Search results for "ErbB"

showing 10 items of 298 documents

The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

2014

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the co…

Cancer ResearchPathologyCetuximabApoptosisHNSCCHNSCCMiceAntineoplastic Combined Chemotherapy ProtocolsNeoplasmPhosphoinositide-3 Kinase InhibitorsMice Inbred BALB CCetuximabCaspase 3TriazinesTOR Serine-Threonine KinasesCetuximab resistanceErbB ReceptorsOncologyHead and Neck NeoplasmsMonoclonalCarcinoma Squamous Cellmedicine.drugmedicine.medical_specialtyMorpholinesPI3K-mTOR inhibitorsMice NudeAntineoplastic AgentsBiologyAntibodies Monoclonal HumanizedCell Line TumorAutophagymedicineCarcinomaAnimalsHumansneoplasmsPI3K/AKT/mTOR pathwayCell Proliferationcetuximab resistanceSquamous Cell Carcinoma of Head and Necktarget therapyCell growthAutophagyCancermedicine.diseaseXenograft Model Antitumor Assaysdigestive system diseasesDrug Resistance NeoplasmPI3K7mTOR inhibitorsCancer researchTranslational TherapeuticsBritish Journal of Cancer
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Co-expression of receptor tyrosine kinases in esophageal adenocarcinoma and squamous cell cancer.

2008

This study aimed to define the co-expression pattern of target receptor tyrosine kinases (RTKs) in human esophageal adenocarcinoma and squamous cell cancer. The co-expression pattern of vascular endothelial growth factor receptor (VEGFR)1-3, platelet-derived growth factor receptor (PDGFR)alpha/beta and epidermal growth factor receptor 1 (EGFR1) was analyzed by RT-PCR in 50 human esophageal cancers (35 adenocarcinomas and 15 squamous cell cancers). In addition, IHC staining was applied for the confirmation of the expression and analysis of RTK localisation. The adenocarcinoma samples revealed VEGFR1 (97%), VEGFR2 (94%), VEGFR3 (77%), PDGFRalpha (91%), PDGFRbeta (85%) and EGFR1 (97%) expressi…

Cancer ResearchPathologymedicine.medical_specialtyReceptor Platelet-Derived Growth Factor alphaEsophageal NeoplasmsAdenocarcinomaReceptor tyrosine kinaseReceptor Platelet-Derived Growth Factor betaGrowth factor receptormedicineHumansEpidermal growth factor receptorVascular Endothelial Growth Factor Receptor-1biologyOncogeneCancerReceptor Protein-Tyrosine KinasesGeneral Medicinemedicine.diseaseVascular Endothelial Growth Factor Receptor-3ImmunohistochemistryVascular Endothelial Growth Factor Receptor-2ErbB ReceptorsOncologyEpidermoid carcinomacardiovascular systembiology.proteinCancer researchCarcinoma Squamous CellAdenocarcinomaPlatelet-derived growth factor receptorOncology reports
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2-Triazenoazaindoles: Α novel class of triazenes inducing transcriptional down-regulation of EGFR and HER-2 in human pancreatic cancer cells

2012

Pancreatic cancer is a complex malignancy arising from the accumulation of genetic and epigenetic defects in the affected cells. Standard chemotherapy for patients with advanced disease shows only modest effects and is associated with considerable toxicity. Overexpression or aberrant activation of members of the epidermal growth factor receptor tyrosine kinase family, which includes EGFR and HER-2, occurs frequently and is associated with multiple drug resistance and decreased patient survival. In this study, we have investigated the therapeutic potential of AS104, a novel compound of the triazene class, with potential inhibitory effects on EGFR. We found that treatment of cells with AS104 …

Cancer ResearchProgrammed cell deathmedicine.medical_specialtyIndolesReceptor ErbB-2EGFRCellpancreatic cancer2-triazenoazaindoles pancreatic cancer cell death EGFR HER-2Down-RegulationApoptosisCell Growth ProcessesBiologyReceptor tyrosine kinasePancreatic cancerInternal medicineCell Line TumormedicineAutophagyHumansMolecular Targeted TherapyOncogeneCell growthCancerArticlesCell cyclemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaErbB ReceptorsPancreatic Neoplasmsmedicine.anatomical_structureEndocrinologycell deathOncologyHER-2Cancer researchbiology.protein2-triazenoazaindolesTriazenesCarcinoma Pancreatic Ductal
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Effects of interferon gamma on the proliferation and modulation of cell-surface structures of human ovarian carcinoma cell lines.

1993

Platinum-containing regimens are very effective in the primary treatment of ovarian cancer. However, upon subsequent treatment most tumors develop multidrug resistance. The clinical application of biological response modifiers like interferon gamma (IFN gamma) in advanced ovarian cancer is therefore of increasing interest. Permanent ovarian cancer cell lines are suitable for investigating the mode of action and the potential clinical effectiveness of such response modifiers. IFN gamma is known to modulate many cellular functions. In this study it was compared for its antiproliferative and antigen-modulatory activity on the expression of tumor-associated (CA-125, HMFG, CEA) and major histoco…

Cancer ResearchReceptor expressionCellInterferon-gammaAntigenEpidermal growth factorAntigens NeoplasmHLA AntigensMHC class ImedicineTumor Cells CulturedHumansAntigens Tumor-Associated CarbohydrateOvarian NeoplasmsMHC class IIbiologyCell growthCell MembraneGeneral Medicinemedicine.diseaseRecombinant ProteinsErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyAntigens Surfacebiology.proteinCancer researchFemaleOvarian cancerCell DivisionJournal of cancer research and clinical oncology
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Identification and validation of novel ERBB2 (HER2, NEU) targets including genes involved in angiogenesis.

2005

V-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2; synonyms HER2, NEU) encodes a transmembrane glycoprotein with tyrosine kinase-specific activity that acts as a major switch in different signal-transduction processes. ERBB2 amplification and overexpression have been found in a number of human cancers, including breast, ovary and kidney carcinoma. Our aim was to detect ERBB2-regulated target genes that contribute to its tumorigenic effect on a genomewide scale. The differential gene expression profile of ERBB2-transfected and wild-type mouse fibroblasts was monitored employing DNA microarrays. Regulated expression of selected genes was verified by RT-PCR and validated by West…

Cancer ResearchReceptor ErbB-2Blotting WesternViral OncogeneDown-RegulationComputational biologyBiologymedicine.disease_causeTransfectionGenomeMiceGene expressionmedicineAnimalsHumansskin and connective tissue diseasesGeneDNA PrimersGlycoproteinsOligonucleotide Array Sequence AnalysisGeneticsRegulation of gene expressionGenomeNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionFibroblastsGenes erbB-2Up-RegulationGene expression profilingGene Expression Regulation NeoplasticCell Transformation NeoplasticOncologyNIH 3T3 CellsDNA microarrayCarcinogenesisSignal TransductionInternational journal of cancer
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HER2 regulates the mammary stem/progenitor cell population driving tumorigenesis and invasion.

2008

The cancer stem cell hypothesis proposes that cancers arise in stem/progenitor cells through disregulation of self-renewal pathways generating tumors, which are driven by a component of 'tumor-initiating cells' retaining stem cell properties. The HER2 gene is amplified in 20-30% of human breast cancers and has been implicated in mammary tumorigenesis as well as in mediating aggressive tumor growth and metastasis. We demonstrate that HER2 overexpression drives mammary carcinogenesis, tumor growth and invasion through its effects on normal and malignant mammary stem cells. HER2 overexpression in normal mammary epithelial cells (NMEC) increases the proportion of stem/progenitor cells as demons…

Cancer ResearchReceptor ErbB-2Cellular differentiationStem cell factorBreast NeoplasmsMice SCIDBiologyStem cell markerAntibodies Monoclonal HumanizedArticleMicePhosphatidylinositol 3-KinasesCancer stem cellMice Inbred NODCell Line TumorGeneticsAnimalsHumansNeoplasm InvasivenessBreastProgenitor cellskin and connective tissue diseasesMolecular BiologyCell ProliferationPhosphoinositide-3 Kinase InhibitorsSettore MED/04 - Patologia GeneraleAntibodies MonoclonalAldehyde DehydrogenaseTrastuzumabEndothelial stem cellImmunologyHER2 Breast Cancer Stem CellsCancer researchNeoplastic Stem CellsFemaleStem cellProto-Oncogene Proteins c-aktAdult stem cellSignal TransductionOncogene
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Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers

2014

Introduction More than 70 common alleles are known to be involved in breast cancer (BC) susceptibility, and several exhibit significant heterogeneity in their associations with different BC subtypes. Although there are differences in the association patterns between BRCA1 and BRCA2 mutation carriers and the general population for several loci, no study has comprehensively evaluated the associations of all known BC susceptibility alleles with risk of BC subtypes in BRCA1 and BRCA2 carriers. Methods We used data from 15,252 BRCA1 and 8,211 BRCA2 carriers to analyze the associations between approximately 200,000 genetic variants on the iCOGS array and risk of BC subtypes defined by estrogen re…

Cancer ResearchReceptor ErbB-2Genes BRCA2BRCALOCIGenes BRCA1MODIFIERSVARIANTSErbB-2610 Medical sciences MedicineDuctalReceptorsMedicine and Health SciencesINVESTIGATORSBreastskin and connective tissue diseasesProgesteroneMedicine(all)Carcinoma Ductal BreastMiddle AgedAdult; Aged; Alleles; Breast Neoplasms; Carcinoma; Carcinoma Ductal Breast; Carcinoma Lobular; Female; Genetic Predisposition to Disease; Heterozygote; Humans; Middle Aged; Neoplasm Grading; Neoplasm Staging; Receptor ErbB-2; Receptors Estrogen; Receptors Progesterone; Genes BRCA1; Genes BRCA2; Cancer Research; OncologyOncologyReceptors EstrogenTUMOR SUBTYPESFemaleReceptors ProgesteroneReceptorResearch ArticleAdultHeterozygote610Breast NeoplasmsMEDULLARY CARCINOMAOVARIAN-CANCERLobularHumansGenetic Predisposition to DiseaseGENOME-WIDE ASSOCIATIONAllelesAgedNeoplasm StagingAdult; Aged; Alleles; Breast Neoplasms; Carcinoma; Carcinoma Ductal Breast; Carcinoma Lobular; Female; Genetic Predisposition to Disease; Heterozygote; Humans; Middle Aged; Neoplasm Grading; Neoplasm Staging; Receptor ErbB-2; Receptors Estrogen; Receptors Progesterone; Genes BRCA1; Genes BRCA2CONSORTIUMCarcinomaBRCA1EstrogenBRCA2Carcinoma LobularESTROGEN-RECEPTORGenesNeoplasm GradingBreast Cancer Research
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ERBB2 Induces an Antiapoptotic Expression Pattern of Bcl-2 Family Members in Node-Negative Breast Cancer

2010

AbstractPurpose: Members of the Bcl-2 family act as master regulators of mitochondrial homeostasis and apoptosis. We analyzed whether ERBB2 influences the prognosis of breast cancer by influencing the proapoptotic versus antiapoptotic balance of Bcl-2 family members.Experimental Design: ERBB2-regulated Bcl-2 family members were identified by inducible expression of ERBB2 in MCF-7 breast cancer cells and by correlation analysis with ERBB2 expression in breast carcinomas. The prognostic relevance of ERBB2-regulated and all additional Bcl-2 family members was determined in 782 patients with untreated node-negative breast cancer. The biological relevance of ERBB2-induced inhibition of apoptosis…

Cancer ResearchReceptor ErbB-2Transplantation HeterologousMedizinApoptosisBreast NeoplasmsBiologyBioinformaticsModels BiologicalBAG1Cohort StudiesMiceBreast cancerDownregulation and upregulationTumor Cells CulturedmedicineAnimalsHumansskin and connective tissue diseasesOligonucleotide Array Sequence AnalysisClusterinGene Expression ProfilingCarcinomaBcl-2 familyCancermedicine.diseaseGenes bcl-2Gene Expression Regulation NeoplasticTransplantationOncologyMultigene FamilyBCL2L13NIH 3T3 CellsCancer researchbiology.proteinFemaleLymph NodesApoptosis Regulatory ProteinsClinical Cancer Research
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Preclinical and Clinical Characterization of Fibroblast-derived Neuregulin-1 on Trastuzumab and Pertuzumab Activity in HER2-positive Breast Cancer.

2021

[Purpose]: To characterize expression of neuregulin-1 (NRG1), an HER3 ligand, in HER2-positive breast cancer and its relation with the efficacy of trastuzumab with or without pertuzumab.

Cancer ResearchStromal cellReceptor ErbB-2medicine.medical_treatmentNeuregulin-1Drug Evaluation PreclinicalBreast NeoplasmsAntibodies Monoclonal HumanizedBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabAntineoplastic Combined Chemotherapy Protocolsmental disordersmedicineTumor Cells CulturedHumansNeuregulin 1skin and connective tissue diseasesneoplasmsNeoadjuvant therapyRetrospective Studiesbiologybusiness.industryFibroblastsTrastuzumabmedicine.diseasebody regionsTreatment OutcomeOncologyCancer cellbiology.proteinCancer researchImmunohistochemistryFemalePertuzumabbusinessmedicine.drug
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Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype

2007

Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.

Cancer ResearchTime FactorsCell of originCellular differentiationBrain tumormacromolecular substancesBiologyMiceProto-Oncogene ProteinsPrecursor cellmedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Cell ProliferationNeoplasm StagingMice KnockoutNeuronsPolycomb Repressive Complex 1Brain NeoplasmsCell growthStem CellsNuclear ProteinsCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseStem Cell Self-RenewalErbB ReceptorsGene Expression Regulation NeoplasticRepressor ProteinsCell Transformation NeoplasticPhenotypeOncologyBMI1AstrocytesMutationCancer cellCancer researchGlioblastomaSignal TransductionCancer Cell
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