PMC1952633, DOI: 10.1172/jci31604.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCells, CulturedDNA-Binding ProteinsDNA, MitochondrialGene DosageGene Expression Regulation, EnzymologicHomeostasisHumansMitochondriaMutationProtein BiosynthesisProtein Serine-Threonine KinasesProtein SubunitsReactive Oxygen SpeciesRibonucleotide ReductasesTumor Suppressor ProteinsUp-RegulationConceptsRibonucleotide reductaseMitochondrial homeostasisRNA interferenceNuclear DNA damage responseAtaxia telangiectasiaATM inhibitor KU-55933Disruption of ATMNormal growth conditionsDNA damage responseMitochondrial transcription factorWild-type fibroblastsCandidate disease lociMtDNA depletion syndromeMtDNA copy numberMitochondrial DNA depletionKU-55933P53R2 subunitsDamage responseTranscription factorsRate-limiting enzymeDe novo synthesisGlobal dysregulationT fibroblastsR1 subunitMitochondrial respirationDisruption of cAMP and Prostaglandin E2 Transport by Multidrug Resistance Protein 4 Deficiency Alters cAMP-Mediated Signaling and Nociceptive Response
Lin ZP, Zhu YL, Johnson DR, Rice KP, Nottoli T, Hains BC, McGrath J, Waxman SG, Sartorelli AC. Disruption of cAMP and Prostaglandin E2 Transport by Multidrug Resistance Protein 4 Deficiency Alters cAMP-Mediated Signaling and Nociceptive Response. Molecular Pharmacology 2007, 73: 243-251. PMID: 17959714, PMCID: PMC2780335, DOI: 10.1124/mol.107.039594.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsNociceptive responsesPG synthesisInflammatory nociceptive responsesInflammatory pain thresholdWild-type miceCyclooxygenase-2 expressionMrp4 knockout miceMultidrug resistance protein 4Accumulation of intracellularMEF cellsMRP4 knockdownNucleotide agentsPain thresholdDisruptions of cAMPPGE metabolitePG levelsEnergy-dependent effluxProtein 4MiceMRP4PG transportIntracellular levelsProstaglandinsATP-binding cassette (ABC) familyPronounced reductionCXCL10-induced regulatory T cells and adenosine signaling promote immunosuppression and progression of epithelial ovarian cancer
Lin A, Moscarelli J, Zhu Y, Lin Z, Ratner E. CXCL10-induced regulatory T cells and adenosine signaling promote immunosuppression and progression of epithelial ovarian cancer. Scientific Reports 2025, 15: 20778. PMID: 40596479, PMCID: PMC12217468, DOI: 10.1038/s41598-025-06812-1.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH Keywords5'-NucleotidaseAdenosineAnimalsApyraseB7-H1 AntigenCarcinoma, Ovarian EpithelialCell Line, TumorChemokine CXCL10Disease Models, AnimalDisease ProgressionFemaleHumansImmune ToleranceInterferon-gammaMiceOvarian NeoplasmsReceptors, CXCR3Signal TransductionT-Lymphocytes, RegulatoryTumor MicroenvironmentConceptsEpithelial ovarian cancerImmunosuppressive tumor microenvironmentRegulatory T cellsAdenosine signalingTumor microenvironmentTumor ascitesOvarian cancerT cellsAnti-cancer immune responseEffector T cell activationUp-regulation of Foxp3Epithelial ovarian cancer progressionProgression of epithelial ovarian cancerCell-mediated suppressionSyngeneic mouse modelT cell activationPEO1 cellsPD-L1Inhibitor bevacizumabMouse survivalIL10 productionProlonged survivalPEO4 cellsAMG487 treatmentEOC cells
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