Search results for "Digest"

showing 10 items of 3038 documents

Efficacy of BET Bromodomain Inhibition in Kras-Mutant Non–Small Cell Lung Cancer

2013

Abstract Purpose: Amplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion, and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that bromodomain and extra-terminal (BET) bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven non–small cell lung cance…

Cancer ResearchLKB1Lung NeoplasmsMutantApoptosisMYCAMP-Activated Protein KinasesProtein Serine-Threonine KinasesBiologyNSCLCmedicine.disease_causeArticleProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)MiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumorKRASmedicineAnimalsRNA Small InterferingLung cancerneoplasmsCell ProliferationMice KnockoutGene knockdownCell growthNuclear ProteinsCancerAzepinesTriazolesBETmedicine.diseaseMolecular biologydigestive system diseasesrespiratory tract diseasesBromodomainOncologyCancer researchRNA InterferenceKRASSignal TransductionTranscription FactorsClinical Cancer Research
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Epidemiological, clinical and molecular characterization of Lynch‐like syndrome: A population‐based study

2019

Colorectal carcinomas that are mismatch repair (MMR)‐deficient in the absence of MLH1 promoter methylation or germline mutations represent Lynch‐like syndrome (LLS). Double somatic events inactivating MMR genes are involved in the etiology of LLS tumors. Our purpose was to define the clinical and broader molecular hallmarks of LLS tumors and the population incidence of LLS, which remain poorly characterized. We investigated 762 consecutive colorectal carcinomas operated in Central Finland in 2000–2010. LLS cases were identified by a stepwise protocol based on MMR protein expression, MLH1 methylation and MMR gene mutation status. LLS tumors were profiled for CpG Island Methylator Phenotype (…

Cancer ResearchMICROSATELLITE INSTABILITYDNA mismatch repairMISMATCH-REPAIR DEFICIENCYGene mutationmedicine.disease_cause0302 clinical medicinelynch syndromeFinlandMolecular Epidemiologyeducation.field_of_studyMutationISLAND METHYLATOR PHENOTYPENONPOLYPOSIS COLORECTAL-CANCERlynch-like syndromeTUMORSLynch syndrome3. Good healthOncology030220 oncology & carcinogenesissyöpätauditColorectal NeoplasmsMutL Protein Homolog 1Lynch-like syndromeAdult3122 CancersPopulationsuolistosyövätCpG island methylator phenotypeBiologyta3111FREQUENCYMLH103 medical and health sciencesGermline mutationcolorectal carcinomaBRAF MUTATIONCOLONmedicineHumansLynchin oireyhtymäeducationneoplasmsMSIAgedRetrospective StudiesCpG Island Methylator PhenotypeMicrosatellite instabilityDNASOMATIC MUTATIONSta3122CpG Island Methylator phenotypemedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesCOPY NUMBERMutationCancer researchInternational Journal of Cancer
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Inactivation of O(6)-methylguanine-DNA methyltransferase by glucose-conjugated inhibitors.

2001

The DNA-repair protein O6-methylguanine-DNA methyltransferase (MGMT) is a decisive determinant of resistance of tumor cells to methylating and chloroethylating anti-cancer drugs. Therefore, selective inhibition of MGMT in tumors is expected to cause tumor sensitization. Several inhibitors of MGMT have been developed which function in both tumors and normal tissue. To deplete MGMT preferentially in tumors, strategies to target the inhibitor to the tumor tissue need to be developed. Here, we report on the properties of glucose-conjugated MGMT inhibitors that might be useful for tumor targeting since tumor cells frequently over-express glucose transporter. O6-Benzylguanine (O6BG), 8-aza-O6-ben…

Cancer ResearchMethyltransferaseGuaninebiologyDNA repairGlucose transporterbiology.organism_classificationDNA methyltransferaseMolecular biologydigestive system diseasesHeLaO(6)-Methylguanine-DNA MethyltransferaseGlucoseOncologyTargeted drug deliveryEnzyme inhibitorbiology.proteinTumor Cells CulturedHumansEnzyme InhibitorsneoplasmsAlkyltransferaseHeLa CellsInternational journal of cancer
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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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MGMT in primary and recurrent human glioblastomas after radiation and chemotherapy and comparison with p53 status and clinical outcome

2007

The DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) plays a pivotal role in alkylating drug resistance. Here, we determined MGMT activity in primary and recurrent glioblastomas (GBM, WHO grade IV) of patients who received radiation therapy (RT) or RT plus chemotherapy with alkylating agents (temozolomide, chloroethylnitrosoureas). The mean MGMT activity of untreated GBM was 37 +/- 45 (range 0-205) fmol/mg proteins. In the 1st, 2nd and 3rd recurrences, MGMT activity increased from 66 +/- 50 (13-194) to 68 +/- 44 (14-143) and 182 +/- 163 (64-423) fmol/mg protein, respectively. Comparing patients who received RT only with RT plus chemotherapy, a significant increase of MGMT …

Cancer ResearchPathologymedicine.medical_specialtyChemotherapyTemozolomideMethyltransferasemedicine.medical_treatmentCancerBiologymedicine.diseasePrimary tumordigestive system diseasesRadiation therapyOncologymedicineCancer researchneoplasmsSurvival analysismedicine.drugAlkyltransferaseInternational Journal of Cancer
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O6-methylguanine-DNA methyltransferase activity and sensitivity to cyclophosphamide and cisplatin in human lung tumor xenografts

1998

The DNA repair protein O6-methylguanine-DNA methyl-transferase (MGMT) is a main determinant of resistance of cells to the cytostatic effects of O6-alkylguanine-generating alkylating agents. The purpose of our study was to assay MGMT activity in cells of lung cancers and to correlate MGMT levels with chemotherapy response to cyclophosphamide (CTX) and cisplatin (DDP). MGMT levels were determined in 14 human lung tumor xenografts. There was a wide variation of MGMT expression in these tumors, ranging from 10 to 984 fmol/mg protein. There was also a wide range in the sensitivity of the xenografts to CTX and DDP, as measured by specific growth delay. When the MGMT levels of the different xenogr…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsMethyltransferaseCyclophosphamidemedicine.medical_treatmentTransplantation HeterologousMice NudeAntineoplastic AgentsBiologyMiceO(6)-Methylguanine-DNA Methyltransferasechemistry.chemical_compoundIn vivoCarcinoma Non-Small-Cell LungCarcinomamedicineAnimalsHumansCyclophosphamideneoplasmsCisplatinChemotherapyDose-Response Relationship DrugO-6-methylguanine-DNA methyltransferasemedicine.diseasedigestive system diseasesNitrogen mustardOncologychemistryCancer researchFemaleCisplatinmedicine.drugInternational Journal of Cancer
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Cathepsin D expression levels in nongynecological solid tumors: clinical and therapeutic implications.

2004

Cathepsin D is a lysosomal acid proteinase which is involved in the malignant progression of breast cancer and other gynecological tumors. Clinical investigations have shown that in breast cancer patients cathepsin D overexpression was significantly correlated with a shorter free-time disease and overall survival, whereas in patients with ovarian or endometrial cancer this phenomenon was associated with tumor aggressiveness and a degree of chemoresistance to various antitumor drugs such as anthracyclines, cis-platinum and vinca alkaloids. Therefore, a lot of research has been undertaken to evaluate the role and the prognostic value of cathepsin D also in other solid neoplasms. However, conf…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsSkin NeoplasmsCathepsin DAntineoplastic AgentsBiologyDigestive System NeoplasmsCathepsin DMetastasisCentral Nervous System NeoplasmsBreast cancerSurgical oncologyNeoplasmsmedicineBiomarkers TumorNeoplasmHumansClinical significanceThyroid NeoplasmsMelanomaEndometrial cancerGeneral Medicinecathepsin D lysosomal proteinases matrix-metalloproteinases metastasis neoplasm plasminogen activator prognosis tumor progressionmedicine.diseaseNeoplasm ProteinsOncologyTumor progressionHead and Neck NeoplasmsDrug DesignCancer researchDisease ProgressionLysosomesUrogenital NeoplasmsClinicalexperimental metastasis
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Activity of O(6)-methylguanine-DNA methyltransferase in relation to p53 status and therapeutic response in ovarian cancer.

1999

The DNA-repair protein O(6)-methylguanine-DNA methyltransferase (alkyltransferase; MGMT) is a major determinant of resistance of cells to various alkylating cytostatic drugs. Its expression in tissues is highly variable, indicating complex regulatory mechanisms involved. Transfection-mediated expression of wild-type p53 has been shown to negatively regulate basal promoter activity of MGMT in vitro. To elucidate whether p53 is involved in regulation of MGMT in tumor tissue, we examined MGMT expression and the p53 status of 140 primary ovarian carcinomas and analyzed the data as to the correlation between MGMT and p53, as well as the survival response of the patients after chemotherapy. We sh…

Cancer ResearchPathologymedicine.medical_specialtyMethyltransferaseTime FactorsCyclophosphamidemedicine.medical_treatmentBiologyDisease-Free Survivalchemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferasePredictive Value of TestsmedicineHumansneoplasmsNeoplasm StagingRetrospective StudiesOvarian NeoplasmsChemotherapyL-Lactate DehydrogenaseCancermedicine.diseaseGenes p53ImmunohistochemistrySurvival Analysisdigestive system diseasesNitrogen mustardCarboplatinOncologychemistryCancer researchFemaleTumor Suppressor Protein p53Ovarian cancermedicine.drugAlkyltransferaseFollow-Up StudiesInternational journal of cancer
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Italian survey of second tumors in patients with diagnosis of GIST (gastrointestinal stromal tumor).

2019

11032 Background: GISTs are the most common mesenchymal tumors of the digestive tract. As of recent, new links are being made between GISTS and secondary malignancies. However, whether the coexistence of GISTs with other tumors is stochastic, or the result of related pathogenetic mechanisms is still unknown. Methods: We retrospectively reviewed clinical and molecular features from all GIST patients with second tumors treated in seven Italian GIST reference centers. Qualitative variables were compared using the Fisher exact test. Results: Clinical data of 184 patients with diagnosis of GIST were evaluated. Median age at diagnosis was 66 years, KIT exon 11 resulted the most frequent mutation…

Cancer ResearchPathologymedicine.medical_specialtyOncologybusiness.industryMesenchymal stem cellmedicineGIST - Gastrointestinal stromal tumorDigestive tractIn patientbusinessneoplasmsdigestive system diseasesJournal of Clinical Oncology
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Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma

2005

Defects in apoptosis signaling in hepatocytes contribute to tumorigenesis in hepatocellular carcinoma (HCC). In addition, treatment with chemotherapeutic drugs is often ineffective in HCC patients due to the apoptosis resistance of cancer cells. Anti-apoptotic members of the Bcl-2 family, including myeloid cell leukemia-1 (Mcl-1), which regulate intrinsic apoptosis induction at the mito-chondrial level, are often overexpressed in human cancer, and are implicated with disease grade and prognosis. Yet, little is known about the role of Mcl-1 in HCC. In this study, we analyzed the relevance of Mcl-1 expression for the apop-tosis resistance of human HCC. Mcl-1 protein expression was considerabl…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularApoptosisBiologyPhosphatidylinositol 3-KinasesEpidermal growth factorhemic and lymphatic diseasesTumor Cells CulturedmedicineHumansneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayAkt/PKB signaling pathwayGene Expression ProfilingLiver NeoplasmsIntrinsic apoptosisPrognosisdigestive system diseasesNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2OncologyImmunologyCancer cellCancer researchMyeloid Cell Leukemia Sequence 1 ProteinHepatocyte growth factorProto-Oncogene Proteins c-aktmedicine.drugInternational Journal of Oncology
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