Search results for " must"

showing 10 items of 65 documents

Molecular aspects of carcinogenesis. Part B

1989

Nitrogen mustards represent a major group of alkylating agents that are used in the chemotherapy of cancer. It is commonly accepted that they exert their cytotoxic effects by their ability to produce interstrand crosslinks in DNA. The main target site of the two identical alkylating moieties is the N-7 position of guanine. By a Maxam-Gilbert-type reaction it is possible to identify "hot spots" for alkylation by nitrogen mustards. Analysis of data obtained reveal the importance of the DNA context for efficient alkylation. For most of~ the compounds the highest reactivity is observed ila regions of G clusters, while in the neighbourhood of cytosine residues alkylation is reduced. As a consequ…

Cancer ResearchGuanineStereochemistrySubstituentGeneral MedicineAlkylationDNA sequencingchemistry.chemical_compoundUracil MustardQuinacrine MustardOncologychemistryCytosineDNAJournal of Cancer Research and Clinical Oncology
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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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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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Induction of DNA breaks and apoptosis in crosslink-hypersensitive V79 cells by the cytostatic drug beta-D-glucosyl-ifosfamide mustard.

2001

To study molecular aspects of cytotoxicity of the anticancer drug β-D-glucose-ifosfamide mustard we investigated the potential of the agent to induce apoptosis and DNA breakage. Since β-D-glucose-ifosfamide mustard generates DNA interstrand crosslinks, we used as an in vitro model system a pair of isogenic Chinese hamster V79 cells differing in their sensitivity to crosslinking agents. CL-V5B cells are dramatically more sensitive (30-fold based on D10 values) to the cytotoxic effects of β-D-glucose-ifosfamide mustard as compared to parental V79B cells. After 48 h of pulse-treatment with the agent, sensitive cells but not the resistant parental line undergo apoptosis and necrosis, with apopt…

Cancer ResearchProgrammed cell deathNecrosisDNA damageDNA repairAntineoplastic AgentsBiologychemistry.chemical_compoundCricetinaemedicineCytotoxic T cellAnimalsExperimental TherapeuticsIfosfamideDNA breaksCytotoxicityapoptosisDNAPhosphoramide MustardMolecular biologyNitrogen mustardEnzyme ActivationCross-Linking ReagentsGlucoseOncologyBiochemistrychemistryApoptosisCaspasescancer therapyPhosphoramide Mustardscyclophosphamidemedicine.symptomDNA DamageBritish journal of cancer
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Assessment of alterations in barrier functionality and induction of proinflammatory and cytotoxic effects after sulfur mustard exposure of an in vitr…

2007

Acute lung injury after sulfur mustard (SM) inhalation is characterized by massive, localized hemorrhage and alveolar edema, which implies severe disruption of the vascular and distal airway barrier. In this study, we tested a recently established in vitro coculture model of the alveolo-capillary barrier for its applicability to investigate acute toxic effects of SM at the human respiratory unit. The epithelial compartment of cocultures was exposed to varying concentrations of SM (0-1000 microM; t = 30 min). Following exposure, functional and structural barrier integrity of cocultures was monitored over a period of 24 h. A 50% reduction of transbilayer electrical resistance (TER) within 12-…

Cell SurvivalHealth Toxicology and MutagenesisDNA FragmentationBiologyLung injuryToxicologyProinflammatory cytokinechemistry.chemical_compoundIn vivoCell Line TumorMustard GasHumansTUNEL assayBlood-Air BarrierInterleukinSulfur mustardMolecular biologyCoculture TechniquesCapillariesPulmonary AlveolichemistryCell cultureImmunologyLiberationChemokinesInflammation MediatorsInhalation toxicology
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mdm2 mRNA expression is associated with survival in ovarian cancer

1997

Expression of mdm-2 mRNA was measured in 90 ovarian-cancer tissue specimens using the S1 nuclease assay, to investigate a possible association between MDM2 expression and prognosis. mdm-2 mRNA expression was an independent prognostic factor for patients with primary ovarian cancer, FIGO (International Federation of Gynecology and Obstetrics) stages III and IV (n = 57), who all received chemotherapy with carboplatin or cisplatin and cyclophosphamide. Median survival time for patients (FIGO stages III and IV) with no detectable expression of mdm-2 mRNA (n = 14) was 171 days, as compared with 839 days for patients (n = 43) with detectable mdm-2 mRNA (p = 0.0194; log-rank test). However, no ass…

CisplatinCancer ResearchPathologymedicine.medical_specialtyChemotherapyendocrine system diseasesCyclophosphamidemedicine.medical_treatmentOvaryBiologymedicine.diseasefemale genital diseases and pregnancy complicationsCarboplatinNitrogen mustardchemistry.chemical_compoundmedicine.anatomical_structureOncologychemistryCarcinomamedicineCancer researchOvarian cancermedicine.drugInternational Journal of Cancer
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Combined Carboplatin plus Ifosfamide and Cisplatin in Patients with Advanced Ovarian Carcinoma. A Phase I–II Study

1998

Abstract Because of the relative lack of overlapping toxicity, carboplatin (PPL) and cisplatin (CDDP) can be easily combined for treatment of ovarian cancer to increase total platinum dose intensity. Ifosfamide (IFO), one of the most effective single agents in ovarian cancer, has a low hematological toxicity when administered in continuous infusion. From January 1991 to December 1993, 34 patients with advanced ovarian cancer, previously untreated with chemo- or radiotherapy, were enrolled in a phase I–II study with the aim of determining the maximum tolerated dose (MTD) of CDDP (on day 8 of a 28-day cycle) in combination with PPL (300 mg/m 2 on day 1) and IFO (4,000 mg/m 2 /24 h by continuo…

Cisplatinmedicine.medical_specialtyChemotherapyIfosfamidebusiness.industrymedicine.medical_treatmentUrologyObstetrics and GynecologyPhases of clinical researchmedicine.diseaseNitrogen mustardCarboplatinSurgerychemistry.chemical_compoundOncologychemistryToxicitymedicinebusinessOvarian cancermedicine.drugGynecologic Oncology
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Observations on the effects of cyclophosphamide, phosphoramide mustard and some activated oxazaphosphorines on murine L1210 leukemia.

1984

The L1210 tumor system was used in vitro and in vivo in comparative studies with activated cyclophosphamide analogs, cyclophosphamide and phosphoramide mustard. All the above compounds gave substantial cell kills (5 logs) of L1210 in vivo at doses that were non-toxic, but slight differences were noted. ASTA Z 7557 had a slight advantage in cure rate over cyclophosphamide when these drugs were given i.v. or i.p. to early tumor (i.p.). However, cyclophosphamide had the advantage in cure rate when drug administration was i.v. to advanced tumor. At equimolar concentrations in vitro ASTA Z 7557 was more cytotoxic than either phosphoramide mustard or acrolein. In vivo, the activated cyclophospham…

CyclophosphamideCell SurvivalPharmacologychemistry.chemical_compoundMiceFibrosisIn vivomedicineAnimalsPharmacology (medical)Clonogenic assayLeukemia L1210CyclophosphamideTumor Stem Cell AssayPharmacologyMice Inbred BALB CDose-Response Relationship Drugbusiness.industryAcroleinTumor Stem Cell Assaymedicine.diseasePhosphoramide MustardIn vitroOncologychemistryMice Inbred DBAPhosphoramide Mustardsbusinessmedicine.drugInvestigational new drugs
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Induction of DNA crosslinks and DNA strand lesions by cyclophosphamide after activation by cytochrome P450 2B1

1997

Cyclophosphamide requires metabolic activation by cytochrome P450 to exert its genotoxic effects. Therefore in vitro studies on its mechanism of action have been limited to the use of self-activating derivatives of cyclophosphamide or to hepatocytes as an activating system. In this study we used a cell line of Chinese hamster lung fibroblasts (V79 cells), genetically engineered to express active cytochrome P450 2B1 as the sole observable cytochrome P450 (SD1 cells). An increase in DNA strand lesions (SL: DNA single-strand breaks and alkali labile sites) was observed between 0.5 and 1.5 mM cyclophosphamide (24 h incubation) which could be classified as alkali labile sites using a modified al…

DNA RepairCyclophosphamideDNA repairDNA damageHealth Toxicology and MutagenesisHamsterBiologyTransfectionCell LineCricetulusCytochrome P-450 Enzyme SystemCricetinaeGeneticsmedicineAnimalsCyclophosphamideMolecular BiologyIncubationBiotransformationDose-Response Relationship Drug4-HydroxycyclophosphamideDNAPhosphoramide MustardBiochemistryCell culturePhosphoramide MustardsDNA Damagemedicine.drugMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Comparative genomics and proteomics of Helicobacter mustelae, an ulcerogenic and carcinogenic gastric pathogen

2010

Abstract Background Helicobacter mustelae causes gastritis, ulcers and gastric cancer in ferrets and other mustelids. H. mustelae remains the only helicobacter other than H. pylori that causes gastric ulceration and cancer in its natural host. To improve understanding of H. mustelae pathogenesis, and the ulcerogenic and carcinogenic potential of helicobacters in general, we sequenced the H. mustelae genome, and identified 425 expressed proteins in the envelope and cytosolic proteome. Results The H. mustelae genome lacks orthologs of major H. pylori virulence factors including CagA, VacA, BabA, SabA and OipA. However, it encodes ten autotransporter surface proteins, seven of which were detec…

DNA BacterialProteomicslcsh:QH426-470Proteomelcsh:BiotechnologyMolecular Sequence DataVirulenceCarcinogenicHelicobacter mustelaeProteomicsFN555004MicrobiologyUlcerogenic03 medical and health sciencesBacterial ProteinsHelicobacterlcsh:TP248.13-248.65medicineGeneticsCagAHelicobacterAmino Acid SequencePhylogeny030304 developmental biology0303 health sciencesComparative Genomic HybridizationbiologyHelicobacter pyloriVirulence030306 microbiologyCancerGene Expression Regulation BacterialGenomicsSequence Analysis DNAHelicobacter pylorimedicine.diseasebiology.organism_classificationdigestive system diseases3. Good healthlcsh:GeneticsProteomeGastritismedicine.symptomSequence AlignmentH. pyloriGenome BacterialBiotechnologyResearch ArticleBMC Genomics
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