Search results for "Patched-1 Receptor"

showing 6 items of 6 documents

Microparticles harbouring Sonic hedgehog morphogen improve the vasculogenesis capacity of endothelial progenitor cells derived from myocardial infarc…

2019

Aims Endothelial progenitor cells (EPC) play a role in endothelium integrity maintenance and regeneration. Decreased numbers of EPC or their impaired function correlates with an increase in cardiovascular events. Thus, EPC are important predictors of cardiovascular mortality and morbidity. Microparticles carrying Sonic hedgehog (Shh) morphogen (MPShh+) trigger pro-angiogenic responses, both in endothelial cells and in ischaemic rodent models. Here, we propose that MPShh+ regulates EPC function, thus enhancing vasculogenesis, and correcting the defects in dysfunctional EPC obtained from acute myocardial infarction (AMI) patients. Methods and results The mechanisms underlying Shh pathway func…

0301 basic medicineEndotheliumNitric Oxide Synthase Type IIIPhysiologyAngiogenesis[SDV]Life Sciences [q-bio]Myocardial InfarctionMice NudeNeovascularization PhysiologicAcute myocardial infarction030204 cardiovascular system & hematologyMicroparticlesZinc Finger Protein GLI103 medical and health sciences0302 clinical medicineVasculogenesisCell-Derived MicroparticlesPhysiology (medical)Paracrine CommunicationVasculogenesismedicineAnimalsHumansHedgehog ProteinsProgenitor cellSonic hedgehogAngiogenic ProteinsCells CulturedComputingMilieux_MISCELLANEOUSEndothelial progenitor cellsbiologybusiness.industryNitric oxideSmoothened ReceptorHedgehog signaling pathwayPatched-1 ReceptorVascular endothelial growth factor A030104 developmental biologymedicine.anatomical_structureCase-Control StudiesKLF2embryonic structuresCancer researchbiology.proteincardiovascular systemCardiology and Cardiovascular MedicinebusinessSignal Transductioncirculatory and respiratory physiology
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PTCH-1 and MDM2 expression in ameloblastoma from a West African sub-population: implication for chemotherapeutics

2015

INTRODUCTION: ameloblastoma is a slow growing, painless odontogenic swelling which can attain sizes that result in severe deformities of the craniofacial complex. It is the most commonly encountered odontogenic tumor in Nigeria. Surgical intervention is currently the method of treatment; however identification of altered molecular pathways may inform chemotherapeutic potential. The Protein Patched homolog 1 (PTCH-1) is overexpressed in ameloblastoma. Also, mutation in the MDM2 gene can reduce the tumor suppressor function of p53 and promote ameloblastoma growth. No study however has characterized the molecular profile of African cases of ameloblastoma with a view to developing chemotherapeu…

AdultMalemdm2Pathologymedicine.medical_specialtyPopulationNigeriaPathology and Forensic MedicinePTCH-1 MdM2 ameloblastoma chemotherapeuticsameloblastomaptch-1HumansMedicineRadiology Nuclear Medicine and imagingDentistry (miscellaneous)ddc:610educationAmeloblastomaStellate reticulumProtein Patched Homolog 1education.field_of_studylcsh:R5-920biologybusiness.industryResearchlcsh:Public aspects of medicinechemotherapeuticsOdontogenic tumorProto-Oncogene Proteins c-mdm2lcsh:RA1-1270General Medicinemedicine.diseaseJaw NeoplasmsGene Expression Regulation NeoplasticPatched-1 ReceptorWest africanstomatognathic diseasesMutationMonoclonalCancer researchbiology.proteinMdm2FemaleSurgeryOral SurgeryAntibodybusinesslcsh:Medicine (General)The Pan African Medical Journal
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Wilms' tumor in patients with 9q22.3 microdeletion syndrome suggests a role for PTCH1 in nephroblastomas

2012

Nephroblastoma (Wilms' tumor; WT) is the most common renal tumor of childhood. To date, several genetic abnormalities predisposing to WT have been identified in rare overgrowth syndromes. Among them, abnormal methylation of the 11p15 region, GPC3 and DIS3L2 mutations, which are responsible for Beckwith-Wiedemann, Simpson-Golabi-Behmel and Perlman syndromes, respectively. However, the underlying cause of WT remains unknown in the majority of cases. We report three unrelated patients who presented with WT in addition to a constitutional 9q22.3 microdeletion and dysmorphic/overgrowth syndrome. The size of the deletions was variable (ie, from 1.7 to 8.9 Mb) but invariably encompassed the PTCH1 …

AdultPatched Receptorsmedicine.medical_specialtyPathologyPTCH1AdolescentNonsense mutationCNVShort ReportReceptors Cell SurfaceBiologymedicine.disease_causeWilms’ tumorWilms TumorFetal MacrosomiaSettore MED/38 - Pediatria Generale E SpecialisticaPregnancyInternal medicineGeneticsmedicineHumansPerlman syndromeChildovergrowthGenetics (clinical)MutationComparative Genomic HybridizationWilms' tumorPTCH1 GeneMicrodeletion syndromeFANCC nephroblastomamedicine.diseaseKidney NeoplasmsPatched-1 ReceptorEndocrinologyPTCH1Settore MED/03 - Genetica MedicaOvergrowth syndromeMutationFemaleChromosome DeletionChromosomes Human Pair 9Comparative genomic hybridization
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Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice

2009

Abstract Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors. We have previously shown that epigenetic silencing of the intact Ptch allele contributes to tumor formation in this model. Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers. A reduction of endogenous DNA methyltransferase1 (Dnmt1) activity significantly reduced tumor incidence in heterozygous Ptch knockout mice. A combined treatment with the Dnmt inhibitor 5-aza-2′deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prev…

DNA (Cytosine-5-)-Methyltransferase 1Patched ReceptorsPatchedCancer Researchmedicine.drug_classGene ExpressionDecitabineReceptors Cell SurfaceBiologyDecitabineHistone DeacetylasesHistonesMice03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsRhabdomyosarcomamedicineAnimalsDNA (Cytosine-5-)-MethyltransferasesGene SilencingMuscle SkeletalRhabdomyosarcoma030304 developmental biologyMedulloblastomaMice Inbred BALB C0303 health sciencesValproic AcidHistone deacetylase inhibitorCancerAcetylationDNA Methylationmedicine.disease3. Good healthHistone Deacetylase InhibitorsMice Inbred C57BLPatched-1 Receptorstomatognathic diseasesOncology030220 oncology & carcinogenesisAzacitidineCancer researchDNMT1Epigenetic therapyMedulloblastomamedicine.drugCancer Research
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Familial seborrhoeic keratosis associated with multiple 'pure reticulated acanthomas' and infundibulocystic basal cell carcinomas.

2017

Background A variety of genodermatoses with multiple cutaneous tumors with germline genetic alterations such as Gorlin syndrome with PTCH1 gene mutations have been described. Other cutaneous syndromes have been associated with somatic gene mutations, such as FGFR3 in familial seborrhoeic keratosis. Objective We describe the clinical, dermoscopic, and histopathological features of multiple cutaneous lesions, mostly infundibulocystic basal cell carcinomas and pure reticulated acanthomas, present in a family affected by familial seborrhoeic keratosis. In addition, we tested for possible germline alterations in the FGFR3 and PTCH1 genes. Methods Ten members of one family were clinically examine…

MalePathologymedicine.medical_specialtySkin NeoplasmsKeratosisDermoscopyDermatologyGene mutationBiologyGermline030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicinemedicineHumansReceptor Fibroblast Growth Factor Type 3Keratosis SeborrheicGerm-Line MutationAgedPolymorphism Geneticmedicine.diagnostic_testApocrinePTCH1 GeneMiddle Agedmedicine.diseaseDermatologyPedigreePatched-1 ReceptorPTCH1Carcinoma Basal Cell030220 oncology & carcinogenesisAcanthomaSkin biopsyFemaleAcanthoma
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Time-point and dosage of gene inactivation determine the tumor spectrum in conditional Ptch knockouts

2009

Mutations in Patched (PTCH) have been associated with tumors characteristic both for children [medulloblastoma (MB) and rhabdomyosarcoma (RMS)] and for elderly [basal cell carcinoma (BCC)]. The determinants of the variability in tumor onset and histology are unknown. We investigated the effects of the time-point and dosage of Ptch inactivation on tumor spectrum using conditional Ptch-knockout mice. Ptch heterozygosity induced prenatally resulted in the formation of RMS, which was accompanied by the silencing of the remaining wild-type Ptch allele. In contrast, RMS was observed neither after mono- nor biallelic postnatal deletion of Ptch. Postnatal biallelic deletion of Ptch led to BCC preca…

PatchedPatched ReceptorsCancer ResearchPathologymedicine.medical_specialtyAgingSkin NeoplasmsGene DosageReceptors Cell SurfaceBiologymedicine.disease_causeGene dosageGastrointestinal epitheliumLoss of heterozygosity03 medical and health sciencesMice0302 clinical medicineRhabdomyosarcomamedicineAnimalsGene SilencingRhabdomyosarcomaMuscle SkeletalGerm-Line MutationPeritoneal Neoplasms030304 developmental biologyGastrointestinal NeoplasmsMedulloblastomaMice Knockout0303 health sciencesMutationMuscle NeoplasmsCystsGeneral MedicinePTCH1 Genemedicine.disease3. Good healthPatched-1 Receptorstomatognathic diseasesCarcinoma Basal Cell030220 oncology & carcinogenesisMutationCancer researchPrecancerous ConditionsCarcinogenesis
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