Search results for "Cyclin-dependent kinase 4"

showing 10 items of 13 documents

Mechanisms of Raf-1 Kinase Inhibitor Protein Dysregulation in Triple-Negative Breast Cancers and Identification of Possible Novel Therapeutic Approac…

2014

Triple-negative breast cancers (TNBCs) are a heterogenous group of breast cancers characterized by poor prognosis because they are not amenable to targeted therapies. We have taken into account that altered expression of Raf-1 kinase inhibitor protein (RKIP), a tumor and metastasis suppressor and a promoter of drug-induced apoptosis, is frequent in TNBCs and may be involved in their aggressive biology. Interestingly, the analysis of the possible mechanisms of RKIP downregulation in TNBCs permits the identification and recapitulation of different possible approaches, including epigenetic modulation, e.g., by DNA demethylating agents or histone deacetylase inhibition, and NF-κB inhibition. Th…

Oncologymedicine.medical_specialtybiologybusiness.industryCyclin-dependent kinase 4Settore MED/06 - Oncologia MedicaInhibitor proteinBiochemistryEpigenetic therapy NF-κB inhibition Raf-1 kinase inhibitor protein triple-negative breast cancersInternal medicineRaf 1 kinaseGeneticsbiology.proteinCancer researchSettore BIO/14 - FarmacologiaMolecular MedicineMedicineIdentification (biology)businessTriple negativeEpigenetic therapyBiotechnology
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Docosahexaenoic acid inhibits cancer cell growth via p27Kip1, CDK2, ERK1/ERK2, and retinoblastoma phosphorylation

2006

Docosahexaenoic acid (DHA), a PUFA of the n-3 family, inhibited the growth of FM3A mouse mammary cancer cells by arresting their progression from the late-G(1) to the S phase of the cell cycle. DHA upregulated p27(Kip1) levels by inhibiting phosphorylation of mitogen-activated protein (MAP) kinases, i.e., ERK1/ERK2. Indeed, inhibition of ERK1/ERK2 phosphorylation by DHA, U0126 [chemical MAPK extracellularly signal-regulated kinase kinase (MEK) inhibitor], and MEK(SA) (cells expressing dominant negative constructs of MEK) resulted in the accumulation of p27(Kip1). MAP kinase (MAPK) inhibition by DHA did not increase p27(Kip1) mRNA levels. Rather, this fatty acid stabilized p27(Kip1) contents…

MAPK/ERK pathwayDocosahexaenoic AcidsMammary Neoplasms AnimalQD415-436fatty acidsenvironment and public healthBiochemistryMiceEndocrinologyCyclin-dependent kinaseCyclin EAnimalsRNA MessengerPhosphorylationCells CulturedCell ProliferationMAPK14biologyKinaseCyclin-dependent kinase 4Cyclin-Dependent Kinase 2Cyclin-dependent kinase 2Retinoblastomafood and beveragesCell BiologyUp-RegulationCell biologyenzymes and coenzymes (carbohydrates)cyclin-dependent kinaseCyclin-dependent kinase complexbiology.proteinPhosphorylationcell cyclelipids (amino acids peptides and proteins)Mitogen-Activated Protein KinasesCyclin-Dependent Kinase Inhibitor p27Journal of Lipid Research
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An increase in neural stem cells and olfactory bulb adult neurogenesis improves discrimination of highly similar odorants

2019

Adult neurogenesis is involved in cognitive performance but studies that manipulated this process to improve brain function are scarce. Here, we characterized a genetic mouse model in which neural stem cells (NSC) of the subventricular zone (SVZ) were temporarily expanded by conditional expression of the cell cycle regulators Cdk4/cyclinD1, thus increasing neurogenesis. We found that supernumerary neurons matured and integrated in the olfactory bulb similarly to physiologically generated newborn neurons displaying a correct expression of molecular markers, morphology and electrophysiological activity. Olfactory performance upon increased neurogenesis was unchanged when mice were tested on r…

MaleNeurogenesisSubventricular zoneMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyDiscrimination LearningMiceNeural Stem Cellsodor discriminationmedicineAnimalsCyclin D1News & ViewsMolecular Biologyneural stem cellsGeneral Immunology and MicrobiologyGeneral NeuroscienceNeurogenesisCyclin-Dependent Kinase 4Cell cycleOlfactory BulbNeural stem cellOlfactory bulbadult neurogenesisDisease Models AnimalElectrophysiologymedicine.anatomical_structurenervous systemOdorOdorantsNeuroscienceNeuroscienceAdult stem cellThe EMBO Journal
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A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma.

1995

A mutated cyclin-dependent kinase 4 (CDK4) was identified as a tumor-specific antigen recognized by HLA-A2. 1-restricted autologous cytolytic T lymphocytes (CTLs) in a human melanoma. The mutated CDK4 allele was present in autologous cultured melanoma cells and metastasis tissue, but not in the patient's lymphocytes. The mutation, an arginine-to-cysteine exchange at residue 24, was part of the CDK4 peptide recognized by CTLs and prevented binding of the CDK4 inhibitor p16INK4a, but not of p21 or of p27KIP1. The same mutation was found in one additional melanoma among 28 melanomas analyzed. These results suggest that mutation of CDK4 can create a tumor-specific antigen and can disrupt the ce…

Cyclin-Dependent Kinase Inhibitor p21Tumor suppressor geneMutantMolecular Sequence DataCell Cycle ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeTransfectionPolymerase Chain ReactionMetastasisCell LineAntigenCyclinsProto-Oncogene ProteinsHLA-A2 AntigenmedicineTumor Cells CulturedAnimalsHumansPoint MutationAmino Acid SequenceCloning MolecularneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15MutationMultidisciplinaryintegumentary systemBase SequenceMelanomaTumor Suppressor ProteinsCyclin-Dependent Kinase 4Cell cyclemedicine.diseaseCyclin-Dependent KinasesCytolysisCancer researchCarrier ProteinsMicrotubule-Associated ProteinsCyclin-Dependent Kinase Inhibitor p27T-Lymphocytes CytotoxicScience (New York, N.Y.)
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Calmodulin binds to p21(Cip1) and is involved in the regulation of its nuclear localization.

1999

p21(Cip1), first described as an inhibitor of cyclin-dependent kinases, has recently been shown to have a function in the formation of cyclin D-Cdk4 complexes and in their nuclear translocation. The dual behavior of p21(Cip1) may be due to its association with other proteins. Different evidence presented here indicate an in vitro and in vivo interaction of p21(Cip1) with calmodulin: 1) purified p21(Cip1) is able to bind to calmodulin-Sepharose in a Ca(2+)-dependent manner, and this binding is inhibited by the calmodulin-binding domain of calmodulin-dependent kinase II; 2) both molecules coimmunoprecipitate when extracted from cellular lysates; and 3) colocalization of calmodulin and p21(Cip…

Cyclin-Dependent Kinase Inhibitor p21CalmodulinMolecular Sequence DataBiologyBiochemistryCell LineCalmodulinIn vivoCyclinsProto-Oncogene ProteinsmedicineAnimalsCyclin D1Amino Acid SequencePhosphorylationMolecular BiologyCyclinCell NucleusSulfonamidesKinaseColocalizationCyclin-Dependent Kinase 4Cell BiologyImmunogold labellingPrecipitin TestsCyclin-Dependent KinasesCell biologyRatsEnzyme ActivationCell nucleusMicroscopy Electronmedicine.anatomical_structurebiology.proteinNuclear localization sequenceProtein BindingThe Journal of biological chemistry
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Involvement of protein kinases in the induction of NO synthase II in human DLD-1 cells

1998

Protein phosphorylation is involved in the induction of nitric oxide synthase II (NOS II, iNOS) in several types of animal cells. Here we have investigated the possible involvement of major protein kinases in the induction of NOS II expression in human DLD-1 cells. In DLD-1 cells, interferon-γ alone induced a submaximal NOS II expression; a cytokine mixture consisting of interferon-γ, tumour necrosis factor-α and interleukin-1β produced maximal NOS II induction. Activators of protein kinase A (forskolin, 8-dibutyryl-cyclic AMP), of protein kinase C (tetradecanoylphorbol-13-acetate), and of protein kinase G (8-bromo cyclic GMP) did not induce NOS II mRNA by themselves, nor did they alter NOS…

PharmacologybiologyMAP kinase kinase kinaseCyclin-dependent kinase 4Cyclin-dependent kinase 2biology.proteinCyclin-dependent kinase 9ASK1c-RafMitogen-activated protein kinase kinaseMolecular biologyMAP2K7British Journal of Pharmacology
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Abemaciclib: safety and effectiveness of a unique cyclin-dependent kinase inhibitor

2020

Introduction: The discovery and the clinical availability of novel cyclin-dependent kinases 4 and 6 inhibitors have profoundly changed the therapeutic scenario of metastatic hormone receptor-positive breast carcinoma. Among these inhibitors, abemaciclib can induce potent and sustained cell cycle arrest and immune system stimulation. Areas covered: This review summarizes the safety profile and clinical efficacy data on abemaciclib alone or in combination with aromatase inhibitors or fulvestrant in metastatic hormone receptor-positive breast carcinoma. The management of patients treated with abemaciclib is the object of this paper. Expert opinion: As shown in phase 2 and 3 clinical trials on …

safetyAminopyridinesBreast Neoplasms030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundabemaciclib breast cancer metastases hormonal receptors safetybreast cancer0302 clinical medicineBreast cancerCyclin-dependent kinaseAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansPharmacology (medical)metastasesskin and connective tissue diseasesFulvestrantProtein Kinase InhibitorsAbemaciclibbiologyAromatase Inhibitorsbusiness.industryKinasehormonal receptorsCyclin-Dependent Kinase 4Cell Cycle CheckpointsCyclin-Dependent Kinase 6General Medicinemedicine.diseaseAbemaciclibchemistry030220 oncology & carcinogenesisQuality of LifeCancer researchbiology.proteinBenzimidazolesFemalesense organsbusinessHormone
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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
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Phase 1/2 study of cyclin-dependent kinase (CDK)4/6 inhibitor palbociclib (PD-0332991) with bortezomib and dexamethasone in relapsed/refractory multi…

2015

This phase 1/2 study was the first to evaluate the safety and efficacy of the cyclin-dependent kinase (CDK) 4/6-specific inhibitor palbociclib (PD-0332991) in sequential combination with bortezomib and dexamethasone in relapsed/refractory multiple myeloma. The recommended phase 2 dose was palbociclib 100 mg orally once daily on days 1-12 of a 21-day cycle with bortezomib 1.0 mg/m2 (intravenous) and dexamethasone 20 mg (orally 30 min pre-bortezomib dosing) on days 8 and 11 (early G1 arrest) and days 15 and 18 (cell cycle resumed). Dose-limiting toxicities were primarily cytopenias; most other treatment-related adverse events were grade≤3. At a bortezomib dose lower than that in other combina…

AdultMaleCancer ResearchCombination therapyPyridinesKaplan-Meier EstimatePalbociclibPharmacologyDexamethasoneDrug Administration SchedulePiperazinesBortezomibRecurrenceCyclin-dependent kinaseAntineoplastic Combined Chemotherapy ProtocolsHumansMedicineMultiple myelomaDexamethasoneAgedNeoplasm StagingAged 80 and overbiologybusiness.industryBortezomibCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6HematologyMiddle AgedCell cyclemedicine.diseaseTreatment OutcomeOncologyDrug Resistance NeoplasmPharmacodynamicsRetreatmentbiology.proteinFemaleDrug MonitoringMultiple Myelomabusinessmedicine.drugLeukemia & Lymphoma
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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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