Search results for "protein kinase inhibitors"

showing 10 items of 211 documents

Small molecule DNA-PK inhibitors as potential cancer therapy: a patent review (2010–present)

2021

Introduction: DNA-dependent protein kinase (DNA-PK) plays a crucial role in the repair of DSBs via non-homologous end joining (NHEJ). Several DNA-PK inhibitors are being investigated for potential anticancer treatment in clinical trials.Area covered: This review aims to give an overview of patents published since 2010 by analyzing the patent space and structure features of scaffolds used in those patents. It also discusses the recent clinical developments and provides perspectives on future challenges and directions in this field.Expert opinion: As a key component of the DNA damage response (DDR) pathway, DNA-PK appears to be a viable drug target for anticancer therapy. The clinical investi…

DNA damageCancer therapyDNA-Activated Protein Kinase01 natural sciencesPatents as Topic03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DevelopmentNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoveryCombination strategyAnimalsHumansMedicineProtein kinase AProtein Kinase InhibitorsPharmacologybusiness.industryGeneral MedicineSmall molecule0104 chemical sciences010404 medicinal & biomolecular chemistrychemistryAnticancer treatment030220 oncology & carcinogenesisPARP inhibitorCancer researchbusinessDNADNA DamageExpert Opinion on Therapeutic Patents
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Future perspectives in hepatocellular carcinoma.

2010

Hepatocellular carcinoma (HCC) is one of the most common and lethal malignancies worldwide. Due to late diagnosis and advanced underlying liver cirrhosis, only limited treatment options with marginal clinical benefits have been available in up to 70% of patients. However, major progress has been achieved with regard to surveillance, early diagnosis, and multimodal treatment approaches during the last years leading to an improvement in prognosis. Particularly, the increasing knowledge of molecular hepatocarcinogenesis today provides the opportunity for targeted therapy. The multikinase inhibitor sorafenib has broadened the therapeutic horizon for patients with advanced disease and is current…

SorafenibOncologyAblation Techniquesmedicine.medical_specialtyCarcinoma Hepatocellularmedicine.medical_treatmentLiver transplantationGastroenterologyTargeted therapyInternal medicinemedicineAdjuvant therapyCombined Modality TherapyHumansChemoembolization TherapeuticPrecision MedicineTranscatheter arterial chemoembolizationProtein Kinase InhibitorsHepatologybusiness.industryLiver NeoplasmsGastroenterologymedicine.diseaseCombined Modality TherapyFibrosisLiver TransplantationHepatocellular carcinomaPersonalized medicinebusinessmedicine.drugForecastingDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
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Differences among young adults, adults and elderly chronic myeloid leukemia patients

2014

Abstract BACKGROUND: The incidence of chronic myeloid leukemia (CML) increases with age, but it is unclear how the characteristics of the disease vary with age. In children, where CML is very rare, it presents with more aggressive features, including huge splenomegaly, higher cell count and higher blast cell percentage. PATIENTS AND METHODS: To investigate if after childhood the disease maintains or loses these characteristics of aggressiveness, we analyzed 2784 adult patients, at least 18 years old, registered by GIMEMA CML WP over a 40-year period. RESULTS: Young adults (YAs: 18-29 years old) significantly differed from adults (30-59 years old) and elderly patients (at least 60 years old)…

MalePediatricsHost responseBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Oncology; HematologyTyrosine kinase inhibitorDiseaseAntineoplastic AgentTyrosin kinase inhibitorProtein-Tyrosine Kinasehemic and lymphatic diseases80 and overAge FactorProspective StudiesYoung adultChronicBCR-ABLAged 80 and overLeukemiaIncidence (epidemiology)Chronic myeloid leukemiaAge FactorsMyeloid leukemiaHematologyMiddle AgedProtein-Tyrosine KinasesPrognosisLeukemiaOncologybcr-abl1FemaleBCR-ABL; chronic myeloid leukemia; prognosis; tyrosine kinase inhibitors; young adultsHumanAdultyoung adultsmedicine.medical_specialtyPrognosiProtein Kinase InhibitorAntineoplastic Agentschronic myeloid leukemia; bcr-abl1; Tyrosin kinase inhibitor; prognosis; young adultsNOYoung Adultchronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young AdultProtein Kinase InhibitorsAgedTyrosine kinase inhibitorsAdult patientsbusiness.industrymedicine.diseaseClinical trialBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Hematology; OncologyProspective StudieBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Medicine (all); Hematology; OncologyImmunologySplenomegalyBCR-ABL PositiveBCR-ABL chronic myeloid leukemia prognosis tyrosine kinase inhibitors young adultsprognosisbusinessSpleenYoung adultsMyelogenous
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Arthrinins A–D: Novel diterpenoids and further constituents from the sponge derived fungus Arthrinium sp.

2011

Bioassay-guided fractionation of a methanolic extract of the fungus Arthrinium sp., isolated from the Mediterranean sponge Geodia cydonium, afforded 10 natural products including five new diterpenoids, arthrinins A-D (1-4) and myrocin D (5). In addition, five known compounds were obtained, which included myrocin A (6), norlichexanthone (7), anomalin A (8), decarboxycitrinone (9) and 2,5-dimethyl-7-hydroxychromone (10). The structures of all isolated compounds were unambiguously elucidated based on extensive 1D and 2D NMR and HR-MS analyzes. The absolute configuration of arthrinins A-D (1-4) was established by the convenient Mosher method performed in NMR tubes and by interpretation of the R…

Vascular Endothelial Growth Factor AClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsBiochemistryMiceAscomycotaCell Line TumorNeoplasmsDrug DiscoveryAnimalsHumansMTT assayCytotoxicityProtein Kinase InhibitorsMolecular BiologyNeovascularization PathologicKinaseChemistryOrganic ChemistryTerpenoidIn vitroPoriferaEndothelial stem cellVascular endothelial growth factor ABiochemistryCell cultureMolecular MedicineDiterpenesProtein KinasesBioorganic & Medicinal Chemistry
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High-dose radiotherapy for oligo-progressive NSCLC receiving EGFR tyrosine kinase inhibitors: Real world data

2020

Background/aim Local ablative treatments for oligo-progressive, EGFR mutated non-small cell lung cancer (mut-NCSLC) may improve long-term disease control and survival. We analyzed the efficacy of hypo-fractionated, high-dose radiation therapy (HDRT), in association with prolonged EGFR tyrosine kinase inhibitors (TKI) in oligo-progressive, EGFR mutant-NSCLC. Patients and methods Progression-free survival-1 (PFS-1, date from initiation of TKI therapy until oligo-progression or death), and progression-free survival-2 (PFS-2, date of focal progression until further progression or death) were evaluated. Results Thirty-six patients were analyzed. The median PFS 1 was 12.5 months. HDHRT consisted …

OncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentEGFR high-dose radiotherapy Non-small cell lung cancer oligo-progressionEGFRGeneral Biochemistry Genetics and Molecular Biologyoligo-progression03 medical and health sciences0302 clinical medicineNon-small cell lung cancerCarcinoma Non-Small-Cell LungInternal medicinemedicineOverall survivalHumansProtein Kinase InhibitorsRetrospective StudiesPharmacologybusiness.industryEGFR Non-small cell lung cancer high-dose radiotherapy oligo-progressionEGFR; High-dose radiotherapy; Non-small cell lung cancer; Oligo-progressionEGFR Tyrosine Kinase Inhibitorshigh-dose radiotherapyDisease controlProgression-Free SurvivalErbB ReceptorsRadiation therapy030220 oncology & carcinogenesisMutationNon small cellbusinessReal world dataResearch Article
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MMP-10/stromelysin-2 promotes invasion of head and neck cancer.

2011

BackgroundPeriostin, IFN-induced transmembrane protein 1 (IFITM1) and Wingless-type MMTV integration site family, member 5B (Wnt-5b) were previously identified as the invasion promoted genes of head and neck squamous cell carcinoma (HNSCC) by comparing the gene expression profiles between parent and a highly invasive clone. We have previously reported that Periostin and IFITM1 promoted the invasion of HNSCC cells. Here we demonstrated that Wnt-5b overexpression promoted the invasion of HNSCC cells. Moreover, stromelysin-2 (matrix metalloproteinase-10; MMP-10) was identified as a common up-regulated gene among Periostin, IFITM1 and Wnt-5b overexpressing HNSCC cells by using microarray data s…

Tumor PhysiologyClone (cell biology)p38 Mitogen-Activated Protein KinasesMetastasisMetastasisMolecular Cell BiologyBasic Cancer ResearchNeoplasm MetastasisRegulation of gene expressionGene knockdownMultidisciplinaryHead and Neck cancerQRTransfectionHead and Neck TumorsExtracellular MatrixUp-RegulationGene Expression Regulation NeoplasticOncologyHead and Neck NeoplasmsGene Knockdown TechniquesCarcinoma Squamous CellMedicineResearch ArticleScience490Oral MedicineBiologyPeriostinHead and Neck Squamous Cell CarcinomaMatrix Metalloproteinase 10stomatognathic systemSettore MED/28 - Malattie OdontostomatologicheCell Line TumormedicineCancer Detection and Diagnosisotorhinolaryngologic diseasesHumansNeoplasm Invasiveness490BiologyExtracellular Matrix AdhesionsProtein Kinase InhibitorsneoplasmsMicroarray analysis techniquesCancers and Neoplasmsmedicine.diseaseMolecular biologyHead and neck squamous-cell carcinomaAntigens DifferentiationWnt Proteinsstomatognathic diseasesCancer researchCell Adhesion MoleculesPLoS ONE
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Cardiotoxicity mechanisms of the combination of BRAF-inhibitors and MEK-inhibitors.

2018

Many new drugs have appeared in last years in the oncological treatment scenario. Each drug carries an important set of adverse events, not less, cardiovascular adverse events. This aspect is even more important considering the increasing use of combination therapies with two drugs, or three drugs as in some ongoing clinical trials. Besides it represents a growing problem for Cardiologists, that face it in every day clinical practice and that will face it probably more and more in the coming years. This work reviews the mechanism of action of BRAF-inhibitors and MEK-inhibitors used together, the pathophysiological mechanisms that lead to cardiovascular toxicity. Particularly, it focuses on …

DrugCardiovascular toxicityBRAF inhibitorProto-Oncogene Proteins B-rafmedicine.medical_specialtyCombination therapySettore MED/06 - Oncologia Medicamedia_common.quotation_subjectDecreased ejection fraction030204 cardiovascular system & hematologyCardiovascular System03 medical and health sciences0302 clinical medicineCardiovascular toxicityAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansPharmacology (medical)Intensive care medicineAdverse effectBRAF inhibitor; Cardio-oncology; Cardiovascular toxicity; Decreased ejection fraction; Hypertension; MEK inhibitor; Pharmacology; Pharmacology (medical)MelanomaProtein Kinase Inhibitorsmedia_commonPharmacologyMitogen-Activated Protein Kinase KinasesCardiotoxicityMEK inhibitorClinical Trials as Topicbusiness.industryMEK inhibitorCancermedicine.diseaseCardiotoxicityClinical trialCardio-oncology030220 oncology & carcinogenesisHypertensionbusinessPharmacologytherapeutics
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The novel dual PI3K/mTOR inhibitor GDC-0941 synergizes with the MEK inhibitor U0126 in non-small cell lung cancer cells.

2011

Lung cancer is a malignant disease with poor outcome, which has led to a search for new therapeutics. The PI3K/Akt/mTOR and Ras/raf/Erk pathways are key regulators of tumor growth and survival. In the present study, their roles were evaluated by MTT assay, flow cytometry and Western blotting in lung cancer cells. We found that a high efficacy of antitumor activity was shown with GDC-0941 treatment in two gefitinib-resistant non-small cell lung cancer (NSCLC) cell lines, A549 and H460. In addition, H460 cells with activating mutations of PIK3CA were relatively more sensitive to GDC-0941 than A549 cells with wild-type PIK3CA. Furthermore, GDC-0941 was highly efficacious in combination with U0…

MAPK/ERK pathwayCancer ResearchIndazolesLung NeoplasmsApoptosisBiologyBiochemistryPhosphatidylinositol 3-KinasesCarcinoma Non-Small-Cell LungCell Line TumorNitrilesGeneticsmedicineButadienesHumansMolecular BiologyProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsSulfonamidesOncogeneCell growthMEK inhibitorTOR Serine-Threonine KinasesCancerDrug SynergismCell cyclemedicine.diseaseG1 Phase Cell Cycle Checkpointsrespiratory tract diseasesEnzyme ActivationOncologyCancer researchMolecular MedicineMitogen-Activated Protein KinasesSignal TransductionMolecular medicine reports
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Stochastic dynamics of leukemic cells under an intermittent targeted therapy

2009

The evolutionary dynamics of cancerous cell populations in a model of Chronic Myeloid Leukemia (CML) is investigated in the presence of an intermittent targeted therapy. Cancer development and progression is modeled by simulating the stochastic evolution of initially healthy cells which can experience genetic mutations and modify their reproductive behavior, becoming leukemic clones. Front line therapy for the treatment of patients affected by CML is based on the administration of tyrosine kinase inhibitors, namely imatinib (Gleevec) or, more recently, dasatinib or nilotinib. Despite the fact that they represent the first example of a successful molecular targeted therapy, the development o…

Statistics and ProbabilityComplex systemsmedicine.medical_treatmentModels BiologicalPiperazinesSettore FIS/03 - Fisica Della MateriaCancer evolutionTargeted therapyLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesStochastic dynamics; Cancer evolution; Complex systemsHumansMedicineComputer SimulationStochastic dynamicMolecular Targeted TherapyProtein Kinase InhibitorsEcology Evolution Behavior and SystematicsStochastic Processesbusiness.industryApplied MathematicsMyeloid leukemiaImatinibmedicine.diseaseSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)DasatinibLeukemiaPyrimidinesImatinib mesylateNilotinibStochastic dynamics Monte Carlo simulationBenzamidesImmunologyCancer cellDisease ProgressionImatinib MesylateCancer researchbusinessmedicine.drug
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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