Search results for "Kinase inhibitor"

showing 10 items of 414 documents

TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

2006

The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutatio…

AdenomaAdenomaGenotypePhysiologyClinical BiochemistryBiologymedicine.disease_causeMethylationEpigenesis GeneticProto-Oncogene Proteins p21(ras)GenotypemedicineCarcinomaHumansEpigeneticsTP53GeneCyclin-Dependent Kinase Inhibitor p16Base SequenceSingle-strand conformation polymorphismCell BiologyMethylationmedicine.diseaseMolecular biologyCell Transformation NeoplasticMutationDisease ProgressionTumor Suppressor Protein p53Carcinogenesis
researchProduct

Posttranslationally modified proteins as mediators of sustained intestinal inflammation.

2006

Oxidative and carbonyl stress leads to generation of N(epsilon)-carboxymethyllysine-modified proteins (CML-mps), which are known to bind the receptor for advanced glycation end products (RAGE) and induce nuclear factor (NF)-kappaB-dependent proinflammatory gene expression. To determine the impact of CML-mps in vivo, RAGE-dependent sustained NF-kappaB activation was studied in resection gut specimens from patients with inflammatory bowel disease. Inflamed gut biopsy tissue demonstrated a significant up-regulation of RAGE and increased NF-kappaB activation. Protein extracts from the inflamed zones, but not from noninflamed resection borders, caused perpetuated NF-kappaB activation in cultured…

AdultCell ExtractsMaleReceptor for Advanced Glycation End ProductsInflammationBiologyInflammatory bowel diseasep38 Mitogen-Activated Protein KinasesPathology and Forensic MedicineProinflammatory cytokineRAGE (receptor)MiceGlycationhemic and lymphatic diseasesGene expressionmedicineAnimalsCalgranulin BHumansCalgranulin AIntestinal MucosaReceptors ImmunologicReceptorProtein Kinase InhibitorsMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3LysineNF-kappa Bnutritional and metabolic diseasesEndothelial Cellsmedicine.diseaseNFKB1Inflammatory Bowel DiseasesIntestinesDisease Models AnimalImmunologyCancer researchFemalemedicine.symptomProtein Processing Post-TranslationalRegular ArticlesThe American journal of pathology
researchProduct

Expression of cell-cycle regulatory proteins cyclin D1, cyclin E, and their inhibitor p21 WAF1/CIP1 in gastric cancer.

1999

The expression and prognostic role of cyclin D1, cyclin E, and p21 (WAF1/CIP1) were immunohistochemically investigated in 413 curatively resected gastric carcinomas. p21 was expressed in 65.4 per cent (n=270), cyclin D1 in 23.7 per cent (n=98), and cyclin E in 13.6 per cent ( n=56) of the tumours. The expression of p21, cyclin D1, and cyclin E was positively associated with the papillary or tubular type of the WHO classification, as well as with the intestinal type according to the Lauren classification. No significant correlation could be found between the expression of p21, cyclin D1 and cyclin E and the parameters pT category, lymph node involvement, and blood vessel and lymphatic vessel…

AdultCyclin-Dependent Kinase Inhibitor p21MaleCyclin ECyclin DCyclin BBiologyPathology and Forensic MedicineImmunoenzyme TechniquesCyclin D1Stomach NeoplasmsCyclinsCyclin EmedicineBiomarkers TumorHumansCyclin D1Lymph nodeCyclinAgedAged 80 and overCancerCell cycleMiddle Agedmedicine.diseasePrognosisNeoplasm ProteinsSurvival Ratemedicine.anatomical_structureGastric Mucosabiology.proteinCancer researchFemaleFollow-Up StudiesThe Journal of pathology
researchProduct

MDM2 and CDKN1A gene polymorphisms and risk of Kaposi's sarcoma in African and Caucasian patients

2010

A single-nucleotide polymorphism in the MDM2 promoter (SNP309; rs2279744) causes elevated transcription of this major negative regulator of p53 in several cancer types. We investigated MDM2 SNP309 and CDKN1A (p21/Waf1/Cip1) codon 31 (rs1801270) polymorphisms in 86 cases of cutaneous Kaposi's sarcoma (KS) from African and Caucasian patients, and 210 healthy controls. A significant increase of the MDM2 SNP309 T/G genotype was observed among classic KS cases (odds ratio 2.38, 95% confidence interval 1.0-5.5). Frequencies of CDKN1A codon 31 genotypes were not significantly different between cases and controls. The results suggest that the MDM2 SNP309 G allele may act as a susceptibility gene fo…

AdultCyclin-Dependent Kinase Inhibitor p21MaleGenotypeHealth Toxicology and MutagenesisClinical BiochemistryBlack PeopleBiologyPolymorphism Single NucleotideBiochemistryWhite PeopleYoung AdultGene FrequencyRisk FactorsGenotypemedicineHumansGenetic Predisposition to DiseaseAlleleYoung adultSarcoma KaposiKaposi's sarcomaAllele frequencyAgedAged 80 and overProto-Oncogene Proteins c-mdm2Odds ratioMiddle Agedmedicine.diseaseConfidence intervalImmunologyCancer researchFemaleSarcomaTumor Suppressor Protein p53
researchProduct

Molecular analysis of the 9p21 locus and p53 genes in Ewing family tumors.

2001

The EWS-ETS rearrangements, and their respective fusion gene products, are specifically associated with histopathologically Ewing family tumors (EFT). These translocations are implicated in generating malignant transformation of EFT, but the presence of additional genetic alterations must be considered in the pathogenesis of such tumors. We analyzed 26 samples (biopsies and/or nude mice xenotransplants) collected from 19 patients with an EFT to determine whether molecular and cytogenetic alterations of the G(1)/S checkpoint genes are implicated in the pathogenesis of EFT. We found inactivating p53 mutations in three (16%) cases, which correlated with a loss of p21(WAF1/Cip1) expression and …

AdultCyclin-Dependent Kinase Inhibitor p21MaleMonosomyTumor suppressor geneAdolescentTransplantation HeterologousGene ExpressionChromosome 9Locus (genetics)Sarcoma EwingBiologymedicine.disease_causePathology and Forensic MedicineFusion geneMiceCyclinsProto-Oncogene ProteinsmedicineAnimalsHumansPoint MutationCyclin D1ChildMolecular BiologyGeneGene AmplificationChromosome MappingCyclin-Dependent Kinase 4Nuclear ProteinsProto-Oncogene Proteins c-mdm2Cell BiologyDNA Methylationmedicine.diseaseGenes p53Survival AnalysisCyclin-Dependent KinasesChromosome 17 (human)Child PreschoolCancer researchFemaleCarcinogenesisChromosomes Human Pair 9Gene DeletionNeoplasm TransplantationLaboratory investigation; a journal of technical methods and pathology
researchProduct

Immunohistochemical expression of p21 in normal tissues of salivary gland, pleomorphic adenoma and carcinoma ex pleomorphic adenoma (undifferentiated…

2009

Objective: Our study aimed to characterize alteration in the immunohistochemical expression of p21 in normal tissue of the salivary gland surrounding pleomorphic adenoma, the tumor cells of pleomorphic adenomas, and carcinoma arising in pleomorphic adenoma. Study design: A selected series of 29 cases of pleomorphic adenomas, and 27 cases of carcinoma ex-pleomorphic adenoma (undifferentiated and adenocarcinoma types) were examined. Results: The results showed that p21 expression was negative in the most components of normal tissue of the salivary gland surrounding pleomorphic adenoma, 24 cases out of 29 of the non tumour duct cells (82.8%), and 28 (96.6%) cases out of 29 of the acinar cells …

AdultCyclin-Dependent Kinase Inhibitor p21MalePathologymedicine.medical_specialtyAdenomaAdenoma PleomorphicAdenocarcinomaSalivary GlandsPleomorphic adenomaYoung AdultmedicineCarcinomaHumansGeneral DentistryAgedAged 80 and overSalivary glandbusiness.industrySalivary Gland Pleomorphic AdenomaMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseSalivary Gland NeoplasmsImmunohistochemistrydigestive system diseasesCarcinoma ex pleomorphic adenomamedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASAdenocarcinomaImmunohistochemistrySurgeryFemalebusiness
researchProduct

Frequent Alteration of the Yin Yang 1/Raf-1 Kinase Inhibitory Protein Ratio in Hepatocellular Carcinoma

2011

The transcription factor Yin Yang 1 (YY1) can favor several aspects of tumorigenesis. In turn, Raf-1 Kinase Inhibitor Protein (RKIP) inhibits the oncogenic activities of MAPK and NF-κB pathways and promotes drug-induced apoptosis. Mutual influences between YY1 and RKIP may exist, and there are already separate evidences that relevant increases in YY1 and reductions in RKIP occur in hepatocellular carcinoma (HCC). However, the levels of the two factors have never been concomitantly examined in HCC. We evaluated by RT-PCR the mRNA levels of YY1, YY1AP, RKIP, and survivin in 35 clinical HCCs (91% HCV-related), in their adjacent cirrhotic tissues and in 6 healthy livers. Immunohistochemical ana…

AdultLiver CirrhosisMaleMAPK/ERK pathwayCarcinoma HepatocellularSettore MED/09 - Medicina InternaSurvivinCell Cycle ProteinsPhosphatidylethanolamine Binding ProteinSettore MED/08 - Anatomia PatologicaBiologymedicine.disease_causeBiochemistryInhibitor of Apoptosis ProteinsSurvivinGeneticsmedicineHumansRNA MessengerHepatocellular carcinomaYY1RKIPMolecular BiologyTranscription factorYY1 Transcription FactorAgedAged 80 and overSettore MED/12 - GastroenterologiaHepatocellular carcinoma Yin Yang 1 Raf-1 Kinase Inhibitor Protein Yin Yang 1-associated proteinKinaseYY1Liver NeoplasmsNuclear ProteinsMiddle AgedHCCSmedicine.diseaseGene Expression Regulation NeoplasticLiverHepatocellular carcinomaembryonic structuresSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineFemaleSettore SECS-S/01 - StatisticaCarcinogenesisTranscription FactorsBiotechnologyOMICS: A Journal of Integrative Biology
researchProduct

Safety and Efficacy of Sorafenib in Patients With Advanced Hepatocellular Carcinoma in Consideration of Concomitant Stage of Liver Cirrhosis

2009

GOALS AND BACKGROUND: The multikinase inhibitor sorafenib provides survival benefit for patients with advanced hepatocellular carcinoma (HCC) and liver cirrhosis (LCI) Child-Pugh A. We report our experiences with sorafenib in advanced HCC, particularly in patients with LCI Child-Pugh B/C, where only limited data are available in regard to safety and efficacy of sorafenib. METHODS: Thirty-four patients with advanced HCC were treated with sorafenib regardless of liver function and prior anticancer therapy. Adverse events (AEs) were graded using Common Toxicity Criteria version 3.0, tumor response was assessed according to Response Evaluation Criteria in Solid Tumors. RESULTS: Fifteen patients…

AdultLiver CirrhosisMaleNiacinamideSorafenibmedicine.medical_specialtyCarcinoma HepatocellularTime FactorsCirrhosisPyridinesAntineoplastic AgentsKaplan-Meier EstimateRisk AssessmentSeverity of Illness IndexGastroenterologyInternal medicinemedicineCarcinomaHumansProspective StudiesProtein Kinase InhibitorsAgedAged 80 and overbusiness.industryPatient SelectionPhenylurea CompoundsBenzenesulfonatesLiver NeoplasmsGastroenterologyCancerMiddle AgedSorafenibmedicine.diseasedigestive system diseasesSurgeryTreatment OutcomeResponse Evaluation Criteria in Solid TumorsHepatocellular carcinomaConcomitantFemaleLiver functionbusinessmedicine.drugJournal of Clinical Gastroenterology
researchProduct

Multicenter Phase I Study of Erdafitinib (JNJ-42756493), Oral Pan-Fibroblast Growth Factor Receptor Inhibitor, in Patients with Advanced or Refractor…

2018

AbstractPurpose:Here, we report results of the first phase I study of erdafitinib, a potent, oral pan-FGFR inhibitor.Patients and Methods:Patients age ≥18 years with advanced solid tumors for which standard antineoplastic therapy was no longer effective were enrolled (NCT01703481). Parts 2 to 4 employed molecular screening for activating FGFR genomic alterations. In patients with such alterations, two selected doses/schedules identified during part 1 dose-escalation [9 mg once daily and 10 mg intermittently (7 days on/7 days off), as previously published (Tabernero JCO 2015;33:3401-8)] were tested.Results:The study included 187 patients. The most common treatment-related adverse events were…

AdultMale0301 basic medicineCancer Researchmedicine.medical_specialtyAdministration OralAntineoplastic AgentsDrug resistanceGastroenterologyYoung Adult03 medical and health sciencesHyperphosphatemia0302 clinical medicineRefractoryErdafitinibNeoplasmsQuinoxalinesInternal medicinemedicineHumansNeoplasmDosingAdverse effectProtein Kinase InhibitorsAgedNeoplasm StagingAged 80 and overbusiness.industryGenetic VariationMiddle AgedPrognosismedicine.diseaseReceptors Fibroblast Growth FactorTreatment Outcome030104 developmental biologyOncologyTolerabilityDrug Resistance Neoplasm030220 oncology & carcinogenesisRetreatmentPyrazolesFemalebusinessClinical Cancer Research
researchProduct

A First-in-Human Phase I Study of the ATP-Competitive AKT Inhibitor Ipatasertib Demonstrates Robust and Safe Targeting of AKT in Patients with Solid …

2016

Abstract Activation of AKT signaling by PTEN loss or PIK3CA mutations occurs frequently in human cancers, but targeting AKT has been difficult due to the mechanism-based toxicities of inhibitors that target the inactive conformation of AKT. Ipatasertib (GDC-0068) is a novel selective ATP-competitive small-molecule inhibitor of AKT that preferentially targets active phosphorylated AKT (pAKT) and is potent in cell lines with evidence of AKT activation. In this phase I study, ipatasertib was well tolerated; most adverse events were gastrointestinal and grade 1–2 in severity. The exposures of ipatasertib ≥200 mg daily in patients correlated with preclinical TGI90, and pharmacodynamic studies co…

AdultMale0301 basic medicineProto-Oncogene Proteins c-aktAdministration OralPharmacologyIpatasertibDrug Administration SchedulePiperazines03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsHumansPTENMedicineProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayAgedbiologybusiness.industryMiddle AgedXenograft Model Antitumor AssaysSmall moleculePyrimidines030104 developmental biologyOncologyCell culture030220 oncology & carcinogenesisPharmacodynamicsbiology.proteinFemalebusinessProto-Oncogene Proteins c-akt
researchProduct