Collin Heer, PhD
Associate Research Scientist in Therapeutic RadiologyAbout
Research
Publications
2026
Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes
Heer C, Elia J, Menon V, Johnson S, Arbelaez S, Friedman S, Lopez-Giraldez F, Sundaram R, Herzon S, Bindra R, Gueble S. 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, PMCID: PMC12783042, DOI: 10.1093/narcan/zcaf052.Peer-Reviewed Original ResearchConceptsDNA-damaging agentsDNA repair genesTranscription-coupled nucleotide excision repairCRISPR knockout screenFanconi anemia pathwayRepair genesClasses of DNA-damaging agentsDNA damage repairChemical diversityNucleotide excision repairKnockout screenMethylation lesionsRepair of lesionsDamaging agentsDDR pathwaysDSB repairGenetic instabilityLN229 glioma cellsExcision repairDamage repairDNA lesionsMonofunctional alkylating agentsTopoisomerase IDNAGenes
2025
Synthesis and Biological Evaluation of Colibactin Derivatives
Airan Y, Fedorova O, Heer C, Rees M, Ronan M, Roth J, Bindra R, Herzon S. Synthesis and Biological Evaluation of Colibactin Derivatives. ACS Chemical Biology 2025, 21: 26-36. PMID: 41419211, PMCID: PMC12856499, DOI: 10.1021/acschembio.5c00639.Peer-Reviewed Original ResearchAuranofin Synergistically Sensitizes KEAP1 Mutant and WT NSCLCs to P-AscH--induced Cell Killing by a Thiol and H2O2 Dependent Mechanism
Sho S, Heer C, Pulliam C, Tomanek-Chalkley A, Marren D, Wasimi S, Lengel A, Gentles M, Dupuy A, Spitz D. Auranofin Synergistically Sensitizes KEAP1 Mutant and WT NSCLCs to P-AscH--induced Cell Killing by a Thiol and H2O2 Dependent Mechanism. Free Radical Biology And Medicine 2025, 240: s42. DOI: 10.1016/j.freeradbiomed.2025.10.122.Peer-Reviewed Original ResearchSomatic CRISPR tumorigenesis and multiomic analysis reveal a pentose phosphate pathway disruption vulnerability in MPNSTs
McGivney G, Brockman Q, Borcherding N, Scherer A, Rauckhorst A, Gutierrez W, Solst S, Heer C, Warrier A, Floyd W, Kirsch D, Knepper-Adrian V, Laverty E, Roughton G, Spitz D, Taylor E, Dodd R. Somatic CRISPR tumorigenesis and multiomic analysis reveal a pentose phosphate pathway disruption vulnerability in MPNSTs. Science Advances 2025, 11: eadu2906. PMID: 40802750, PMCID: PMC12346278, DOI: 10.1126/sciadv.adu2906.Peer-Reviewed Original ResearchConceptsPentose phosphate pathwayMalignant peripheral nerve sheath tumor growthMultiomics analysisGlucose-6-phosphate dehydrogenaseRate-limiting enzymeNADPH metabolismG6PD transcriptionPhosphate pathwayMalignant peripheral nerve sheath tumorMPNST developmentTranscription factor Nrf2TCGA samplesPentoseRedox-regulated transcription factors Nrf2G6PDMetabolomic featuresGene signatureTumor transformationTumorigenesisTargetable vulnerabilitiesNrf2Standard-of-care chemotherapyPeripheral nerve sheath tumorsGrowthPoor survival rateMitoregulin Promotes Cell Cycle Progression in Non-Small Cell Lung Cancer Cells
Stein C, Linzer C, Heer C, Witmer N, Cochran J, Spitz D, Boudreau R. Mitoregulin Promotes Cell Cycle Progression in Non-Small Cell Lung Cancer Cells. International Journal Of Molecular Sciences 2025, 26: 1939. PMID: 40076565, PMCID: PMC11899852, DOI: 10.3390/ijms26051939.Peer-Reviewed Original ResearchConceptsMitochondrial H2 O2 levelsNon-small cell lung cancerG1 arrestReactive oxygen speciesG1 phaseCyclin D1 abundanceG1 phase of cell cycleCell cycle progressionPhase of cell cycleLung cancer cellsMitoregulinRoGFP2-Orp1Non-small cell lung cancer cellsCycle progressionCell cycleG1/S transitionMitochondrial energeticsGene expressionRedox sensorCell survivalThioredoxin reductaseLung adenocarcinomaProportion of cellsProtein changesButhionine sulfoximine
2021
HGG-33. EXPLOITING METABOLIC DEFECTS WITH NAMPT INHIBITORS IN DIPG
Muraleedharan R, Heer C, Sundam R, Brenner C. HGG-33. EXPLOITING METABOLIC DEFECTS WITH NAMPT INHIBITORS IN DIPG. Neuro-Oncology 2021, 23: i24-i24. PMCID: PMC8168214, DOI: 10.1093/neuonc/noab090.097.Peer-Reviewed Original ResearchDiffuse intrinsic pontine gliomaH3K27M mutationM mutationNicotinamide phosphoribosyl transferaseNeural progenitor cellsMetabolic defectsH3K27MNicotinamide phosphoribosyl transferase inhibitorDIPG cellsSynthetic lethal drug screenShort-term viability assaysIntrinsic pontine gliomaLethal pediatric brain tumorsLimited treatment optionsCell linesPediatric brain tumorsInduced expressionEffects of FK866H3K27M-mutantIsogenic cell linesPontine gliomaFollow-up studyInhibitors in vitroTreatment optionsProgenitor cellsAvasopasem manganese synergizes with hypofractionated radiation to ablate tumors through the generation of hydrogen peroxide
Sishc B, Ding L, Nam T, Heer C, Rodman S, Schoenfeld J, Fath M, Saha D, Pulliam C, Langen B, Beardsley R, Riley D, Keene J, Spitz D, Story M. Avasopasem manganese synergizes with hypofractionated radiation to ablate tumors through the generation of hydrogen peroxide. Science Translational Medicine 2021, 13 PMID: 33980575, PMCID: PMC8314936, DOI: 10.1126/scitranslmed.abb3768.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerPreclinical xenograft modelsAvasopasem manganeseXenograft models of non-small cell lung cancerHead and neck squamous cell carcinomaPhase I-II clinical trialHigh dosesModel of non-small cell lung cancerStereotactic ablative body radiotherapyNeck squamous cell carcinomaHead and neck cancerPhase 3 clinical trialsRadiation-Induced MucositisDamage to normal tissueCell lung cancerMammary adenocarcinoma modelSquamous cell carcinomaKilling of cancer cellsTreatment synergyPancreatic ductal adenocarcinomaHypofractionated radiationConditional overexpressionTumor irradiationOverexpression of catalaseAdenocarcinoma modelInhibition of CD38 and supplementation of nicotinamide riboside ameliorate lipopolysaccharide‐induced microglial and astrocytic neuroinflammation by increasing NAD+
Roboon J, Hattori T, Ishii H, Takarada‐Iemata M, Nguyen D, Heer C, O'Meally D, Brenner C, Yamamoto Y, Okamoto H, Higashida H, Hori O. Inhibition of CD38 and supplementation of nicotinamide riboside ameliorate lipopolysaccharide‐induced microglial and astrocytic neuroinflammation by increasing NAD+. Journal Of Neurochemistry 2021, 158: 311-327. PMID: 33871064, PMCID: PMC8282715, DOI: 10.1111/jnc.15367.Peer-Reviewed Original ResearchMeSH KeywordsADP-ribosyl Cyclase 1AnimalsApigeninAstrocytesChemokinesCytokinesGene DeletionHippocampusInflammationInjections, IntraventricularLipopolysaccharidesMacrophage ActivationMaleMembrane GlycoproteinsMiceMice, Inbred ICRMice, KnockoutMicrogliaNADNerve DegenerationNF-kappa BNiacinamidePyridinium CompoundsConceptsGlial activationNicotinamide ribosideDeletion of CD38Intracerebroventricular injectionSupplementation of nicotinamide ribosideLPS-induced inflammatory responseInflammatory responseTreatment of primary astrocytesInduction of cytokinesInjection of LPSInhibition of CD38Cuprizone-induced demyelinationIntracerebroventricular injection of LPSCellular energy metabolismInnate immune systemBrain's innate immune systemNF-kB signaling pathwayCD38 expressionLipopolysaccharide (LPS)-induced neuroinflammationControl of neuroinflammationNicotinamide adenine dinucleotideCD38LPS administrationPre-administrationCalcium homeostasis
2020
Succinate Accumulation Links Mitochondrial MnSOD Depletion to Aberrant Nuclear DNA Methylation and Altered Cell Fate.
Cramer-Morales K, Heer C, Mapuskar K, Domann F. Succinate Accumulation Links Mitochondrial MnSOD Depletion to Aberrant Nuclear DNA Methylation and Altered Cell Fate. Journal Of Experimental Pathology 2020, 1: 60-70. PMID: 33585836, PMCID: PMC7876477.Peer-Reviewed Original ResearchSuccinate dehydrogenaseRegulation of TET enzymesNuclear DNA methylationErythroid phenotypeAltering cell fateInhibition of SDH activityTET enzyme activityHuman erythroleukemia cell lineErythroleukemia cell lineTET enzymesMitochondrial originDNA methylationCell fateMitochondrial superoxide dismutaseEpigenetic reprogrammingGenetic strategiesTET activitySuccinate accumulationDecreased succinate dehydrogenaseAconitase activityRetrograde signaling moleculesHEL cellsSuccinate levelsHEL 92.1.7Succinate dehydrogenase activityCoronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity
Heer C, Sanderson D, Voth L, Alhammad Y, Schmidt M, Trammell S, Perlman S, Cohen M, Fehr A, Brenner C. Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity. Journal Of Biological Chemistry 2020, 295: 17986-17996. PMID: 33051211, PMCID: PMC7834058, DOI: 10.1074/jbc.ra120.015138.Peer-Reviewed Original ResearchConceptsPoly(ADP-ribose) polymeraseMurine hepatitis virusADP-riboseNAD synthesisSource of ADP-riboseNicotinamide ribosideCellular NADCellular antiviral responseNAD biosynthetic pathwayAvailability of NADPoly(ADP-ribose) polymerase expressionDNA damage responseExpression of genesMono(ADP-ribosylNAD metabolomeBiosynthetic pathwaySuperfamily membersModel coronavirusDamage responsePARP activityAntiviral activityAntiviral responseNADNAD levelsInnate immunity
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