2018
Bullous disorders associated with anti–PD-1 and anti–PD-L1 therapy: A retrospective analysis evaluating the clinical and histopathologic features, frequency, and impact on cancer therapy
Siegel J, Totonchy M, Damsky W, Berk-Krauss J, Castiglione F, Sznol M, Petrylak DP, Fischbach N, Goldberg SB, Decker RH, Stamatouli AM, Hafez N, Glusac EJ, Tomayko MM, Leventhal JS. Bullous disorders associated with anti–PD-1 and anti–PD-L1 therapy: A retrospective analysis evaluating the clinical and histopathologic features, frequency, and impact on cancer therapy. Journal Of The American Academy Of Dermatology 2018, 79: 1081-1088. PMID: 30025829, DOI: 10.1016/j.jaad.2018.07.008.Peer-Reviewed Original ResearchMeSH KeywordsAdrenal Cortex HormonesAgedAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic Agents, ImmunologicalB7-H1 AntigenDrug EruptionsFemaleHumansLichenoid EruptionsMaleMiddle AgedNeoplasm ProteinsNeoplasmsNivolumabPemphigoid, BullousProgrammed Cell Death 1 ReceptorRetrospective StudiesSkin Diseases, VesiculobullousTertiary Care CentersTreatment OutcomeConceptsPD-L1 therapyAnti-PD-1/PD-L1 therapyBullous disordersBullous eruptionPD-1/PD-L1 therapyCell death ligand-1 therapyAnti-programmed cell death 1Cancer therapyDeath ligand 1 therapySingle tertiary care centerLinear IgA bullous dermatosisYale-New Haven HospitalDistinct therapeutic challengesInterruption of immunotherapyPositive tumor responseSteroid-sparing agentTertiary care centerIgA bullous dermatosisCell death 1New Haven HospitalStable diseaseSystemic corticosteroidsSystemic steroidsMaintenance therapyL1 therapy
2013
Molecular Phenotypes in Triple Negative Breast Cancer from African American Patients Suggest Targets for Therapy
Lindner R, Sullivan C, Offor O, Lezon-Geyda K, Halligan K, Fischbach N, Shah M, Bossuyt V, Schulz V, Tuck DP, Harris LN. Molecular Phenotypes in Triple Negative Breast Cancer from African American Patients Suggest Targets for Therapy. PLOS ONE 2013, 8: e71915. PMID: 24260093, PMCID: PMC3832509, DOI: 10.1371/journal.pone.0071915.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerNegative breast cancerInsulin-like growth factor-1African American patientsAA patientsBreast cancerAmerican patientsAA tumorsHigher breast cancer mortalityLuminal androgen receptorBreast cancer mortalityDistinct transcriptional programsBasal-like subtypeBasal-like phenotypeGrowth factor-1Expression of VEGFHigher tumor vascularizationDrug response profilesEA tumorsRetrospective cohortTNBC patientsEA patientsPoor prognosisTNBC casesTNBC subtypes
2004
HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo
Fischbach NA, Rozenfeld S, Shen W, Fong S, Chrobak D, Ginzinger D, Kogan SC, Radhakrishnan A, Le Beau MM, Largman C, Lawrence HJ. HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo. Blood 2004, 105: 1456-1466. PMID: 15522959, DOI: 10.1182/blood-2004-04-1583.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsBone Marrow CellsCell DifferentiationCell Line, TransformedCell ProliferationCell Transformation, NeoplasticErythropoiesisFemaleHomeodomain ProteinsKaryotypingLeukemia, MyeloidLymphopoiesisMiceMice, CongenicMice, Inbred C57BLMyeloid Ecotropic Viral Integration Site 1 ProteinMyeloid Progenitor CellsNeoplasm ProteinsPhenotypeTime FactorsConceptsHematopoietic stem cellsMurine bone marrowPre-B-cell leukemia transcription factor 1Potential cooperative interactionsHox gene expressionMyelomonocytic precursorsHematopoietic stem cell expansionStructure-function relationshipsStem cell expansionHox genesTranscription factor 1Homeobox genesHox familyHuman myeloid leukemiaDNA bindingGene expressionMalignant hematopoiesisHOXB6Gene transferAberrant activationMonocytic differentiationCell expansionDirect interactionStem cellsHuman acute myeloid leukemia