Search results for "malignant"

showing 10 items of 283 documents

Novel 1H‑Pyrrolo[2,3‑b]pyridine Derivative Nortopsentin Analogues: Synthesis and Antitumor Activity in Peritoneal Mesothelioma Experimental Models

2013

In this study, we describe the synthesis of new nortopsentin analogues, 1H-pyrrolo[2,3-b]pyridine derivatives and their biological effects in experimental models of diffuse malignant peritoneal mesothelioma (DMPM), a rare and rapidly fatal disease, poorly responsive to conventional therapies. The three most active compounds, 1f (3-[2-(5-fluoro-1-methyl-1H-indol-3- yl)-1,3-thiazol-4-yl]-1H-pyrrolo[2,3-b]pyridine), 3f (3-[2-(1H-indol-3-yl)-1,3- thiazol-4-yl]-1-methyl-1H-pyrrolo[2,3-b]pyridine), and 1l (3-[2-(5-fluoro-1- methyl-1H-indol-3-yl)-1,3-thiazol-4-yl]-1-methyl-1H-pyrrolo[2,3-b] pyridine), which were shown to act as cyclin-dependent kinase 1 inhibitors, consistently reduced DMPM cell p…

CDK1 inhibitorsmalignant peritoneal mesothelioma3‑b]pyridineNortopsentin Analogues1H‑Pyrrolo[21H‑Pyrrolo[23‑b]pyridineCDK1 inhibitorsNortopsentin AnalogueSettore CHIM/08 - Chimica Farmaceuticamalignant peritoneal mesothelioma; 1H‑Pyrrolo[2; 3‑b]pyridine; Nortopsentin Analogues; CDK1 inhibitors
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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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Malignant transformation of the liver tumour precursor cell line OC/CDE 22 by the four stereoisomeric fjord region 3,4-dihydrodiol 1,2-epoxides of be…

1995

In previous work we established the rat liver oval cell line OC/CDE 22 in order to study in vitro mechanisms of liver cell transformation. We have now exposed OC/CDE 22 cells to each of the four optically active fjord region dihydrodiol epoxides of benzo[c]phenanthrene to investigate their capacity for malignant transformation of liver cells. All four configurational isomers, which are among the most potent carcinogenic metabolites of polycyclic aromatic hydrocarbons tested in murine tumour models, malignantly transform OC/CDE 22 cells at a 2 microM dose level, resulting in a similar colony-forming efficiency in soft agar. Inoculation of the transformed cells into newborn syngeneic rats pro…

Cancer ResearchBenzo(c)phenanthreneMalignant transformationRats Sprague-Dawleychemistry.chemical_compoundLiver Neoplasms ExperimentalTumor Cells CulturedmedicineAnimalsCarcinogenConfluencyCell growthLiver cellStereoisomerismGeneral MedicinePhenanthrenesRatsCell Transformation Neoplasticmedicine.anatomical_structureLiverchemistryBiochemistryCell cultureHepatocyteCarcinogensPrecancerous ConditionsCell DivisionCarcinogenesis
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Abstract 3512: MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2014

Abstract The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect …

Cancer ResearchCancerBiologymedicine.diseaseWarburg effectIn vitroMalignant transformationTransplantationOncologyImmunologySurvivinmedicineCancer researchmedicine.symptomneoplasmsAnaplasiaCancer Research
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Cytokines in cancer therapy

1989

The treatment options for patients with cancer are presently limited to surgical and radiotherapeutic strategies for localized disease and the systemic use of cytotoxic drugs for disseminated disease. So far, chemotherapy remains the mainstay for the treatment of metastatic cancer. Treatment results, however, have been stagnant particularly for the more frequent cancers such as lung cancer, breast cancer and colorectal cancer. Current research is seeking new concepts of cancer treatment, based upon a more profound understanding of tumor cell biology. The oncogenetic defect in neoplastic cells is a genetic alteration in a primordial cancer cell, which subsequently leads to clonal expansion a…

Cancer ResearchColorectal cancerCancerGeneral MedicineBiologymedicine.diseaseSomatic evolution in cancerMalignant transformationCell therapyBreast cancerOncologyCancer cellmedicineCancer researchNeoplastic transformationJournal of Cancer Research and Clinical Oncology
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Coordinate mutation and transformation of mouse fibroblasts: induction by nitroquinoline oxide and modulation by caffeine

1981

Mutation and malignant transformation were followed in the same cells. Mouse fibroblasts (C3H 10T 1/2) were mutated and transformed by 4-nitroquinoline-1-oxide with similar, approximately linear dose-responses. The presence of caffeine immediately after exposure to 4-nitroquinoline-1-oxide potently inhibited mutation and transformation at high but not at low doses of 4-nitroquinoline-1-oxide. Whilst the coordinate induction of mutation and transformation could be explained by both a common target (DNA) or a common reactive species hitting several targets, the identical modulation by a DNA repair inhibitor of both end points suggests fundamental similarities in the nature of the lesions lead…

Cancer ResearchDNA repairDrug ResistanceBiologyMalignant transformationMicechemistry.chemical_compoundCaffeinemedicineAnimalsA-DNAOuabainFibroblastCells CulturedMice Inbred C3HNitroquinolinesDrug SynergismGeneral MedicineMolecular biology4-Nitroquinoline-1-oxideTransformation (genetics)Cell Transformation Neoplasticmedicine.anatomical_structurechemistryMutationMutation (genetic algorithm)Cancer researchCaffeineDNACarcinogenesis
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Pimasertib Versus Dacarbazine in Patients With Unresectable NRAS-Mutated Cutaneous Melanoma: Phase II, Randomized, Controlled Trial with Crossover

2020

This study investigated the efficacy and safety of pimasertib (MEK1/MEK2 inhibitor) versus dacarbazine (DTIC) in patients with untreated NRAS-mutated melanoma. Phase II, multicenter, open-label trial. Patients with unresectable, stage IIIc/IVM1 NRAS-mutated cutaneous melanoma were randomized 2:1 to pimasertib (60 mg

Cancer ResearchGastroenterologypimasertiblaw.invention0302 clinical medicineRandomized controlled triallawClinical endpoint030212 general & internal medicineMalignant melanomaHazard ratioProgression-free survivalSciences bio-médicales et agricoleslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthDacarbazineOncology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology030220 oncology & carcinogenesismedicine.symptomPimasertibmedicine.drugQuality of lifemedicine.medical_specialtyNauseaDacarbazinemalignant melanomadacarbazine[SDV.CAN]Life Sciences [q-bio]/CancerN-(2 3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamideNeutropeniaN-(23-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamidelcsh:RC254-282Article03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerInternal medicinemedicineProgression-free survivalAdverse effectbusiness.industry[SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatologymedicine.diseaseadverse eventsCancérologiequality of lifeAdverse events[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologybusinessprogression-free survival[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
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Ha-rasVa112 but not p53Ser247 leads to a significant neoplastic transformation rate of the putative rat liver stem cells (oval cell)

1996

In order to test the controversially discussed hypothesis that oval cells are part of a liver stem cell compartment and can give rise to cholangiocellular as well as hepatocellular carcinomas in the course of liver carcinogenesis, we transfected an oval cell line established in our laboratory with an oncogenically activated genomic Ha-ras clone (pUC EJ 6.6), carrying a valine at position 12 instead of the wild-type glycine, or a rat p53 cDNA mutated by site-directed mutagenesis at codon 247, which corresponds to codon 249 in the human p53. This codon is of particular interest since it represents a mutation hotspot observed in hepatocellular carcinoma especially in regions with high aflatoxi…

Cancer ResearchPathologymedicine.medical_specialtyCellLiver Stem CellGeneral MedicineBiologymedicine.diseasemedicine.disease_causeMolecular biologyMalignant transformationmedicine.anatomical_structureCell cultureHepatocellular carcinomamedicineNeoplastic transformationStem cellCarcinogenesisCarcinogenesis
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Role of the Ha-ras gene in the malignant transformation of rat liver oval cells.

1997

We have shown that the oval cell line OCICDE 22 can be transformed by the highly carcinogenic fiord-region diol epoxides of benzo[c]phenanthrene. Mutational activation of the ras proto-oncogene family has been proposed to be a critical event in the formation of tumors induced by polycyclic aromatic hydrocarbons. Therefore, we investigated whether in the earlier transformed OCICDE 22 cells any point mutations were detected in the ras proto-oncogene. The results indicate that the malignant transformation of OCICDE 22 cells by the 4 stereoisomeric benzo[c]phenan-threne diol epoxides in vitro is independent of activation of the Ha-ras proto-oncogene. In addition, Northern and Western blot analy…

Cancer ResearchPathologymedicine.medical_specialtyCellular differentiationBiologymedicine.disease_causeTransfectionProto-Oncogene MasMalignant transformationCell LineRats Sprague-DawleyLiver Neoplasms ExperimentalmedicineAnimalsHumansCell LineageCarcinogenOncogeneCarcinomaCell DifferentiationEpithelial CellsTransfectionPhenanthrenesMolecular biologyIn vitroRatsGene Expression Regulation NeoplasticCell Transformation NeoplasticGenes rasOncologyLiverUrinary Bladder NeoplasmsCell cultureCarcinogensNeoplastic Stem CellsBile DuctsCarcinogenesisNeoplasm TransplantationInternational journal of cancer
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Claudin-18 splice variant 2 is a pan-cancer target suitable for therapeutic antibody development

2008

Abstract Purpose: Antibody-based cancer therapies have emerged as the most promising therapeutics in oncology. The purpose of this study was to discover novel targets for therapeutic antibodies in solid cancer. Experimental Design: We combined data mining and wet-bench experiments to identify strictly gastrocyte lineage–specific cell surface molecules and to validate them as therapeutic antibody targets. Results: We identified isoform 2 of the tight junction molecule claudin-18 (CLDN18.2) as a highly selective cell lineage marker. Its expression in normal tissues is strictly confined to differentiated epithelial cells of the gastric mucosa, but it is absent from the gastric stem cell zone. …

Cancer ResearchPathologymedicine.medical_specialtymicemedicine.drug_classMolecular Sequence DataGene ExpressionBiologyMonoclonal antibodyMalignant transformationAntigenmedicineProtein IsoformsAnimalsHumansNeoplasms Glandular and EpithelialMembrane Proteins/geneticsAntibodies Monoclonal/immunologyProtein Isoforms/immunologyBase SequenceReverse Transcriptase Polymerase Chain ReactionNeoplasms Glandular and Epithelial/drug therapyAntibodies MonoclonalImmunotherapy ActiveMembrane ProteinsCancermedicine.diseaseFlow CytometryImmunohistochemistryImmunotherapy Active/methodsOncologyCancer cellClaudinsbiology.proteinCancer researchImmunohistochemistryAntibodyStem cell
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