Adam Krysztofiak, PhD
Associate Research Scientist in Therapeutic RadiologyDownloadHi-Res Photo
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Therapeutic Radiology
PO Box 208040
New Haven, CT 06520
United States
Publications Overview
- 15 Publications
- 367 Citations
- 9 Yale Co-Authors
Research Interests
Contact Info
Therapeutic Radiology
PO Box 208040
New Haven, CT 06520
United States
Publications Overview
- 15 Publications
- 367 Citations
- 9 Yale Co-Authors
Research Interests
Contact Info
Therapeutic Radiology
PO Box 208040
New Haven, CT 06520
United States
Publications Overview
- 15 Publications
- 367 Citations
- 9 Yale Co-Authors
Research Interests
About
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Titles
Associate Research Scientist in Therapeutic Radiology
Appointments
Therapeutic Radiology
Associate Research ScientistPrimary
Other Departments & Organizations
- All Institutions
- Radiobiology
- Therapeutic Radiology
Education & Training
- Postdoctoral Associate
- Yale School of Medicine
- PhD
- University of Duisburg-Essen, Cancer and Radiation Biology (2019)
- MSc
- Poznan University of Medical Sciences, Pharmacy (2015)
Research
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Overview
Medical Research Interests
Biochemistry; Cell Biology; DNA Breaks; DNA Damage; DNA Repair; Molecular Biology; Proton Therapy; Radiation Oncology; Radiation, Ionizing; Radiobiology; Radiotherapy
Public Health Interests
Cancer; Metabolism; Pharmaceuticals and Medical Devices
ORCID
0000-0001-7813-7806
Research at a Glance
Research Interests
Research topics Adam Krysztofiak is interested in exploring.
Yale Co-Authors
Frequent collaborators of Adam Krysztofiak's published research.
Publications Timeline
A big-picture view of Adam Krysztofiak's research output by year.
Faye Rogers, PhD
Peter M. Glazer, MD, PhD
Daniel Andrés Colón-Ríos
Yanfeng Liu
Demetrios Braddock, MD, PhD
Eric Hoyeon Song, MD, PhD
15Publications
367Citations
Publications
Featured Publications
Direct targeting of amplified gene loci for proapoptotic anticancer therapy
Kaushik Tiwari M, Colon-Rios DA, Tumu HCR, Liu Y, Quijano E, Krysztofiak A, Chan C, Song E, Braddock DT, Suh HW, Saltzman WM, Rogers FA. Direct targeting of amplified gene loci for proapoptotic anticancer therapy. Nature Biotechnology 2021, 40: 325-334. PMID: 34711990, PMCID: PMC8930417, DOI: 10.1038/s41587-021-01057-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDNA double-strand breaksTriplex-forming oligonucleotidesDNA damage responseDouble-strand breaksDrug resistanceGene amplificationP53-independent apoptosisHER2-positive breastOvarian cancer modelHuman tumor xenograftsInduction of apoptosisGenomic lociNumber of drugsCellular functionsDamage responseGene locusProtein productsHER2-positive cancer cellsDriver genesClinical efficacyCombat drug resistanceDNA damageHER2 amplificationTherapeutic strategiesTumor xenograftsMetabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdown
Krysztofiak A, Szymonowicz K, Hlouschek J, Xiang K, Waterkamp C, Larafa S, Goetting I, Vega-Rubin-de-Celis S, Theiss C, Matschke V, Hoffmann D, Jendrossek V, Matschke J. Metabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdown. IScience 2021, 24: 103366. PMID: 34825138, PMCID: PMC8603201, DOI: 10.1016/j.isci.2021.103366.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCommon metabolic responseCompensatory glycolysisDSB repair kineticsMitochondrial respiratory chainRepair kineticsRadiation-induced DNAFuture mechanistic studiesDNA repairDNA repair kineticsRespiratory chainCancer metabolismMitochondrial functionStress conditionsMetabolic vulnerabilitiesCancer cell linesMetabolic targetsCancer cellsCell linesMitochondrial recoveryGlycolysisNew hypothesisMetabolic responseMetabolismMechanistic studiesDiscoveryVulnerability of IDH1-Mutant Cancers to Histone Deacetylase Inhibition via Orthogonal Suppression of DNA Repair
Dow J, Krysztofiak A, Liu Y, Colon-Rios DA, Rogers FA, Glazer PM. Vulnerability of IDH1-Mutant Cancers to Histone Deacetylase Inhibition via Orthogonal Suppression of DNA Repair. Molecular Cancer Research 2021, 19: 2057-2067. PMID: 34535560, PMCID: PMC8642278, DOI: 10.1158/1541-7786.mcr-21-0456.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHistone deacetylase inhibitor vorinostatPatient-derived tumor xenograftsHomology-directed repairIsocitrate dehydrogenase 1/2 mutationsHistone deacetylase inhibitionIDH1 mutant cellsGreater cell deathHDACi treatmentInhibitor vorinostatTumor xenograftsDeacetylase inhibitionIDH1/2 mutationsPotential biomarkersSpecific cancersMutant cancersCancerCancer cellsDNA repair defectsMalignancyVorinostatDNA double-strand breaksGliomasHistone hypermethylationCell deathPARPiProton Irradiation Increases the Necessity for Homologous Recombination Repair Along with the Indispensability of Non-Homologous End Joining
Szymonowicz K, Krysztofiak A, van der Linden J, Kern A, Deycmar S, Oeck S, Squire A, Koska B, Hlouschek J, Vüllings M, Neander C, Siveke J, Matschke J, Pruschy M, Timmermann B, Jendrossek V. Proton Irradiation Increases the Necessity for Homologous Recombination Repair Along with the Indispensability of Non-Homologous End Joining. Cells 2020, 9: 889. PMID: 32260562, PMCID: PMC7226794, DOI: 10.3390/cells9040889.Peer-Reviewed Original ResearchCitationsAltmetricHigh-throughput Evaluation of Protein Migration and Localization after Laser Micro-Irradiation
Oeck S, Malewicz NM, Krysztofiak A, Turchick A, Jendrossek V, Glazer PM. High-throughput Evaluation of Protein Migration and Localization after Laser Micro-Irradiation. Scientific Reports 2019, 9: 3148. PMID: 30816253, PMCID: PMC6395640, DOI: 10.1038/s41598-019-39760-8.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDNA damage sitesDNA repair proteinsProtein of interestHistone dynamicsHistone phosphorylationProtein fociHigh-throughput analysisProtein modificationRepair proteinsDNA damageDamage sitesSingle nucleusMultiple fluorescence channelsHigh-throughput evaluationRepair kineticsProtein migrationProteinAnalysis of accumulationFluorescence channelsPhosphorylationDNACellsAccumulationLocalizationMigration
2025
PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7
Colón-Ríos D, Dow J, Krysztofiak A, Liu Y, Rogers F, Glazer P. PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7. NAR Cancer 2025, 7: zcaf047. PMID: 41357766, PMCID: PMC12675010, DOI: 10.1093/narcan/zcaf047.Peer-Reviewed Original ResearchThis study investigates how IDH1-mutant cancers develop resistance to PARP inhibitors through loss of end protection factors, 53BP1 and REV7, and shows that the drug cediranib can overcome this resistance, highlighting potential therapeutic strategies for improving cancer treatment outcomes.Cell-penetrating antibody enhances nuclear delivery of triplex-forming oligonucleotides targeting HER2-positive cancers
Minnah A, Tubéns N, Krysztofiak A, Liu Y, Glazer P, Rogers F. Cell-penetrating antibody enhances nuclear delivery of triplex-forming oligonucleotides targeting HER2-positive cancers. Molecular Therapy - Nucleic Acids 2025, 36: 102720. PMID: 41127334, PMCID: PMC12538099, DOI: 10.1016/j.omtn.2025.102720.Peer-Reviewed Original ResearchAltmetricConceptsNucleic acid therapiesNuclear deliveryBreast cancer modelHER2-positive cancersTriplex-forming oligonucleotidesCancer treatment optionsTumor-targeting propertiesPrecision cancer therapyAnti-DNA monoclonal antibodyTreatment optionsCancer modelsCell-penetrating antibodiesBinding extracellular DNACancer therapyClinical translationMonoclonal antibodiesDelivery efficiencyIn vitroNecrotic regionsTherapyExtracellular DNADelivery systemAntibodiesDeliveryHER2
2024
Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition
Rackear M, Quijano E, Ianniello Z, Colón-Ríos D, Krysztofiak A, Abdullah R, Liu Y, Rogers F, Ludwig D, Dwivedi R, Bleichert F, Glazer P. Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition. Oncotarget 2024, 15: 699-713. PMID: 39352803, PMCID: PMC11444335, DOI: 10.18632/oncotarget.28651.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsTumor targetingMonoclonal antibody therapyTumor-specific targetingCell uptakeNucleic acid bindingCell surface antigensAntibody therapyHuman variantsClinical successCell-penetrating antibodiesAcid bindingSystemic administrationSurface antigensTumorRAD51 inhibitionAntibody platformMechanism of cell penetrationBind RAD51AntibodiesFull-lengthSpecific targetsCell penetrationDisease targetsCellsAutoantibodies
2022
The Pathogenic R3052W BRCA2 Variant Disrupts Homology-Directed Repair by Failing to Localize to the Nucleus
Jimenez-Sainz J, Krysztofiak A, Garbarino J, Rogers F, Jensen RB. The Pathogenic R3052W BRCA2 Variant Disrupts Homology-Directed Repair by Failing to Localize to the Nucleus. Frontiers In Genetics 2022, 13: 884210. PMID: 35711920, PMCID: PMC9197106, DOI: 10.3389/fgene.2022.884210.Peer-Reviewed Original ResearchCitationsAltmetricConceptsDominant-negative alleleDNA damage responseDNA repair functionDNA strand exchangeHomology-directed repairGenome instabilityCellular functionsDamage responseDNA bindingNegative allelesStrand exchangeRepair functionGermline missense variantsCell survivalFunction mutationsMissense variantsRAD51Pathogenic allelesSimple lossPARP inhibitorsCytoplasmProteinAllelesHomologyDNA
2018
Relating Linear Energy Transfer to the Formation and Resolution of DNA Repair Foci After Irradiation with Equal Doses of X-ray Photons, Plateau, or Bragg-Peak Protons
Oeck S, Szymonowicz K, Wiel G, Krysztofiak A, Lambert J, Koska B, Iliakis G, Timmermann B, Jendrossek V. Relating Linear Energy Transfer to the Formation and Resolution of DNA Repair Foci After Irradiation with Equal Doses of X-ray Photons, Plateau, or Bragg-Peak Protons. International Journal Of Molecular Sciences 2018, 19: 3779. PMID: 30486506, PMCID: PMC6320817, DOI: 10.3390/ijms19123779.Peer-Reviewed Original ResearchCitationsAltmetric
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Therapeutic Radiology
PO Box 208040
New Haven, CT 06520
United States
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Hunter Building
15 York Street, Fl 2, Rm 210
New Haven, CT 06510
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203.785.7585