2017
CDK4/6 inhibition triggers anti-tumour immunity
Goel S, DeCristo MJ, Watt AC, BrinJones H, Sceneay J, Li BB, Khan N, Ubellacker JM, Xie S, Metzger-Filho O, Hoog J, Ellis MJ, Ma CX, Ramm S, Krop IE, Winer EP, Roberts TM, Kim HJ, McAllister SS, Zhao JJ. CDK4/6 inhibition triggers anti-tumour immunity. Nature 2017, 548: 471-475. PMID: 28813415, PMCID: PMC5570667, DOI: 10.1038/nature23465.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationBiological MimicryBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Disease Models, AnimalFemaleHumansInterferonsMicePhosphorylationProtein Kinase InhibitorsRepressor ProteinsRNA, Double-StrandedSignal TransductionT-Lymphocytes, RegulatoryTranscriptomeVirusesA randomized, double-blinded, controlled study of tucatinib (ONT-380) vs. placebo in combination with capecitabine (C) and trastuzumab (Tz) in patients with pretreated HER2+ unresectable locally advanced or metastatic breast carcinoma (mBC) (HER2CLIMB).
Anders C, Murthy R, Hamilton E, Borges V, Cameron D, Carey L, Müller V, Curigliano G, Gelmon K, Hortobagyi G, Krop I, Loibl S, Pivot X, Pegram M, Slamon D, Hurvitz S, Tsai M, Winer E. A randomized, double-blinded, controlled study of tucatinib (ONT-380) vs. placebo in combination with capecitabine (C) and trastuzumab (Tz) in patients with pretreated HER2+ unresectable locally advanced or metastatic breast carcinoma (mBC) (HER2CLIMB). Journal Of Clinical Oncology 2017, 35: tps1107-tps1107. DOI: 10.1200/jco.2017.35.15_suppl.tps1107.Peer-Reviewed Original ResearchProgression-free survivalMetastatic breast carcinomaBrain metsIndependent data monitoring committeeClinical benefit ratePhase 1b studyDuration of responseIndependent central reviewPrimary study objectiveData monitoring committeeCNS progressionEGFR agentsPo bidBrain metastasesAdult patientsObjective responseOverall survivalCentral reviewStudy treatmentT-DM1CNS therapyTrastuzumab emtansineBenefit rateSelective small molecule inhibitorsBreast carcinoma
2004
Frequent HIN-1 promoter methylation and lack of expression in multiple human tumor types.
Krop I, Player A, Tablante A, Taylor-Parker M, Lahti-Domenici J, Fukuoka J, Batra SK, Papadopoulos N, Richards WG, Sugarbaker DJ, Wright RL, Shim J, Stamey TA, Sellers WR, Loda M, Meyerson M, Hruban R, Jen J, Polyak K. Frequent HIN-1 promoter methylation and lack of expression in multiple human tumor types. Molecular Cancer Research 2004, 2: 489-94. PMID: 15383627, DOI: 10.1158/1541-7786.489.2.9.Peer-Reviewed Original ResearchConceptsHIN-1 expressionHIN-1 methylationHIN-1Breast carcinomaPancreatic carcinomaSmall cell lung cancerNormal tissuesMajority of lungCell lung cancerSquamous cell carcinomaMultiple human cancer typesPromoter methylationMultiple human tumor typesBronchial epithelial cellsHuman cancer typesHuman tumor typesNoncancer patientsCell carcinomaPromoter methylation statusLung cancerBronchial lavagePremalignant changesLack of expressionLung carcinomaProstate tumors
2003
Lack of HIN-1 methylation in BRCA1-linked and "BRCA1-like" breast tumors.
Krop I, Maguire P, Lahti-Domenici J, Lodeiro G, Richardson A, Johannsdottir HK, Nevanlinna H, Borg A, Gelman R, Barkardottir RB, Lindblom A, Polyak K. Lack of HIN-1 methylation in BRCA1-linked and "BRCA1-like" breast tumors. Cancer Research 2003, 63: 2024-7. PMID: 12727813.Peer-Reviewed Original ResearchConceptsHIN-1 methylationBreast tumorsHIN-1BRCA1 tumorsSporadic breast tumorsFamilial breast cancer patientsBreast cancer patientsSpecific breast cancer subtypesBreast cancer riskBreast cancer subtypesSporadic breast carcinomasGerm-line mutationsPromoter methylation statusCancer patientsHER2 statusBreast carcinomaHistopathological phenotypeEstrogen receptorCancer riskCandidate tumor suppressor geneCancer subtypesSporadic casesTumorsCancer typesTumor suppressor gene
2001
HIN-1, a putative cytokine highly expressed in normal but not cancerous mammary epithelial cells
Krop I, Sgroi D, Porter D, Lunetta K, LeVangie R, Seth P, Kaelin C, Rhei E, Bosenberg M, Schnitt S, Marks J, Pagon Z, Belina D, Razumovic J, Polyak K. HIN-1, a putative cytokine highly expressed in normal but not cancerous mammary epithelial cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2001, 98: 9796-9801. PMID: 11481438, PMCID: PMC55532, DOI: 10.1073/pnas.171138398.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBlotting, NorthernBlotting, WesternBreastBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, Intraductal, NoninfiltratingCarcinoma, LobularCell DivisionCells, CulturedChlorocebus aethiopsCHO CellsCOS CellsCricetinaeCricetulusCytokinesDNA MethylationEpithelial CellsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene LibraryGene SilencingGenes, Tumor SuppressorGrowth InhibitorsHumansMolecular Sequence DataNeoplasm ProteinsPromoter Regions, GeneticRecombinant Fusion ProteinsRNA, MessengerRNA, NeoplasmSequence AlignmentSequence Homology, Amino AcidTransfectionTumor Cells, CulturedTumor Suppressor ProteinsConceptsHIN-1 expressionHIN-1Mammary epithelial cellsPutative cytokineEpithelial cellsBreast cancer cell linesHuman breast carcinomaCancerous mammary epithelial cellsBreast cancer cellsCancer cell linesDuctal carcinomaLobular carcinomaPrimary tumorPreinvasive lesionsBreast carcinomaCandidate tumor suppressor geneMolecular alterationsTumor suppressor geneCarcinomaCancer cellsGene expression profilesCell linesCytokinesSuppressor geneCell growth