Search results for "INHIBITOR"

showing 10 items of 3742 documents

BCR-ABL1 Doubling-Times and Halving-Times May Predict CML Response to Tyrosine Kinase Inhibitors

2019

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDisease ResponseChronic Myeloid LeukemiaBCR-ABL1/ABL1IShalving-timelcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinehemic and lymphatic diseasesBCR-ABL1/ABL1; IS; Chronic Myeloid Leukemia; Doubling-time; Halving-time; Tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineDoubling timeOriginal ResearchBCR-ABL1/ABL1Oncogenebusiness.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDiscontinuationdoubling-time030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisCohortISBCR-ABL1/ABL1 ISbusinessTyrosine kinaseFrontiers in Oncology
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HDAC5 Inhibitors as a Potential Treatment in Breast Cancer Affecting Very Young Women

2020

Background: Breast cancer in very young women (BCVY) defined as &lt

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDose dependencelcsh:RC254-282ArticleLMK-23503 medical and health sciences0302 clinical medicineBreast cancerbreast cancerOlder patientsInternal medicinemedicineskin and connective tissue diseasesPathologicalHDAC5 inhibitorsHistone deacetylase 5young womenbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyOncologyApoptosisCell culture030220 oncology & carcinogenesishistone deacetylaseHistone deacetylasebusiness
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Abstract PD3-06: Neratinib + fulvestrant for HER2-mutant, HR-positive, metastatic breast cancer: Updated results from the phase 2 SUMMIT trial

2019

Abstract Background: HER2 mutations define a rare subset of metastatic breast cancer (MBC) with a unique mechanism of oncogenic addiction to HER2 signaling. Neratinib, an irreversible pan-HER tyrosine kinase inhibitor, has demonstrated single-agent clinical activity in HER2-mutant MBC. In HER2-mutant, HR+ MBC, neratinib + fulvestrant (N+F) appears synergistic vs single-agent neratinib, possibly due to more complete inhibition of bi-directional signaling between HER2 and estrogen receptors. Here we describe interim efficacy results of the expanded HER2-mutant, HR+ MBC cohort treated with N+F from SUMMIT (NCT01953926). Methods: HR+ MBC patients (pts) with HER2 mutations documented by local te…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyFulvestrantmedicine.drug_classbusiness.industryEstrogen receptorCancermedicine.diseaseMetastatic breast cancerTyrosine-kinase inhibitor03 medical and health sciences030104 developmental biology0302 clinical medicineBreast cancerOncology030220 oncology & carcinogenesisInternal medicineNeratinibmedicineskin and connective tissue diseasesbusinessAdverse effectmedicine.drugCancer Research
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The Role of Molecular Profiling to Predict the Response to Immune Checkpoint Inhibitors in Lung Cancer.

2019

Immune checkpoint inhibitors radically changed the treatment of patients with non-small cell lung cancer (NSCLC). However, only one-quarter of patients benefit from these new therapies when used as monotherapy. The assessment of Program Death Ligand-1 (PD-L1) tumor expression by immunohistochemistry is used to select potential responder patients, but this not an optimal marker since it does not predict the absence of anti PD-1 efficacy. Despite this shortcoming, PD-L1 remains the gold standard biomarker in many studies and the only biomarker available for clinicians. In addition to histological markers, transcriptomic and exome analyses have revealed potential biomarkers requiring further c…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentImmune checkpoint inhibitorsReviewlcsh:RC254-282Transcriptome03 medical and health sciences0302 clinical medicineInternal medicinemedicineLung cancerExomebusiness.industrySurrogate endpointbiomarkersImmunotherapymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncology030220 oncology & carcinogenesisBiomarker (medicine)ImmunohistochemistryimmunotherapyLung cancerbusinessCancers
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Targeted Therapy in Advanced Melanoma With Rare BRAF Mutations

2019

PURPOSE BRAF/MEK inhibition is a standard of care for patients with BRAF V600E/K–mutated metastatic melanoma. For patients with less frequent BRAF mutations, however, efficacy data are limited. METHODS In the current study, 103 patients with metastatic melanoma with rare, activating non-V600E/K BRAF mutations that were treated with either a BRAF inhibitor (BRAFi), MEK inhibitor (MEKi), or the combination were included. BRAF mutation, patient and disease characteristics, response, and survival data were analyzed. RESULTS Fifty-eight patient tumors (56%) harbored a non-E/K V600 mutation, 38 (37%) a non-V600 mutation, and seven had both V600E and a rare BRAF mutation (7%). The most frequent mu…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentMedizinmedicine.disease_causeTargeted therapy03 medical and health sciences0302 clinical medicineInternal medicineJournal ArticleMedicineProgression-free survivalneoplasmsSurvival rateMutationbusiness.industryMEK inhibitorMelanomamedicine.disease3. Good healthRegimen030104 developmental biologyOncology030220 oncology & carcinogenesisbusinessV600EJournal of Clinical Oncology
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Recent Advances in Desmoid Tumor Therapy

2020

The desmoid tumor is a locally aggressive proliferative disease within the family of soft-tissue sarcomas. Despite its relatively good prognosis, the clinical management of desmoid tumors requires constant multidisciplinary evaluation due to its highly variable clinical behavior. Recently, active surveillance has being regarded as the appropriate strategy at diagnosis, as indolent persistence or spontaneous regressions are not uncommon. Here, we review the most recent advances in desmoid tumor therapy, including low-dose chemotherapy and treatment with tyrosine kinase inhibitors. We also explore the recent improvements in our knowledge of the molecular biology of this disease, which are lea…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentProliferative diseasedesmoid tumorDiseaseReviewchemotherapylcsh:RC254-282aggressive fibromatosis03 medical and health sciences0302 clinical medicineInternal medicinedesmoid tumor; aggressive fibromatosis; active surveillance; chemotherapy; tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineChemotherapybusiness.industryactive surveillanceTumor therapyaggressive fibromatosimedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensClinical trialbody regions030104 developmental biologyOncology030220 oncology & carcinogenesisAggressive fibromatosisGood prognosisbusinessCancers
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A study of PD-L1 expression in KRAS mutant non-small cell lung cancer cell lines exposed to relevant targeted treatments.

2017

We investigated PD-L1 changes in response to MEK and AKT inhibitors in KRAS mutant lung adenocarcinoma (adeno-NSCLC). PD-L1 expression was quantified using immunofluorescence and co-culture with a jurkat cell-line transfected with NFAT-luciferase was used to study if changes in PD-L1 expression in cancer cell lines were functionally relevant. Five KRAS mutant cell lines with high PD-L1 expression (H441, H2291, H23, H2030 and A549) were exposed to GI50 inhibitor concentrations of a MEK inhibitor (trametinib) and an AKT inhibitor (AZD5363) for 3 weeks. Only 3/5 (H23, H2030 and A549) and 2/5 cell lines (H441 and H23) showed functionally significant increases in PD-L1 expression when exposed to…

0301 basic medicineOncologyCell signalingLung NeoplasmsLuminescenceImmunofluorescenceMutantCancer Treatmentlcsh:MedicineSignal transductionERK signaling cascademedicine.disease_causeJurkat cellsB7-H1 AntigenLung and Intrathoracic TumorsMajor Histocompatibility ComplexWhite Blood Cells0302 clinical medicineAnimal CellsCarcinoma Non-Small-Cell LungMedicine and Health Scienceslcsh:ScienceTrametinibMultidisciplinarymedicine.diagnostic_testT CellsChemistryPhysicsElectromagnetic RadiationMEK inhibitorSignaling cascadesOncology030220 oncology & carcinogenesisPhysical SciencesKRASCellular TypesResearch Articlemedicine.medical_specialtyGeneral Science & TechnologyImmune CellsImmunologyResearch and Analysis MethodsImmunofluorescenceFluorescence03 medical and health sciencesCell Line TumorInternal medicineMD MultidisciplinarymedicineHumansImmunoassaysBlood Cellslcsh:RCancers and NeoplasmsBiology and Life SciencesCell BiologyCoculture TechniquesNon-Small Cell Lung Cancerrespiratory tract diseasesGenes ras030104 developmental biologyCell cultureMutationImmunologic TechniquesCancer researchClinical ImmunologyCancer biomarkerslcsh:QClinical MedicinePLoS ONE
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Combinaisons de chimiothérapie ou de radiothérapie et d’inhibiteurs de checkpoints

2018

Les progrès récents de l’immunothérapie en oncologie dus au développement des anticorps anti-PD1/PDL1 révolutionnent la prise en charge des patients. Malgré tout, l’efficacité de ces traitements en monothérapie est limitée à une sous-population représentant environ 25 à 30 % des patients dans la plupart des indications. Le développement de nouvelles stratégies se base sur les combinaisons entre les traitements standards (chimiothérapie cytotoxique et radiothérapie) et l’immunothérapie afin de trouver des combinaisons synergiques.

0301 basic medicineOncologyChemotherapymedicine.medical_specialtybusiness.industrymedicine.medical_treatmentImmune checkpoint inhibitorsCancerImmunotherapyCytotoxic chemotherapymedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyRadiation therapy03 medical and health sciences030104 developmental biology0302 clinical medicineCancer immunotherapy030220 oncology & carcinogenesisInternal medicinemedicineCombined Modality TherapybusinessBiologie Aujourd'hui
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Compassionate use of everolimus for refractory epilepsy in a patient with MTOR mosaic mutation

2020

Abstract The MTOR gene encodes the mechanistic target of rapamycin (mTOR), which is a core component of the PI3K-AKT-mTOR signaling pathway. Postzygotic MTOR variants result in various mosaic phenotypes, referred to in OMIM as Smith-Kinsgmore syndrome or focal cortical dysplasia. We report here the case of a patient, with an MTOR mosaic gain-of-function variant (p.Glu2419Lys) in the DNA of 41% skin cells, who received compassionate off-label treatment with everolimus for refractory epilepsy. This 12-year-old-girl presented with psychomotor regression, intractable seizures, hypopigmentation along Blaschko's lines (hypomelanosis of Ito), asymmetric regional body overgrowth, and ocular anomali…

0301 basic medicineOncologyCompassionate Use Trialsmedicine.medical_specialty[SDV]Life Sciences [q-bio]030105 genetics & heredityMuscle hypertrophyCraniofacial Abnormalities03 medical and health sciencesInternal medicineGeneticsmedicineHumansEverolimusChildMechanistic target of rapamycinProtein Kinase InhibitorsGenetics (clinical)PI3K/AKT/mTOR pathwayHypopigmentationEverolimusbiologybusiness.industryMosaicismTOR Serine-Threonine KinasesNeuropsychologyGeneral MedicineCortical dysplasiamedicine.disease3. Good healthClinical trialMalformations of Cortical Development[SDV] Life Sciences [q-bio]030104 developmental biologyPhenotypeGain of Function Mutationbiology.proteinFemaleEpilepsies Partialmedicine.symptombusinessmedicine.drug
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Recommendations for the implementation of BRCA testing in ovarian cancer patients and their relatives

2019

The current availability of new Poly(ADP-ribose) Polymerase (PARP)-inhibitors for the treatment of ovarian cancer patients independently of the presence of a BRCA pathogenic variant, together with the validation of somatic test for the analysis of BRCA1/2 genes, involves the need to optimise the guidelines for BRCA testing. The AIOM-SIGU-SIBIOC-SIAPEC-IAP Italian Scientific Societies, in this position paper, recommend the implementation of BRCA testing with 2 main objectives: the first is the identification of ovarian cancer patients with higher probability of benefit from specific anticancer treatments (test for response to therapy); the second goal, through BRCA testing in the family memb…

0301 basic medicineOncologyGenetic testingendocrine system diseasesSettore MED/03 - GENETICA MEDICAMedical OncologyBiochemistrychemistry.chemical_compound0302 clinical medicineGermline mutationPARP inhibitorsTrabectedinSocieties MedicalOvarian Neoplasmsmedicine.diagnostic_testBRCA1 ProteinHematologyfemale genital diseases and pregnancy complicationsOncologyItaly030220 oncology & carcinogenesisFemalemedicine.drugHumanmedicine.medical_specialtyGenetic counselingOlaparib03 medical and health sciencesGeneticSomatic mutationsOvarian cancerMedicalInternal medicineBRCA1; BRCA2; Genetic testing; Germline mutations; Ovarian cancer; PARP inhibitors; Somatic mutations; BRCA1 Protein; BRCA2 Protein; Biochemistry; Female; Genetic Testing; Genetics; Humans; Italy; Medical Oncology; Ovarian Neoplasms; Germ-Line Mutation; Societies MedicalGeneticsmedicineGenetic predispositionHumansRucaparibGermline mutationsGerm-Line MutationGenetic testingBRCA2 Proteinbusiness.industrySomatic mutationOvarian NeoplasmCancermedicine.diseaseBRCA1BRCA2BRCA1; BRCA2; Genetic testing; Germline mutations; Ovarian cancer; PARP inhibitors; Somatic mutations030104 developmental biologyPARP inhibitorchemistrySocietiesOvarian cancerbusiness
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