Gary Bellinger
Lab Manager - Politi LabCards
Titles
Lab Manager, Research Associate II-MS, MEDCCC Research Affairs/YCC
About
Titles
Lab Manager - Politi Lab
Lab Manager, Research Associate II-MS, MEDCCC Research Affairs/YCCBiography
Specialist of Rodent Surgery and Therapeutic Intervention.
Leads highly specailized mouse surgeries including the transplantation of tumors from one mouse to another. Utilize pharmacological, physiologicol, and/or surgical techniques in small animals. Use pharmacologicol tools in preclinical animal models to evaluate in vivo efficacy and tolerability (includes study design, animal handling, dosing via numerous routes, blood and tissue sampling and data collection, analysis, and interpretation).
Education & Training
- Specialist in Rodent Surgery
- Weill Cornell Medical Center (2013)
- Senior Research Associate II
- Harvard Medical School (2012)
- Senior Associate Scientist
- Pfizer Global Research & Development (2008)
- Research Associate
- Yale School of Medicine (2007)
- BS
- Southern CT State University, Biology (1999)
Research
Overview
Medical Subject Headings (MeSH)
Autoimmune Diseases; Male Urogenital Diseases; Otorhinolaryngologic Diseases; Surgical Procedures, Operative; Therapeutics
Research at a Glance
Yale Co-Authors
Frequent collaborators of Gary Bellinger's published research.
Publications Timeline
A big-picture view of Gary Bellinger's research output by year.
David F. Stern, PhD
Aarti Bhatia, MD, MPH
Barbara Burtness, MD
Benjamin L. Judson, MD, MBA
Saral Mehra, MD, MBA, FACS
15Publications
2,866Citations
Publications
2022
Pyruvate kinase M1 suppresses development and progression of prostate adenocarcinoma
Davidson S, Schmidt D, Heyman J, O'Brien J, Liu A, Israelsen W, Dayton T, Sehgal R, Bronson R, Freinkman E, Mak H, Fanelli G, Malstrom S, Bellinger G, Carracedo A, Pandolfi P, Courtney K, Jha A, DePinho R, Horner J, Thomas C, Cantley L, Loda M, Vander Heiden M. Pyruvate kinase M1 suppresses development and progression of prostate adenocarcinoma. Cancer Research 2022, 82: 2403-2416. PMID: 35584006, PMCID: PMC9256808, DOI: 10.1158/0008-5472.can-21-2352.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2017
Demethylation Therapy as a Targeted Treatment for Human Papillomavirus–Associated Head and Neck Cancer
Biktasova A, Hajek M, Sewell A, Gary C, Bellinger G, Deshpande HA, Bhatia A, Burtness B, Judson B, Mehra S, Yarbrough WG, Issaeva N. Demethylation Therapy as a Targeted Treatment for Human Papillomavirus–Associated Head and Neck Cancer. Clinical Cancer Research 2017, 23: 7276-7287. PMID: 28916527, DOI: 10.1158/1078-0432.ccr-17-1438.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsClinical trialsHNSCC cellsMatrix metalloproteinasesHuman papillomavirus-associated headNeck squamous cell carcinomaSquamous cell carcinomaAbility of HPVClin Cancer ResTumor cell proliferationNeck cancer cellsWindow trialsCell carcinomaEffective therapyPreclinical modelsHPVHPV oncogenesMouse modelMouse blood vesselsDNA demethylating agentHNSCCXenografted tumorsHPV genesIFN responseTherapyTumor samplesLoss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner
Wamsley JJ, Gary C, Biktasova A, Hajek M, Bellinger G, Virk R, Issaeva N, Yarbrough WG. Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner. Oncogenesis 2017, 6: e314-e314. PMID: 28394357, PMCID: PMC5520489, DOI: 10.1038/oncsis.2017.12.Peer-Reviewed Original ResearchCitationsAltmetricConceptsDNA damage-induced cell deathDamage-induced cell deathSide effectsDNA damageDNA damaging treatmentsMutant p53Cell lung cancerSerious side effectsWild-type p53 cellsP53-dependent mannerCommon cancer therapiesMajority of cancersCell fateProtein bindsSensitivity of cellsLung cancerP53 regulatorsCellular DNACell deathDamage DNAMutation statusHuman cancersDamaging treatmentsAnticancer effectsType p53
2016
Phosphoinositide 3-kinase inhibitors induce DNA damage through nucleoside depletion
Juvekar A, Hu H, Yadegarynia S, Lyssiotis C, Ullas S, Lien E, Bellinger G, Son J, Hok R, Seth P, Daly M, Kim B, Scully R, Asara J, Cantley L, Wulf G. Phosphoinositide 3-kinase inhibitors induce DNA damage through nucleoside depletion. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: e4338-e4347. PMID: 27402769, PMCID: PMC4968752, DOI: 10.1073/pnas.1522223113.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAminopyridinesAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell ProliferationDNA DamageDNA, NeoplasmFemaleHumansMice, Inbred C57BLMice, Inbred NODMice, KnockoutMice, SCIDMorpholinesNucleosidesPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsPoly(ADP-ribose) Polymerase InhibitorsTriple Negative Breast NeoplasmsConceptsDNA damagePI3KDNA synthesisNonoxidative pentose phosphate pathwayProtein kinase AktPentose phosphate pathwayKinase AktPI3K inhibitor BKM120DNA repairPI3K inhibitorsPI3K inhibitionPhosphate pathwayCarbon flux studiesCell deathNucleotide synthesisNucleotide triphosphatesMutational backgroundK inhibitionK inhibitorsGenetic aberrationsMouse modelPARP inhibitionInhibitorsBRCA1Triple-negative breast cancerSelective antitumor activity of roscovitine in head and neck cancer
Gary C, Hajek M, Biktasova A, Bellinger G, Yarbrough WG, Issaeva N. Selective antitumor activity of roscovitine in head and neck cancer. Oncotarget 2016, 7: 38598-38611. PMID: 27233076, PMCID: PMC5122414, DOI: 10.18632/oncotarget.9560.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsNeck cancerSide effectsGrowth of HPVHPV-negative tissuesHPV-positive headCancer cellsHuman papilloma virusTargeted therapeutic optionsDetectable side effectsNeck cancer cellsNormal cellsDNA damageRoscovitine administrationHPV positivityCyclin-dependent kinase inhibitorTherapeutic optionsUnwanted side effectsPapilloma virusCdk-7Xenografted tumorsP53-dependent cell deathSignificant DNA damageSelective antitumor activitySensitivity of cellsKinase inhibitors
2014
Pyruvate Kinase Isoform Expression Alters Nucleotide Synthesis to Impact Cell Proliferation
Lunt S, Muralidhar V, Hosios A, Israelsen W, Gui D, Newhouse L, Ogrodzinski M, Hecht V, Xu K, Acevedo P, Hollern D, Bellinger G, Dayton T, Christen S, Elia I, Dinh A, Stephanopoulos G, Manalis S, Yaffe M, Andrechek E, Fendt S, Vander Heiden M. Pyruvate Kinase Isoform Expression Alters Nucleotide Synthesis to Impact Cell Proliferation. Molecular Cell 2014, 57: 95-107. PMID: 25482511, PMCID: PMC4289430, DOI: 10.1016/j.molcel.2014.10.027.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProliferation arrestPKM1 expressionCell proliferationImpacts cell proliferationPrimary cellsPyruvate kinase isoformsNormal cell proliferationPKM2 lossGene expressionKinase isoformsCell cycleCell differentiationNucleotide levelCell growthNucleotide synthesisPKM2 deletionExpression impairsPKM2DNA synthesisMetabolic stateExpressionDeletionProliferationCellsArrest
2013
Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors
Emerling B, Hurov J, Poulogiannis G, Tsukazawa K, Choo-Wing R, Wulf G, Bell E, Shim H, Lamia K, Rameh L, Bellinger G, Sasaki A, Asara J, Yuan X, Bullock A, DeNicola G, Song J, Brown V, Signoretti S, Cantley L. Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors. Cell 2013, 155: 844-857. PMID: 24209622, PMCID: PMC4070383, DOI: 10.1016/j.cell.2013.09.057.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell RespirationCellular SenescenceEmbryo, MammalianGene Knockdown TechniquesGenes, LethalHeterograftsHumansMiceNeoplasm TransplantationPhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen SpeciesSignal TransductionTumor Suppressor Protein p53ConceptsReactive oxygen speciesP53-null tumorsBreast cancer cell linesCancer cell linesBreast cancerType 2Druggable classesAbsence of p53Tumor formationInhibits growthCell linesCancerHomozygous deletionMiceTP53Oxygen speciesP53Enhanced levelsHigh levelsDramatic reductionXenograftsLittermatesTumorsSynthetic lethalityPKM2 Isoform-Specific Deletion Reveals a Differential Requirement for Pyruvate Kinase in Tumor Cells
Israelsen WJ, Dayton TL, Davidson SM, Fiske BP, Hosios AM, Bellinger G, Li J, Yu Y, Sasaki M, Horner JW, Burga LN, Xie J, Jurczak MJ, DePinho RA, Clish CB, Jacks T, Kibbey RG, Wulf GM, Di Vizio D, Mills GB, Cantley LC, Vander Heiden M. PKM2 Isoform-Specific Deletion Reveals a Differential Requirement for Pyruvate Kinase in Tumor Cells. Cell 2013, 155: 397-409. PMID: 24120138, PMCID: PMC3850755, DOI: 10.1016/j.cell.2013.09.025.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsBase SequenceBreast NeoplasmsExonsFemaleGene DeletionGene Knockout TechniquesHeterograftsHumansIsoenzymesMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLModels, MolecularMolecular Sequence DataMutagenesisMutationNeoplasm MetastasisNeoplasm TransplantationPyruvate KinaseRNA SplicingConceptsTumor cellsPKM2 expressionPKM1 expressionTumor formationMammary tumor formationTumor cell proliferationPyruvate kinase M2 isoformPyruvate kinase expressionBreast cancerNull tumorsHuman tumorsTumorsKinase expressionCell proliferationCell populationsPKM2 deletionPKM2 activityCancerPKM2Anabolic metabolismMetabolic requirementsPyruvate kinaseM2 isoformDifferent metabolic requirementsMetformin Decreases Glucose Oxidation and Increases the Dependency of Prostate Cancer Cells on Reductive Glutamine Metabolism
Fendt S, Bell E, Keibler M, Davidson S, Wirth G, Fiske B, Mayers J, Schwab M, Bellinger G, Csibi A, Patnaik A, Blouin M, Cantley L, Guarente L, Blenis J, Pollak M, Olumi A, Vander Heiden M, Stephanopoulos G. Metformin Decreases Glucose Oxidation and Increases the Dependency of Prostate Cancer Cells on Reductive Glutamine Metabolism. Cancer Research 2013, 73: 4429-4438. PMID: 23687346, PMCID: PMC3930683, DOI: 10.1158/0008-5472.can-13-0080.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProstate cancer cellsProstate cancerCancer cellsGlutamine metabolismReductive glutamine metabolismCancer cell proliferationPresence of metforminCancer cell linesGlucose oxidationCancer outcomesMouse modelAttenuated proliferationMetforminEpidemiology studiesCancerGlutamine anaplerosisCell proliferationPatientsCell linesProliferative defectMetabolismOutcomesProliferationCellsTumorsAMPK-Dependent Degradation of TXNIP upon Energy Stress Leads to Enhanced Glucose Uptake via GLUT1
Wu N, Zheng B, Shaywitz A, Dagon Y, Tower C, Bellinger G, Shen C, Wen J, Asara J, McGraw T, Kahn B, Cantley L. AMPK-Dependent Degradation of TXNIP upon Energy Stress Leads to Enhanced Glucose Uptake via GLUT1. Molecular Cell 2013, 49: 1167-1175. PMID: 23453806, PMCID: PMC3615143, DOI: 10.1016/j.molcel.2013.01.035.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsThioredoxin-interacting proteinAMP-dependent protein kinaseGLUT1 messenger RNAMessenger RNAEnergy stressArrestin family proteinGlucose uptakeGlucose transporter GLUT1Negative feedback loopFamily proteinsProtein kinaseProtein productionEnhanced glucose uptakeGLUT1 functionBiochemical mechanismsLong-term adaptationTransporter GLUT1ADP ratioEnergy homeostasisGLUT1Rapid degradationProteinGlucose influxFeedback loopUptake