Search results for "P21"

showing 10 items of 131 documents

A subset of flavaglines inhibits KRAS nanoclustering and activation.

2020

The RAS oncogenes are frequently mutated in human cancers and among the three isoforms (KRAS, HRAS and NRAS), KRAS is the most frequently mutated oncogene. Here, we demonstrate that a subset of flavaglines, a class of natural anti-tumour drugs and chemical ligands of prohibitins, inhibit RAS GTP loading and oncogene activation in cells at nanomolar concentrations. Treatment with rocaglamide, the first discovered flavagline, inhibited the nanoclustering of KRAS, but not HRAS and NRAS, at specific phospholipid-enriched plasma membrane domains. We further demonstrate that plasma membrane-associated prohibitins directly interact with KRAS, phosphatidylserine and phosphatidic acid, and these int…

:Bioengineering [Engineering]Neuroblastoma RAS viral oncogene homologGene isoformLung NeoplasmsGTP'[SDV]Life Sciences [q-bio]AucunBiology: Biochemistry biophysics & molecular biology [F05] [Life sciences]medicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRocaglamideCarcinoma Non-Small-Cell LungmedicineKRASHumansdrug therapy;geneticsgeneticsHRASProhibitin: Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant]neoplasmsComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesOncogeneLipid nanoclusterOncogenesCell Biologydigestive system diseases3. Good healthrespiratory tract diseasesPhospholipidchemistry030220 oncology & carcinogenesisMutationCancer researchKRASFlavaglineRocaglamideProhibitinSignal Transduction
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TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

2006

The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutatio…

AdenomaAdenomaGenotypePhysiologyClinical BiochemistryBiologymedicine.disease_causeMethylationEpigenesis GeneticProto-Oncogene Proteins p21(ras)GenotypemedicineCarcinomaHumansEpigeneticsTP53GeneCyclin-Dependent Kinase Inhibitor p16Base SequenceSingle-strand conformation polymorphismCell BiologyMethylationmedicine.diseaseMolecular biologyCell Transformation NeoplasticMutationDisease ProgressionTumor Suppressor Protein p53Carcinogenesis
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Expression of cell-cycle regulatory proteins cyclin D1, cyclin E, and their inhibitor p21 WAF1/CIP1 in gastric cancer.

1999

The expression and prognostic role of cyclin D1, cyclin E, and p21 (WAF1/CIP1) were immunohistochemically investigated in 413 curatively resected gastric carcinomas. p21 was expressed in 65.4 per cent (n=270), cyclin D1 in 23.7 per cent (n=98), and cyclin E in 13.6 per cent ( n=56) of the tumours. The expression of p21, cyclin D1, and cyclin E was positively associated with the papillary or tubular type of the WHO classification, as well as with the intestinal type according to the Lauren classification. No significant correlation could be found between the expression of p21, cyclin D1 and cyclin E and the parameters pT category, lymph node involvement, and blood vessel and lymphatic vessel…

AdultCyclin-Dependent Kinase Inhibitor p21MaleCyclin ECyclin DCyclin BBiologyPathology and Forensic MedicineImmunoenzyme TechniquesCyclin D1Stomach NeoplasmsCyclinsCyclin EmedicineBiomarkers TumorHumansCyclin D1Lymph nodeCyclinAgedAged 80 and overCancerCell cycleMiddle Agedmedicine.diseasePrognosisNeoplasm ProteinsSurvival Ratemedicine.anatomical_structureGastric Mucosabiology.proteinCancer researchFemaleFollow-Up StudiesThe Journal of pathology
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MDM2 and CDKN1A gene polymorphisms and risk of Kaposi's sarcoma in African and Caucasian patients

2010

A single-nucleotide polymorphism in the MDM2 promoter (SNP309; rs2279744) causes elevated transcription of this major negative regulator of p53 in several cancer types. We investigated MDM2 SNP309 and CDKN1A (p21/Waf1/Cip1) codon 31 (rs1801270) polymorphisms in 86 cases of cutaneous Kaposi's sarcoma (KS) from African and Caucasian patients, and 210 healthy controls. A significant increase of the MDM2 SNP309 T/G genotype was observed among classic KS cases (odds ratio 2.38, 95% confidence interval 1.0-5.5). Frequencies of CDKN1A codon 31 genotypes were not significantly different between cases and controls. The results suggest that the MDM2 SNP309 G allele may act as a susceptibility gene fo…

AdultCyclin-Dependent Kinase Inhibitor p21MaleGenotypeHealth Toxicology and MutagenesisClinical BiochemistryBlack PeopleBiologyPolymorphism Single NucleotideBiochemistryWhite PeopleYoung AdultGene FrequencyRisk FactorsGenotypemedicineHumansGenetic Predisposition to DiseaseAlleleYoung adultSarcoma KaposiKaposi's sarcomaAllele frequencyAgedAged 80 and overProto-Oncogene Proteins c-mdm2Odds ratioMiddle Agedmedicine.diseaseConfidence intervalImmunologyCancer researchFemaleSarcomaTumor Suppressor Protein p53
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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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Immunohistochemical expression of p21 in normal tissues of salivary gland, pleomorphic adenoma and carcinoma ex pleomorphic adenoma (undifferentiated…

2009

Objective: Our study aimed to characterize alteration in the immunohistochemical expression of p21 in normal tissue of the salivary gland surrounding pleomorphic adenoma, the tumor cells of pleomorphic adenomas, and carcinoma arising in pleomorphic adenoma. Study design: A selected series of 29 cases of pleomorphic adenomas, and 27 cases of carcinoma ex-pleomorphic adenoma (undifferentiated and adenocarcinoma types) were examined. Results: The results showed that p21 expression was negative in the most components of normal tissue of the salivary gland surrounding pleomorphic adenoma, 24 cases out of 29 of the non tumour duct cells (82.8%), and 28 (96.6%) cases out of 29 of the acinar cells …

AdultCyclin-Dependent Kinase Inhibitor p21MalePathologymedicine.medical_specialtyAdenomaAdenoma PleomorphicAdenocarcinomaSalivary GlandsPleomorphic adenomaYoung AdultmedicineCarcinomaHumansGeneral DentistryAgedAged 80 and overSalivary glandbusiness.industrySalivary Gland Pleomorphic AdenomaMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseSalivary Gland NeoplasmsImmunohistochemistrydigestive system diseasesCarcinoma ex pleomorphic adenomamedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASAdenocarcinomaImmunohistochemistrySurgeryFemalebusiness
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Phenotypic analysis of individuals with Costello syndrome due to HRAS p.G13C.

2011

Costello syndrome is characterized by severe failure-to-thrive, short stature, cardiac abnormalities (heart defects, tachyarrhythmia, and hypertrophic cardiomyopathy (HCM)), distinctive facial features, a predisposition to papillomata and malignant tumors, postnatal cerebellar overgrowth resulting in Chiari 1 malformation, and cognitive disabilities. De novo germline mutations in the proto-oncogene HRAS cause Costello syndrome. Most mutations affect the glycine residues in position 12 or 13, and more than 80% of patients share p.G12S. To test the hypothesis that subtle genotype-phenotype differences exist, we report the first cohort comparison between 12 Costello syndrome individuals with p…

AdultHeart Defects CongenitalMalemedicine.medical_specialtyAdolescentrasopathy.RASopathyShort statureProto-Oncogene MasArticleProto-Oncogene Proteins p21(ras)Young AdultGermline mutationSettore MED/38 - Pediatria Generale E SpecialisticaCostello syndromePregnancyInternal medicineNeoplasmsGeneticsMedicineHumansHRASChildGenetics (clinical)business.industryloose anagen hairCostello SyndromeMacrocephalyHypertrophic cardiomyopathyBrainInfantgenotype–phenotype correlationmedicine.diseaseDermatologyMagnetic Resonance ImagingMusculoskeletal AbnormalitiesEndocrinologyPhenotypeChild PreschoolFaceMutationFemalemedicine.symptombusinessMultifocal atrial tachycardiaAmerican journal of medical genetics. Part A
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Relation of early tumor shrinkage (ETS) observed in first‐line treatment to efficacy parameters of subsequent treatment in FIRE‐3 (AIOKRK0306)

2016

We explored the association of early tumor shrinkage (ETS) and non-ETS with efficacy of first-line and consecutive second-line treatment in patients with KRAS wild-type metastatic colorectal cancer treated in FIRE-3. Assessment of tumor shrinkage was based on the sum of longest diameters of target lesions, evaluated after 6 weeks of treatment. Shrinkage was classified as ETS (shrinkage by ≥ 20%), mETS (shrinkage by 0 to20%), mPD (minor progression0 to20%) and PD (progression ≥20%). Overall survival (OS) was 33.2 (95% CI 28.0-38.4) months in ETS patients, while non-ETS was associated with less favorable outcome (mETS 24.0 (95% CI 21.2-26.9) months, mPD 19.0 (95% CI 13.0-25.0) months, PD 12.8…

AdultMale0301 basic medicineCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancerLeucovorinCetuximabKaplan-Meier Estimatemedicine.disease_causeGastroenterologyDisease-Free SurvivalProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAgedShrinkageCetuximabbusiness.industryRemission InductionTumor shrinkageMiddle Agedmedicine.diseaseBevacizumabTreatment Outcome030104 developmental biologyOncologyFluorouracil030220 oncology & carcinogenesisFOLFIRICamptothecinFemaleFluorouracilKRASColorectal Neoplasmsbusinessmedicine.drugInternational Journal of Cancer
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High concordance of KRAS status between primary colorectal tumors and related metastatic sites: implications for clinical practice.

2008

Abstract Purpose. Several studies have suggested that KRAS somatic mutations may predict resistance to cetuximab- and panitumumab-based treatments in metastatic colorectal cancer (CRC) patients. Nevertheless, most experiences were conducted on samples from primaries. The aim of this study was to evaluate the grade of concordance in terms of KRAS status between primaries and related metastases. Patients and Methods. We analyzed KRAS codon 12 and 13 mutations from formalin-fixed sections of 107 CRC primaries and related metastases. Eight pairs were excluded from the analysis because of the low amount of tumor tissue in the available samples. The main characteristics were: 50 men, 49 women; me…

AdultMaleOncologyCancer Researchmedicine.medical_specialtyColorectal cancerConcordancemedicine.disease_causeProto-Oncogene Proteins p21(ras)Proto-Oncogene ProteinsInternal medicinemedicineHumansPanitumumabNeoplasm MetastasisneoplasmsAgedRetrospective StudiesAged 80 and overCetuximabbusiness.industryRetrospective cohort studyMiddle Agedmedicine.diseasedigestive system diseasesConfidence intervalErbB ReceptorsClinical PracticeGenes rasOncologyMutationras ProteinsFemaleKRASKRAScolorectal tumorsColorectal Neoplasmsbusinessmedicine.drug
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Refractory Acne and 21-Hydroxylase Deficiency in a Selected Group of Female Patients.

2009

<i>Background:</i> Excessive androgen production, suspected in women when acne is accompanied by hirsutism and menstrual irregularities, may be due to congenital adrenal hyperplasia. This inherited disorder of cortisol biosynthesis is caused in more than 90–95% of all cases by 21-hydroxylase deficiency (21-OHD). The steroid 21-hydroxylase gene <i>(CYP21)</i> has a high degree of variability. <i>Objective:</i> This study was conducted to evaluate <i>CYP21 </i>gene mutations in a selected group of women with papulopustular and comedonal acne refractory to treatment, irregular menses and hirsutism. <i>Methods:</i> 30 out of 61 women e…

Adultmedicine.medical_specialtyAdolescentDrug ResistancePhysiologyDermatologyAdrenocorticotropic hormoneYoung AdultSettore MED/38 - Pediatria Generale E SpecialisticaPapulopustularInternal medicineAcne VulgarismedicineHumansPoint MutationCongenital adrenal hyperplasiaGenetic TestingRefractory acne Excessive androgen production Non-classical 21-hydroxylase deficiency CYP21 gene mutations.AcnehirsutismAdrenal Hyperplasia Congenitalmedicine.diagnostic_testbiologybusiness.industry17-alpha-HydroxyprogesteroneACTH stimulation test21-Hydroxylasemedicine.diseasePolycystic ovaryEndocrinologybiology.proteinFemaleSteroid 21-HydroxylaseHyperandrogenismbusinessPolycystic Ovary Syndrome
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