Search results for "Progress"

showing 10 items of 1620 documents

Myeloid-Derived Suppressor Cells in Multiple Myeloma: Pre-Clinical Research and Translational Opportunities

2014

Immunosuppressive cells have been reported to play an important role in tumor-progression mainly because of their capability to promote immune-escape, angiogenesis, and metastasis. Among them, myeloid-derived suppressor cells (MDSCs) have been recently identified as immature myeloid cells, induced by tumor-associated inflammation, able to impair both innate and adaptive immunity. While murine MDSCs are usually identified by the expression of CD11b and Gr1, human MDSCs represent a more heterogeneous population characterized by the expression of CD33 and CD11b, low or no HLA-DR, and variable CD14 and CD15. In particular, the last two may alternatively identify monocyte-like or granulocyte-lik…

Cancer ResearchAngiogenesisCD33MDSCInflammationReview Articlelcsh:RC254-282Immune systemImmunesuppressionmedicinecancerimmunosuppressionbusiness.industryAcquired immune systemlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenspreclinical modelsmedicine.anatomical_structuremyelomaOncologyTumor progressionImmunologyMyeloid-derived Suppressor CellBone marrowmedicine.symptombusinesspre-clinical modelsFrontiers in Oncology
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The role of hypoxia-induced factors in tumor progression.

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Describe hypoxia-induced mechanisms for cell survival. Discuss hypoxia-induced gene expression. Relate hypoxia and glucose metabolism. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit atCME.TheOncologist.com Hypoxia is a common characteristic of locally advanced solid tumors that has been associated with diminished therapeutic response and, more recently, with malignant progression, that is, an increasing probability of recurrence, locoregional spread, and distant metastasis. Emerging evidence indicates that the effect of hypoxia on malignant progression is mediated by a…

Cancer ResearchAngiogenesisCell SurvivalRegulatorBiologyNeoplasmsmedicineHumansNuclear proteinSelection GeneticTranscription factorG alpha subunitRegulation of gene expressionHelix-Loop-Helix MotifsNuclear ProteinsHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaDNA-Binding ProteinsGene Expression Regulation NeoplasticCell Transformation NeoplasticGlucoseOncologyTumor progressionImmunologyCancer researchDisease ProgressionHypoxia-Inducible Factor 1medicine.symptomTranscription FactorsThe oncologist
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CtIP silencing as a novel mechanism of tamoxifen resistance in breast cancer.

2007

AbstractAcquired resistance to the antiestrogen tamoxifen constitutes a major clinical challenge in breast cancer therapy. However, the mechanisms involved are still poorly understood. Using serial analysis of gene expression, we identified CtIP, a BRCA1- and CtBP-interacting protein, as one of the most significantly down-regulated transcripts in estrogen receptor α–positive (ER+) MCF-7 tamoxifen-resistant breast cancer cells. We further confirmed the association of CtIP down-regulation with tamoxifen resistance in an additional ER+ breast cancer line (T47D), strengthening the relevance of the phenomenon observed. In additional studies, we found CtIP protein expression in a majority of ER+ …

Cancer ResearchAntineoplastic Agents HormonalEstrogen receptorDown-RegulationBreast NeoplasmsDisease-Free SurvivalBreast cancerCell Line TumormedicineGene silencingHumansSerial analysis of gene expressionGene Silencingskin and connective tissue diseasesMolecular BiologyEndodeoxyribonucleasesbusiness.industryCancerNuclear ProteinsAntiestrogenmedicine.diseaseGrowth InhibitorsGene Expression Regulation NeoplasticTamoxifenOncologyDrug Resistance NeoplasmCancer researchFemalebusinessCarrier ProteinsTamoxifenProgressive diseasemedicine.drugMolecular cancer research : MCR
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MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
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Genetic evolution of T-cell resistance in the course of melanoma progression

2014

Abstract Purpose: CD8+ T lymphocytes can kill autologous melanoma cells, but their activity is impaired when poorly immunogenic tumor phenotypes evolve in the course of disease progression. Here, we analyzed three consecutive melanoma lesions obtained within one year of developing stage IV disease for their recognition by autologous T cells. Experimental Design: One skin (Ma-Mel-48a) and two lymph node (Ma-Mel-48b, Ma-Mel-48c) metastases were analyzed for T-cell infiltration. Melanoma cell lines established from the respective lesions were characterized, determining the T-cell–stimulatory capacity, expression of surface molecules involved in T-cell activation, and specific genetic alteratio…

Cancer ResearchB7 Antigensmedicine.medical_treatmentMedizinGene ExpressionT-Lymphocyte Subsetshemic and lymphatic diseasesCluster AnalysisLymphocytesNeoplasm MetastasisLymph nodeMelanomaTumorImmunogenicityMelanomaSingle Nucleotidemedicine.anatomical_structurePhenotypeButorphanolOncologyDisease ProgressionCytokinesEvolutionT cellHuman leukocyte antigenBiologyPolymorphism Single NucleotideArticleCell LineEvolution MolecularLymphocytes Tumor-InfiltratingCell Line TumormedicineHumansGenetic Predisposition to DiseaseTumor-InfiltratingAllelePolymorphismneoplasmsAllelesNeoplasm StagingHistocompatibility Antigens Class IMolecularImmunotherapymedicine.diseaseAlleles; B7 Antigens; Butorphanol; Cell Line Tumor; Cluster Analysis; Cytokines; Disease Progression; Gene Expression; Genetic Predisposition to Disease; Histocompatibility Antigens Class I; Humans; Lymphocytes Tumor-Infiltrating; Melanoma; Mutation; Neoplasm Metastasis; Neoplasm Staging; Phenotype; Polymorphism Single Nucleotide; T-Lymphocyte Subsets; beta 2-Microglobulin; Evolution Molecular; Oncology; Cancer ResearchImmunologyMutationbeta 2-MicroglobulinCD8
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Immunomodulation and Anti-inflammatory Roles of Polyphenols as Anticancer Agents

2011

Cancers are the largest cause of mortality and morbidity in industrialized countries. Several new concepts have emerged in relation to mechanisms that contribute to the regulation of carcinogenesis processes and associated inflammatory effects such as the modulation of innate immune cells and adaptive immune cells that could infiltrate the tumor. In the tumor microenvironment, there is a delicate balance between antitumor immunity and tumor-originated proinflammatory activity, which weaken antitumor immunity. Consequently; modulation of immune cells and inflammatory processes represent attractive targets for therapeutic intervention in malignant diseases with the goal to restore the sensiti…

Cancer ResearchBiological AvailabilityInflammationBiologymedicine.disease_causeAntioxidantsProinflammatory cytokineImmunomodulationImmune systemNeoplasmsmedicineAnimalsHumansPharmacologyTumor microenvironmentInnate immune systemAnti-Inflammatory Agents Non-SteroidalPolyphenolsfood and beveragesAntineoplastic Agents PhytogenicTumor progressionCancer cellImmunologyMolecular Medicinemedicine.symptomCarcinogenesisAnti-Cancer Agents in Medicinal Chemistry
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Selective inhibition of HDAC6 regulates expression of the oncogenic driver EWSR1-FLI1 through the EWSR1 promoter in Ewing sarcoma

2021

Ewing sarcoma (EWS) is an aggressive bone and soft tissue tumor of children and young adults in which the principal driver is a fusion gene, EWSR1-FLI1. Although the essential role of EWSR1-FLI1 protein in the regulation of oncogenesis, survival, and tumor progression processes has been described in-depth, little is known about the regulation of chimeric fusion-gene expression. Here, we demonstrate that the active nuclear HDAC6 in EWS modulates the acetylation status of specificity protein 1 (SP1), consequently regulating the SP1/P300 activator complex binding to EWSR1 and EWSR1-FLI1 promoters. Selective inhibition of HDAC6 impairs binding of the activator complex SP1/P300, thereby inducing…

Cancer ResearchCarcinogenesisSarcoma EwingBiologymedicine.disease_causeHistone Deacetylase 6ArticleFusion genePaediatric cancerDownregulation and upregulationGeneticsmedicineHumansDoxorubicinPromoter Regions GeneticMolecular BiologyActivator (genetics)Proto-Oncogene Protein c-fli-1AcetylationOncogenesmedicine.diseaseTumor progressionFLI1Cancer researchSarcomaCarcinogenesismedicine.drug
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Phase III randomised clinical trial comparing primary surgery versus neoadjuvant chemotherapy in advanced epithelial ovarian cancer with high tumour …

2016

Abstract Objective To establishing whether neoadjuvant chemotherapy (NACT) followed by interval debulking surgery (IDS) is superior primary debulking surgery (PDS) in terms of clinical outcome as well as peri-operative morbidity in advanced epithelial ovarian cancer (AEOC) endowed with high tumour load (HTL). Material and methods This is a single-Institution, superiority, randomised phase III trial enrolling supposed AEOC women. Patients considered pre-operatively eligible were triaged to staging laparoscopy to assess the predictive index (PI) of tumour load. All AEOC women with PI ≥ 8 or ≤ 12 (considered as HTL) were included. They were randomly assigned (1:1 ratio) to undergo either PDS f…

Cancer ResearchCarcinoma Ovarian EpithelialRandomised clinical trialCarboplatinCytoreductionchemistry.chemical_compoundPostoperative Complications0302 clinical medicineQuality of lifeAntineoplastic Combined Chemotherapy ProtocolsNeoplasms Glandular and EpithelialOvarian Neoplasms030219 obstetrics & reproductive medicineCytoreduction Surgical ProceduresMiddle AgedDebulkingOncologyChemotherapy Adjuvant030220 oncology & carcinogenesisFemalemedicine.symptomAdultQuality of lifemedicine.medical_specialtyAdolescentPaclitaxelNauseaOperative TimeYoung Adult03 medical and health sciencesOvarian cancerBody ImagemedicineHumansProgression-free survivalAgedAnalysis of VarianceAdvanced ovarian cancer; Cytoreduction; Laparoscopy; Peri-operative complications; Quality of life; Randomised clinical trialbusiness.industryPeri-operative complicationsPerioperativeLength of StayCarboplatinSurgeryClinical trialSettore MED/40 - GINECOLOGIA E OSTETRICIAchemistryAdvanced ovarian cancerLaparoscopyPeri-operative complicationComplicationbusiness
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Tumor Hypoxia: Causative Factors, Compensatory Mechanisms, and Cellular Response

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Explain the effect of hypoxia on resistance to treatment. Describe the causes of tumor hypoxia. Characterize cellular response to hypoxia. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit at CME.TheOncologist.com Hypoxia is a characteristic feature of locally advanced solid tumors resulting from an imbalance between oxygen (O2) supply and consumption. Major causative factors of tumor hypoxia are abnormal structure and function of the microvessels supplying the tumor, increased diffusion distances between the nutritive blood vessels and the tumor cells, and reduced O2 tra…

Cancer ResearchCell SurvivalAnemiamedicine.medical_treatmentPhotodynamic therapyDiseaseNeoplasmsmedicineHumansNeovascularization PathologicTumor hypoxiabusiness.industryAnemiaTumor OxygenationHypoxia (medical)medicine.diseaseAdaptation PhysiologicalCell HypoxiaOxygenRadiation therapyCell Transformation NeoplasticOncologyDrug Resistance NeoplasmImmunologyDisease ProgressionCancer researchHemoglobinmedicine.symptombusinessThe Oncologist
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Pimasertib Versus Dacarbazine in Patients With Unresectable NRAS-Mutated Cutaneous Melanoma: Phase II, Randomized, Controlled Trial with Crossover

2020

This study investigated the efficacy and safety of pimasertib (MEK1/MEK2 inhibitor) versus dacarbazine (DTIC) in patients with untreated NRAS-mutated melanoma. Phase II, multicenter, open-label trial. Patients with unresectable, stage IIIc/IVM1 NRAS-mutated cutaneous melanoma were randomized 2:1 to pimasertib (60 mg

Cancer ResearchGastroenterologypimasertiblaw.invention0302 clinical medicineRandomized controlled triallawClinical endpoint030212 general & internal medicineMalignant melanomaHazard ratioProgression-free survivalSciences bio-médicales et agricoleslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthDacarbazineOncology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology030220 oncology & carcinogenesismedicine.symptomPimasertibmedicine.drugQuality of lifemedicine.medical_specialtyNauseaDacarbazinemalignant melanomadacarbazine[SDV.CAN]Life Sciences [q-bio]/CancerN-(2 3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamideNeutropeniaN-(23-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamidelcsh:RC254-282Article03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerInternal medicinemedicineProgression-free survivalAdverse effectbusiness.industry[SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatologymedicine.diseaseadverse eventsCancérologiequality of lifeAdverse events[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologybusinessprogression-free survival[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
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