Search results for "PTEN phosphohydrolase"

showing 10 items of 41 documents

Response to Stanich et al.: Correspondence regarding-PTEN hamartoma tumor syndromes in childhood-Description of two cases and a proposal for follow-u…

2014

The follow-up protocol, which we describe in this study can serve as a practical proposal for clinicians, and as a basis for future studies. We strongly urge the clinician to start an early surveillance of the gastrointestinal tract including regular endoscopy. The main management goals in PHTS patients are to detect colon cancer early, and to prevent polyp-related complications (bowel obstruction from intussusception). The presence of multiple nonmalignant polyps in patients with PTEN mutations may complicate noninvasive methods of colon evaluation [Tan et al., 2012]. In addition, there is a high variability in severity of polyps progression, and the malignant potential of these lesions is…

Oncologymedicine.medical_specialtybiologybusiness.industryMedicine (all)PTEN Phosphohydrolasemedicine.diseaseptenGeneticInternal medicineGeneticsmedicinebiology.proteinHamartomaPTENHumansFemalebusinessHamartoma Syndrome MultipleGenetics (clinical)Human
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Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases.

2017

Natural products or nutraceuticals promote anti-aging, anti-cancer and other health-enhancing effects. A key target of the effects of natural products may be the regulation of the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway. This review will focus on the effects of curcumin (CUR), berberine (BBR) and resveratrol (RES), on the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway, with a special focus on GSK-3. These natural products may regulate the pathway by multiple mechanisms including: reactive oxygen species (ROS), cytokine receptors, mirco-RNAs (miRs) and many others. CUR is present the root of turmeric (Curcuma longa). CUR is used in the treatment of many disorders, especially in those involving inflammatory p…

0301 basic medicineCancer ResearchCurcuminBerberinemTORC1PharmacologyResveratrolMechanistic Target of Rapamycin Complex 1Protective AgentsNatural product03 medical and health scienceschemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesBerberineGeneticNeoplasmsOsteoarthritisStilbenesGeneticsPTENHumansCurcumaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInflammationNatural productsbiologyBerberine; Curcumin; Natural products; ResveratrolPTEN PhosphohydrolaseNeurodegenerative Diseasesbiology.organism_classification030104 developmental biologyBiochemistrychemistryGene Expression RegulationCardiovascular DiseasesResveratrolbiology.proteinCurcuminMolecular MedicineProto-Oncogene Proteins c-aktSignal Transduction
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Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cas…

MAPK/ERK pathwayPremature agingMAP Kinase Signaling SystemTargeted Therapy Therapy Resistance Mutations Raf Akt PI3K mTORMtorReviewsPi3kPI3KReceptor tyrosine kinaseAkt; Mtor; Mutations; Pi3k; Raf; Targeted therapy; Therapy resistance;Targeted therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineAnimalsHumansPTENExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbiologyChemistryTOR Serine-Threonine KinasesAktTherapy resistancePTEN PhosphohydrolaseTargeted TherapyTherapy ResistanceRafProtein phosphatase 2MAP Kinase Kinase Kinases3. Good healthCell biologyOncology030220 oncology & carcinogenesisMutationras ProteinsmTORCancer researchbiology.proteinraf KinasesMitogen-Activated Protein KinasesSignal transductionProto-Oncogene Proteins c-aktMutationsSignal TransductionOncotarget
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The dark side of the moon: The PI3K/PTEN/AKT pathway in colorectal carcinoma

2009

Wild-type KRAS status is required but not sufficient to confer sensitivity to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) in colorectal cancer patients. As a consequence, one of the major challenges is to identify, in non-mutant KRAS patients, other markers that can predict lack of response to this therapy. Small series have investigated the clinical effect of PIK3CA mutations on resistance to anti-EGFR mAbs and discrepant results have been observed. Furthermore, PTEN loss in metastases may be predictive of resistance to anti-EGFR mAbs, even if PTEN determination is far from an immediate clinical application. The introduction of modulators of the PI3K/AKT/mTOR …

PTENCancer ResearchClass I Phosphatidylinositol 3-KinasesPrognosiSettore MED/06 - Oncologia MedicaColorectal cancerCetuximabColorectal NeoplasmPhosphoinositide 3-kinasemedicine.disease_causePhosphatidylinositol 3-KinasesAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineHumansPTENPanitumumabEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayClass I Phosphatidylinositol 3-KinaseAntineoplastic Combined Chemotherapy ProtocolbiologyCetuximabAKTMTORPanitumumabPTEN PhosphohydrolaseAntibodies MonoclonalGeneral MedicinePrognosismedicine.diseaseErbB ReceptorsOncologyMutationbiology.proteinCancer researchReceptor Epidermal Growth FactorKRASPhosphatidylinositol 3-KinaseColorectal NeoplasmsProto-Oncogene Proteins c-aktHumanSignal Transductionmedicine.drug
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PI3K pathway mutations and PTEN levels in primary and metastatic breast cancer.

2011

Abstract The purpose of this work was to determine whether there are differences in PIK3CA mutation status and PTEN protein expression between primary and matched metastatic breast tumors as this could influence patient management. Paraffin sections of 50 μm were used for DNA extraction and slides of 3 μm for immunohistochemistry (IHC) and FISH. Estrogen receptor, progesterone receptor, and HER2 IHC were repeated in a central laboratory for both primary tumors and metastases. PTEN levels were assessed by IHC and phosphoinositide 3-kinase (PI3K) pathway mutations were detected by a mass spectroscopy–based approach. Median age was 48 years (range: 30–83 years). Tumor subtype included 72% horm…

AdultCancer Researchmedicine.medical_specialtyClass I Phosphatidylinositol 3-KinasesReceptor ErbB-2Breast Neoplasmsmedicine.disease_causeArticleMetastasisMetastasisPhosphatidylinositol 3-KinasesBreast cancerInternal medicineBreast CancermedicinePTENHumansPTEN lossReceptorneoplasmsPI3K/AKT/mTOR pathwayAgedAged 80 and overMutationbiologyPTEN PhosphohydrolaseMiddle Agedmedicine.diseaseMetastatic breast cancerEndocrinologyOncologyReceptors EstrogenMutationbiology.proteinCancer researchImmunohistochemistryFemalePIK3CA mutationsReceptors ProgesteroneSignal TransductionMolecular cancer therapeutics
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miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Line…

2020

Gastric cancer (GC) is one of the most common and lethal gastrointestinal malignancies worldwide. Many studies have shown that development of GC and other malignancies is mainly driven by alterations of cellular signaling pathways. MicroRNAs (miRNAs) are small noncoding molecules that function as tumor-suppressors or oncogenes, playing an essential role in a variety of fundamental biological processes. In order to understand the functional relevance of miRNA dysregulation, studies analyzing their target genes are of major importance. Here, we chose to analyze two miRNAs, miR-20b and miR-451a, shown to be deregulated in many different malignancies, including GC. Deregulated expression of miR…

MaleCell signalingAntagonists & inhibitorsCaveolin 1ApoptosisCatalysisTuberous Sclerosis Complex 1 ProteinArticleInorganic Chemistrylcsh:ChemistryMicePhosphatidylinositol 3-KinasesStomach NeoplasmsCell Line TumormicroRNAPTENAnimalsHumans616.33-006.6 [udc]Physical and Theoretical ChemistryMolecular BiologyProtein kinase Blcsh:QH301-705.5SpectroscopyPI3K/AKT/mTOR pathwaybiologyTOR Serine-Threonine Kinasesgastric cancerOrganic ChemistryPTEN PhosphohydrolaseAntagomirsGeneral MedicineStomach neoplasms ; genetics ; MicroRNAs ; genetics ; Phosphoinositide-3 Kinase Inhibitors ; Phosphatidylinositol 3-Kinase ; metabolism ; Proto-Oncogene Proteins c-akt ; antagonists&inhibitors ; Proto-Oncogene Proteins c-akt ; metabolism ; TOR Serine-Threonine Kinases ; antagonists&inhibitors ; TOR Serine-Threonine Kinases ; metabolism ; Signal transduction ; drug effects ; Disease models animal ; MicemiR-451aComputer Science ApplicationsmicroRNAsDisease Models Animallcsh:Biology (General)lcsh:QD1-999biology.proteinCancer researchFemalemiR-20bSignal transductionCarrier ProteinsProto-Oncogene Proteins c-aktTXNIPSignal TransductionPI3K/AKT/mTOR signaling pathwayInternational Journal of Molecular Sciences
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Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways.

2011

Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for ther…

MAPK/ERK pathwayPTENTumor suppressor genekinase inhibitorPhysiologymedicine.medical_treatmentClinical Biochemistrygrowth factor receptorAntineoplastic AgentsDrug resistancePharmacologyBiologyTargeted therapy03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptormedicinePTENAnimalsHumansExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesTOR Serine-Threonine KinasesPTEN PhosphohydrolaseCell BiologyMAP Kinase Kinase Kinases3. Good healthErbB ReceptorsDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationCancer researchbiology.proteinraf KinasesProto-Oncogene Proteins c-aktDrug resistance therapeutic sensitivity targeted therapy RAF ERKACUTE MYELOID LEUKAEMIASignal TransductionJournal of cellular physiology
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Bone morphogenetic protein 4 induces differentiation of colorectal cancer stem cells and increases their response to chemotherapy in mice.

2010

BACKGROUND & AIMS: The limited clinical response observed in many patients with colorectal cancer may be related to the presence of chemoresistant colorectal can- cer stem cells (CRC-SCs). Bone morphogenetic protein 4 (BMP4) promotes the differentiation of normal colonic stem cells. We investigated whether BMP4 might be used to induce differentiation of CRC-SCs and for therapeutic purposes. METHODS: CRC-SCs were isolated from 25 tumor samples based on expression of CD133 or using a selection culture medium. BMP4 expression and activity on CRC-SCs were evaluated in vitro; progeny of the stem cells were evaluated by immunofluorescence, immuno- blot, and flow cytometry analyses. The potential …

MaleOrganoplatinum CompoundsCellular differentiationDrug ResistanceApoptosisBone Morphogenetic Protein 4Colon Cancer; Drug Resistance; Neoplasia; Tumor Resistance to Chemotherapy; AC133 Antigen; Adenomatous Polyposis Coli; Aged; Aged 80 and over; Animals; Antigens CD; Antineoplastic Agents; Apoptosis; Bone Morphogenetic Protein 4; Cell Differentiation; Cells Cultured; Colorectal Neoplasms; Female; Fluorouracil; Glycoproteins; Humans; Male; Mice; Microsatellite Instability; Middle Aged; Mutation; Neoplastic Stem Cells; Organoplatinum Compounds; PTEN Phosphohydrolase; Peptides; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Smad4 Protein; GastroenterologyMice80 and overBone morphogenetic protein receptorAC133 AntigenCells CulturedSmad4 ProteinAged 80 and overCulturedColon Cancerintegumentary systemGastroenterologyCell DifferentiationBMP4 colon stem cellsMiddle AgedCDOxaliplatinTumor Resistance to ChemotherapyBone morphogenetic protein 4Adenomatous Polyposis Coliembryonic structuresNeoplastic Stem CellsFemaleMicrosatellite InstabilityFluorouracilStem cellColorectal Neoplasmsanimal structuresCellsAntineoplastic AgentsBiologyBone morphogenetic proteinSettore MED/04 - PATOLOGIA GENERALECancer stem cellAntigens CDPTENAnimalsHumansAntigensneoplasmsPI3K/AKT/mTOR pathwayAgedGlycoproteinsNeoplasiaHepatologyPTEN Phosphohydrolasedigestive system diseasesMutationCancer researchbiology.proteinPhosphatidylinositol 3-KinasePeptidesProto-Oncogene Proteins c-aktGastroenterology
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Humoral immune responses of lung cancer patients against the Transmembrane Phosphatase with TEnsin homology (TPTE).

2015

Abstract Objective The cancer/testis (C/T) antigen Transmembrane Phosphatase with TEnsin homology (TPTE) is aberrantly expressed in many tumors including lung cancer. In the present study, we analyzed TPTE-auto-antibodies in lung cancer patients. Methods Using a crude-lysate ELISA, we analyzed a large cohort of 307 sera from lung cancer patients and 47 healthy donors for TPTE-specific autoantibodies. Sero-reactivity was correlated with clinical parameters and patients’ survival. Results TPTE-specific antibodies were detected in 41 of 307 (13.4%) sera from lung cancer patients. Based on an optimal cut-off value calculated by ROC curve analysis sensitivity for diagnosing lung cancer was 52% a…

Pulmonary and Respiratory MedicineOncologyMaleCancer Researchmedicine.medical_specialtyPathologyLung NeoplasmsAntibodies NeoplasmImmune systemAntigenAntigens NeoplasmInternal medicineTensinsmedicineTensinHumansLung cancerAutoantibodiesbiologybusiness.industryMicrofilament ProteinsAutoantibodyPTEN PhosphohydrolaseMembrane ProteinsMiddle Agedmedicine.diseasePrognosisImmunity HumoralOncologybiology.proteinCancer/testis antigensFemaleNY-ESO-1AntibodybusinessLung cancer (Amsterdam, Netherlands)
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Binding of PTEN to specific PDZ domains contributes to PTEN protein stability and phosphorylation by microtubule-associated serine/threonine kinases

2005

The tumor suppressor phosphatase PTEN is a key regulator of cell growth and apoptosis that interacts with PDZ domains from regulatory proteins, including MAGI-1/2/3, hDlg, and MAST205. Here we identified novel PTEN-binding PDZ domains within the MAST205-related proteins, syntrophin-associated serine/threonine kinase and MAST3, characterized the regions of PTEN involved in its interaction with distinctive PDZ domains, and analyzed the functional consequences on PTEN of PDZ domain binding. Using a panel of PTEN mutations, as well as PTEN chimeras containing distinct domains of the related protein TPTE, we found that the PTP and C2 domains of PTEN do not affect PDZ domain binding and that the …

Tumor Suppressor Proteins/chemistry/ metabolismTime FactorsAmino Acid MotifsPlasma protein bindingBiochemistryMicrotubulesSerineDiscs Large Homolog 1 ProteinProtein structureSaccharomyces cerevisiae/metabolismPhosphorylationGlutathione Transferaseddc:616Nucleoside-Phosphate Kinase/metabolismbiologyChemistryDystrophin-Associated Proteins/ chemistrySignal transducing adaptor proteinProtein-Serine-Threonine Kinases/metabolismRecombinant Fusion Proteins/chemistryGuanylate KinaseCell biologyCOS CellsMicrotubule-Associated Proteins/metabolismPhosphorylationProteins/metabolismGlutathione Transferase/metabolismMicrotubule-Associated ProteinsMicrotubules/ metabolismPlasmidsProtein BindingCèl·lulesRecombinant Fusion ProteinsPDZ domainSaccharomyces cerevisiaeProtein Serine-Threonine KinasesTransfectionModels BiologicalTwo-Hybrid System TechniquesDiscs Large Homolog 1 ProteinPTENAnimalsHumansImmunoprecipitationProteïnes supressores de tumorsMolecular BiologyAdaptor Proteins Signal TransducingTumor Suppressor ProteinsPTEN PhosphohydrolaseProteinsMembrane ProteinsCell BiologyPlasmids/metabolismPhosphoric Monoester HydrolasesProtein Structure TertiaryDystrophin-Associated ProteinsMutationCancer researchbiology.proteinNucleoside-Phosphate KinaseCarrier ProteinsGuanylate KinasesPhosphoric Monoester Hydrolases/chemistry/ metabolism
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