Search results for "cell cycle."

showing 10 items of 803 documents

Expression of serologically identified tumor antigens in acute leukemias.

2003

Cancer/testis antigens (CTA) are an expanding family of immunogenic proteins selectively expressed in human neoplasms. As little is known about the expression of serologically identified CTA in leukemias so far, we investigated the expression of 5 CT genes (SSX-1, HOM-MEL-40/SSX-2, HOM-TES-14/SCP-1, SCP-3 and NY-ESO-1) in leukemic blood samples obtained from patients with either acute lymphatic leukemias (ALL) or myelocytic leukemia (AML). RT-PCR-analyses showed no expression of any of the CT-genes in the leukemia samples of 19 patients with AML, whereas frequent expression was found in ALL. In the 17 ALL cases studied, SCP3a, SSX-1, HOM-MEL-40/SXX-2 and HOM-TES-14/SCP-1 were expressed in 4…

MaleCancer ResearchCell Cycle ProteinsSerologyAntigenTesticular NeoplasmsAntigens Neoplasmhemic and lymphatic diseasesBiomarkers TumorMedicineHumansRNA MessengerGeneDNA Primersbusiness.industryGene Expression Regulation LeukemicReverse Transcriptase Polymerase Chain ReactionCancerMembrane ProteinsNuclear ProteinsProteinsHematologyPrecursor Cell Lymphoblastic Leukemia-Lymphomamedicine.diseaseNeoplasm ProteinsDNA-Binding ProteinsRepressor ProteinsLeukemiaLeukemia Myeloid AcuteLymphatic systemOncologyImmunologyCancer/testis antigensMyelocytic leukemiabusinessLeukemia research
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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Chronic administration of green tea extract to TRAMP mice induces the collapse of Golgi apparatus in prostate secretory cells and results in alterati…

2011

Considering its long latency, prostate cancer (PCa) represents an ideal target for chemoprevention strategies. Green tea extract (GTE) has been proved to be one of the most promising natural substances capable of inhibiting PCa progression in animal models (transgenic adenocarcinoma of mouse prostate), as well as in humans. However, the cellular targets of the GTE action are mostly unknown. The main objective of this work was to investigate whether the endoplasmic reticulum (ER) and the Golgi apparatus (GA), known to be actively involved in sensing stress stimuli and initiating and propagating cell death signalling, may represent the subcellular targets of GTE action. To this end, 42 TRAMP …

MaleCancer ResearchCellGolgi ApparatusMice TransgenicGreen tea extractAdenocarcinomaEndoplasmic ReticulumCatechinsymbols.namesakeMicegreen tea extract; chemoprevention; prostate cancer; clusterin; ultrastructure; transgenic adenocarcinoma of mouse prostate.medicineAnimalsClusterinbiologyTeaEndoplasmic reticulumProstatic NeoplasmsCell cycleGolgi apparatusCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureClusterinOncologyApoptosisgreen tea extract chemoprevention prostate cancer clusterin ultrastructure transgenic adenocarcinoma of mouse prostatesymbolsbiology.proteinProtein Processing Post-TranslationalTrampInternational journal of oncology
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Synergistic Antioncogenic Activity of Azacitidine and Curcumin in Myeloid Leukemia Cell Lines and Patient Samples.

2019

Background/aim Azacitidine (AZA) is a hypomethylating agent used in myeloid neoplasms, however, approximately half of patients show treatment failure or relapse. This in vitro study investigated the effect of the combination of AZA with the natural compound curcumin (CUR) in increasing its efficacy. Materials and methods We analyzed the effects of AZA plus CUR on proliferation, apoptosis, cell cycle and differentiation in myeloid leukemic cell lines (U-937, HL-60, K-562, and OCI-AML3) and bone marrow samples of patients. Results The results showed a synergy between AZA and CUR in all leukemic lines and in most leukemic samples, with a decrease in proliferation and an increase in apoptosis c…

MaleCancer ResearchMyeloidCurcuminAzacitidineAntineoplastic AgentsApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansAgedAged 80 and overbusiness.industryCell CycleMyeloid leukemiaCell DifferentiationDrug SynergismGeneral MedicineCell cyclemedicine.anatomical_structureOncologychemistryHypomethylating agentApoptosisLeukemia Myeloid030220 oncology & carcinogenesisMyelodysplastic SyndromesCancer researchCurcuminAzacitidineFemaleBone marrowbusinessmedicine.drugAnticancer research
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Bax mutation and overexpression inversely correlate with immature phenotype and prognosis of childhood germ cell tumors

2007

Primary childhood germ cell tumors (GCTs) represent a rare and heterogeneous group of tumors that varies in histologic differentiation, age of presentation and clinical outcome. In malignant neoplasms, apoptosis is a prognostic marker and a predictive factor of response to therapy. Therefore, the study of the expression and mutation of molecules involved in the regulation of apoptosis could be useful in order to both predict the clinical outcome and design self-tailored therapeutic approaches. We retrospectively analysed tissue samples of 54 childhood GCTs. The expression of p53 and BAX protein was assessed by immunohistochemistry (IHC). Moreover, we investigated the presence of mutations i…

MaleCancer ResearchPathologymedicine.medical_specialtyAdolescentBcl-2-associated X proteinmedicineHumansChildRetrospective Studiesbcl-2-Associated X ProteinOncogenebiologyImmunochemistryInfant NewbornCancerInfantGeneral MedicineCell cycleNeoplasms Germ Cell and Embryonalmedicine.diseaseGenes p53PrognosisMolecular medicinePhenotypeOncologyChild PreschoolMutationbiology.proteinImmunohistochemistryImmature teratomaFemaleGerm cell tumorsTumor Suppressor Protein p53
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Overexpression of cyclin D1 and interaction between p27Kip1 and tumour thickness predict lymph node metastases occurrence in lower lip squamous cell …

2005

We have attempted to identify those subgroups of patients most likely to develop lymph node metastases from squamous cell carcinoma of the lower lip (LLSSC). A total of 97 subjects, who did not undergo elective neck dissection, were recruited into the 60-month disease-free survival study. After univariate analysis, tumour size, histological grading, maximal thickness, perineural invasion and immunoreactivity to cyclin D1 and p27Kip1 proteins proved to be significant factors. Tests of the effect of interaction between p27Kip1 LI and tumour thickness yielded that the impact of tumour thickness on the risk of lymph node metastases was modified by the percentage of p27Kip1 positive cells. Subse…

MaleCancer ResearchPathologymedicine.medical_specialtyp27Kip1medicine.medical_treatmentPerineural invasionCell Cycle ProteinsSettore MED/08 - Anatomia PatologicaMetastasisLymph node metastasiCyclin D1Squamous cell carcinomaBiomarkers TumorCarcinomaHumansMedicineCyclin D1Lymph nodeTumour thickness.AgedAged 80 and overbusiness.industryTumor Suppressor ProteinsNeck dissectionMiddle AgedPrognosismedicine.diseaseImmunohistochemistryLymph node metastasis; Squamous cell carcinoma; Lower lip; Cyclin D1; p27Kip1; Tumour thickness.medicine.anatomical_structureOncologyEpidermoid carcinomaLymphatic MetastasisLip NeoplasmsLower lipCarcinoma Squamous CellRegression AnalysisImmunohistochemistryFemaleOral SurgerybusinessCyclin-Dependent Kinase Inhibitor p27Oral Oncology
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Pyrrolotetrazinones deazaanalogues of temozolomide induce apoptosis in Jurkat cell line: involvement of tubulin polymerization inhibition.

2009

Pyrrolotetrazinones are a new class of azolotetrazinones endowed with a high, remarkable antiproliferative activity in human tumor cultured cells. They hold the deaza skeleton of the antitumor drug temozolomide, although preliminary investigations indicated a different mechanism of action. To understand their mechanism(s) of action along with their target at molecular level, four derivatives were selected on the basis of their activity on a panel of human tumor cell lines and they were investigated in depth in a T leukemia cell line (Jurkat). Flow cytometric analysis of cell cycle after treatment with pyrrolotetrazinones has demonstrated that they were able to induce an arrest of the cell c…

MaleCancer ResearchProgrammed cell deathCarcinoma HepatocellularCell SurvivalCellGene ExpressionAntineoplastic AgentsApoptosisPhosphatidylserinesBiologyToxicologyJurkat cellsMicrotubulesMicrotubule polymerizationJurkat CellsMiceTubulinCell Line TumormedicineTemozolomideAnimalsHumansPharmacology (medical)Cell Proliferationbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialMice Inbred BALB CCaspase 3Cell CycleCell MembraneCell cycleSettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsCell biologyMitochondriaDacarbazinemedicine.anatomical_structureOncologyMechanism of actionBiochemistryProto-Oncogene Proteins c-bcl-2ApoptosisCell culturemedicine.symptomPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesPyrrolotetrazinoneCancer chemotherapy and pharmacology
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Reduced expression of Hugl-1, the human homologue of Drosophila tumour suppressor gene lgl, contributes to progression of colorectal cancer.

2005

The human gene, human giant larvae (Hugl-1/Llg1/Lgl1) has significant homology to the Drosophila tumour suppressor gene lethal(2)giant larvae (lgl). The lgl gene codes for a cortical cytoskeleton protein, Lgl, that binds Myosin II and is involved in maintaining cell polarity and epithelial integrity. The human protein, Hugl-1 contains several conserved functional domains found in Lgl, suggesting that these proteins may have closely related functions. Whether loss of Hugl expression plays a role in human tumorigenesis has so far not been extensively investigated. Thus, we evaluated tumour tissues from 94 patients undergoing surgery for colorectal cancer (CRC) for loss of Hugl-1 transcription…

MaleCancer ResearchTranscription Geneticmedicine.disease_causeCell MovementNeoplasmsGene expressionDrosophila ProteinsIntestinal MucosaCytoskeletonReverse Transcriptase Polymerase Chain ReactionCell CycleCell migrationCell DifferentiationMiddle AgedImmunohistochemistryGene Expression Regulation NeoplasticDrosophila melanogasterDisease ProgressionFemaleColorectal NeoplasmsAdenomaAdultTumor suppressor geneBlotting WesternGreen Fluorescent ProteinsDown-RegulationBiologyCell LineDownregulation and upregulationCell Line TumorGeneticsmedicineCell AdhesionAnimalsHumansCell adhesionMolecular BiologyGeneTumor Suppressor ProteinsCarcinomaProteinsProtein Structure TertiaryCytoskeletal ProteinsMicroscopy FluorescenceTumor progressionImmunologyCancer researchCaco-2 CellsCarcinogenesisOncogene
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Blood flow, oxygenation, metabolic and energetic status in different clonal subpopulations of a rat rhabdomyosarcoma.

1998

Differentiation of a tumor plays an important role in terms of biological aggressiveness. The question arises as to whether this is reflected in differences in the metabolic and energetic status of solid tumors. The aim of this study was to analyze the influence of clonal tumor cell differentiation on the microenvironment of rat rhabdomyosarcomas. Two distinct lines of a rhabdomyosarcoma (BA-HAN-1) with different histomorphological properties were used (line F1, co-existence of mononuclear stellate cells and multinuclear myotube-like giant tumor cells; G8, polygonal, mononuclear tumor cells). Solid tumors were grown s.c. on the hind food dorsum of Lewis rats. Tumor oxygenation was measured …

MaleCancer Researchmedicine.medical_specialtyPartial PressureCellular differentiationBiologyAdenosine TriphosphateInternal medicineRhabdomyosarcomaTumor Cells CulturedmedicineAnimalsGlycolysisLactic AcidRhabdomyosarcomaOncogeneTumor OxygenationCell cyclemedicine.diseaseRatsOxygenGlucoseEndocrinologyOncologyRats Inbred LewImmunologyHepatic stellate cellFemaleSarcomaEnergy MetabolismCell DivisionNeoplasm TransplantationInternational Journal of Oncology
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Effects of phenylbutyrate on proliferation and apoptosis in human prostate cancer cells in vitro and in vivo.

1999

Phenylbutyrate (PB) is a potent differentiating agent and currently under investigation for the treatment of prostate cancer (CaP) and other malignancies. We have studied the impact of PB in vitro and in vivo on differentiation, proliferation and apoptosis in the LNCaP and LuCaP 23.1 prostate cancer xenograft models. In vitro we found that i) PB increased PSA secretion/cell, ii) inhibited cell proliferation in a time- and dose-dependent manner resulting in a cell cycle arrest in G1-phase and iii) induced apoptosis at concentrations of 2.5 mM after 3 days of treatment. In PB treated animals tumor growth stabilized or regressed. Combination of castration and PB treatment had a synergistic ant…

MaleCancer Researchmedicine.medical_specialtyProgrammed cell deathTransplantation HeterologousMice NudeAntineoplastic AgentsApoptosisBiologyPhenylbutyrateMiceProstate cancerIn vivoInternal medicineLNCaPTumor Cells CulturedmedicineAnimalsHumansMice Inbred BALB CCell growthCell CycleProstatic NeoplasmsCancerCell Differentiationmedicine.diseasePhenylbutyratesDisease Models AnimalEndocrinologyOncologyCancer cellAndrogensCancer researchCell DivisionNeoplasm TransplantationInternational Journal of Oncology
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