Search results for "25"

showing 10 items of 3263 documents

Underuse of long-term routine hospital follow-up care in patients with a history of breast cancer?

2011

Abstract Background After primary treatment for breast cancer, patients are recommended to use hospital follow-up care routinely. Long-term data on the utilization of this follow-up care are relatively rare. Methods Information regarding the utilization of routine hospital follow-up care was retrieved from hospital documents of 662 patients treated for breast cancer. Utilization of hospital follow-up care was defined as the use of follow-up care according to the guidelines in that period of time. Determinants of hospital follow up care were evaluated with multivariate analysis by generalized estimating equations (GEE). Results The median follow-up time was 9.0 (0.3-18.1) years. At fifth and…

Cancer ResearchPediatricsMultivariate analysisAftercareComorbidityGUIDELINESGeelaw.inventionCohort StudiesRandomized controlled triallawNetherlandsAged 80 and overSURVIVORSmedicine.diagnostic_testBreast neoplasmFollow-upNeoplasms Second PrimaryMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCombined Modality TherapyUtilizationOncologyPractice Guidelines as TopicRECURRENCESHormonal therapyFemaleGuideline AdherenceHEALTHResearch ArticleCohort studyMammographyAdultmedicine.medical_specialtyOutpatient Clinics HospitalAntineoplastic Agents HormonalMatched-Pair AnalysisBreast Neoplasmslcsh:RC254-282Breast cancerGeneticsmedicineHumansMammographyMETAANALYSISAgedbusiness.industryPatient Acceptance of Health Caremedicine.diseaseComorbidityTRENDSRANDOMIZED-TRIALHealth Care SurveysPhysical therapyPatient ComplianceUPDATESURVEILLANCE MAMMOGRAPHYbusinessFollow-Up Studies
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Management of orphan symptoms: ESMO Clinical Practice Guidelines for diagnosis and treatment†

2020

### Highlights There is no clear definition of orphan symptoms. There is a group of symptoms that are seldom evaluated in most symptom assessment tools which can be considered as orphan symptoms.1 These are generally prevalent symptoms that are unaddressed in clinical practice, yet often not reported by the patients or by healthcare professionals.2 Orphan symptoms may be defined as symptoms not regularly assessed in clinical practice, and consequently little studied and not properly treated. No epidemiological or clinical studies generally exist to gauge the prevalence of the symptoms chosen; nevertheless, these symptoms are distressing for patients and their families. Orphan symptoms remai…

Cancer ResearchPediatricsmedicine.medical_specialtydiagnosisoncological therapiesMEDLINElcsh:RC254-282Quality of lifeEpidemiologymedicine1506Restless legs syndromeOriginal Researchtreatmentbusiness.industryEvidence-based medicineorphan symptomsmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRectal tenesmusclinical practice guidelines; diagnosis; oncological therapies; orphan symptoms; treatmentOncologymedicine.symptombusinessMyoclonusclinical practice guidelinesMuscle crampESMO Open
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Clinical impact of the immunome in lymphoid malignancies: the role of Myeloid-Derived Suppressor Cells

2015

The better definition of the mutual sustainment between neoplastic cells and immune system has been translated from the bench to the bedside acquiring value as prognostic factor. Additionally, it represents a promising tool for improving therapeutic strategies. In this context, myeloid-derived suppressor cells have gained a central role in tumor developing with consequent therapeutic implications. In this review, we will focus on the biological and clinical impact of the study of myeloid-derived suppressor cells in the settings of lymphoid malignancies.

Cancer ResearchPrognostic factorLymphomaMDSCMDSCsContext (language use)ReviewBioinformaticslcsh:RC254-282law.inventionImmune systemlawmedicinebusiness.industrymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHematologic Diseasesmicroenvironment3. Good healthLymphomaImmunomeOncologyMyeloid-derived Suppressor CellCancer researchSuppressorbusinessprognosticationFrontiers in Oncology
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Topotecan-triggered degradation of topoisomerase I is p53-dependent and impacts cell survival.

2005

Abstract The anticancer drug topotecan belongs to the group of topoisomerase I (topo I) inhibitors. In the presence of topotecan, topo I cleaves the DNA but is unable to religate the single-strand break. This leads to stabilization of topo I-DNA–bound complexes and the accumulation of DNA strand breaks that may interfere with DNA replication. The molecular mechanism of controlling the repair of topo I-DNA covalent complexes and its impact on sensitivity of cells to topotecan is largely unknown. Here, we used mouse embryonic fibroblasts expressing wild-type p53 and deficient in p53, in order to elucidate the role of p53 in topotecan-induced cell death. We show that p53-deficient mouse embryo…

Cancer ResearchProgrammed cell deathendocrine system diseasesDNA damageLeupeptinsAntineoplastic AgentsApoptosisBiologyTopoisomerase-I Inhibitorchemistry.chemical_compoundMiceMG132medicineAnimalsHumanscdc25 PhosphatasesCHEK1Enzyme InhibitorsTopoisomeraseCell CycleDNA NeoplasmFibroblastsMolecular biologyEnzyme ActivationOncologychemistryDNA Topoisomerases Type IApoptosisCheckpoint Kinase 1MutationCancer researchbiology.proteinTopotecanTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanProtein Kinasesmedicine.drugDNA DamageCancer research
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Large-scale proteomic identification of S100 proteins in breast cancer tissues

2010

Abstract Background Attempts to reduce morbidity and mortality in breast cancer is based on efforts to identify novel biomarkers to support prognosis and therapeutic choices. The present study has focussed on S100 proteins as a potentially promising group of markers in cancer development and progression. One reason of interest in this family of proteins is because the majority of the S100 genes are clustered on a region of human chromosome 1q21 that is prone to genomic rearrangements. Moreover, there is increasing evidence that S100 proteins are often up-regulated in many cancers, including breast, and this is frequently associated with tumour progression. Methods Samples of breast cancer t…

Cancer ResearchProteomeBlotting WesternBreast NeoplasmsBioinformaticsS100 proteinlcsh:RC254-282Cohort StudiesBreast cancerSurgical oncologyBiomarkers TumorGeneticsmedicineHumansElectrophoresis Gel Two-DimensionalBreastNeoplasm MetastasisSettore BIO/06 - Anatomia Comparata E CitologiaGeneproteomicbusiness.industryS100 ProteinsChromosomePrognosismedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary tumorS100 proteinOncologybreast cancer tissuesSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationProteomeFemaleStem cellbusinessResearch ArticleBMC Cancer
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The Proton-Boron Reaction Increases the Radiobiological Effectiveness of Clinical Low- and High-Energy Proton Beams: Novel Experimental Evidence and …

2021

Protontherapy is a rapidly expanding radiotherapy modality where accelerated proton beams are used to precisely deliver the dose to the tumor target but is generally considered ineffective against radioresistant tumors. Proton-Boron Capture Therapy (PBCT) is a novel approach aimed at enhancing proton biological effectiveness. PBCT exploits a nuclear fusion reaction between low-energy protons and 11B atoms, i.e. p+11B→ 3α (p-B), which is supposed to produce highly-DNA damaging α-particles exclusively across the tumor-conformed Spread-Out Bragg Peak (SOBP), without harming healthy tissues in the beam entrance channel. To confirm previous work on PBCT, here we report new in-vitro data obtained…

Cancer ResearchProtonmedicine.medical_treatmentSobpBragg peakBSH030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineRadioresistancemedicineIrradiationRC254-282Original Researchprotontherapycancer cell killingChemistryalpha-particleNeoplasms. Tumors. Oncology. Including cancer and carcinogensProton-Boron ReactionRadiation therapyCell killingchromosome aberrationsOncology030220 oncology & carcinogenesisCancer researchproton-boron (B) fusion-enhanced proton therapy (PBFEPT)chromosome aberrationBeam (structure)Frontiers in Oncology
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C-Kit and Its Ligand Stem Cell Factor: Potential Contribution to Prostate Cancer Bone Metastasis

2008

AbstractThe tyrosine kinase receptor c-kit and its ligand stem cell factor (SCF) have not been explored in prostate cancer (PC) bone metastasis. Herein, we found that three human PC cell lines and bone marrow stromal cells express a membrane-bound SCF isoform and release a soluble SCF. Bone marrow stromal cells revealed strong expression of c-kit, whereas PC cells showed very low levels of the receptor or did not express it all. Using an experimental model of PC bone metastasis, we found that intraosseous bone tumors formed by otherwise c-kit–negative PC3 cells strongly expressed c-kit, as demonstrated using immunohistochemical and Western blot analyses. Subcuta-neous PC3 tumors were, howev…

Cancer ResearchStromal cellbiologyBone metastasisStem cell factorlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaselcsh:RC254-282Receptor tyrosine kinaseProstate cancermedicine.anatomical_structureCell culturemedicineCancer researchbiology.proteinImmunohistochemistryBone marrowNeoplasia
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Identification of Risk Loci for Radiotoxicity in Prostate Cancer by Comprehensive Genotyping of

2021

Simple Summary Genetic variability in transforming growth factor beta pathway (TGFB) has been reported to affect adverse events in radiotherapy. We investigated 40 germline polymorphisms in peripheral blood cells, covering the entire common genetic variability in the TGFβ1 ligand (gene TGFB1) and the TGFβ receptor-1 (TGFBR1) in 240 patients treated with primary radiotherapy for prostate cancer. Human lymphoblastoid cell lines (LCLs) were used to assess whether TGFB1 and TGFBR1 polymorphisms impact DNA repair capacity following single irradiation with 3 Gy. Upon adjustment for multiplicity testing, for one polymorphism (rs10512263 in TGFBR1, C-variant allele, n = 35), a statistically signifi…

Cancer ResearchTGFBDNA repairSNPLeu10ProArticle03 medical and health sciencesProstate cancerchemistry.chemical_compound0302 clinical medicineGenotypeMedicineGenetic variabilityAlleleGenotypingRC254-282radiotherapyTGBF1030304 developmental biology0303 health sciencesirradiationbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogenstoxicitybiomarkersLCLmedicine.diseaseprostate cancerAcute toxicity3. Good healthrs10512263side effectsOncologychemistry030220 oncology & carcinogenesisCancer researchbusinessCytosineCancers
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RB acute loss induces centrosome amplification and aneuploidy in murine primary fibroblasts

2006

AbstractBackgroundIncorrect segregation of whole chromosomes or parts of chromosome leads to aneuploidy commonly observed in cancer. The correct centrosome duplication, assuring assembly of a bipolar mitotic spindle, is essential for chromosome segregation fidelity and preventing aneuploidy. Alteration of p53 and pRb functions by expression of HPV16-E6 and E7 oncoproteins has been associated with centrosome amplification. However, these last findings could be the result of targeting cellular proteins in addition to pRb by HPV16-E7 oncoprotein. To get a more detailed picture on the role of pRb in chromosomal instability and centrosome amplification, we analyzed the effects of the acute loss …

Cancer ResearchTime FactorsTranscription GeneticRbCentrosomes AneuploidyGene ExpressionMitosisAneuploidyBiologyRetinoblastoma Proteinlcsh:RC254-282Chromosome segregationMiceChromosome instabilityGene duplicationmedicineAnimalsCentrosome duplicationMitosisCells CulturedCentrosomeResearchGene AmplificationFibroblastsAneuploidylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseSettore BIO/18 - GeneticaSpindle checkpointOncologyCentrosomeCancer researchMolecular MedicineMolecular Cancer
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Epigenetic Alterations Upstream and Downstream of p53 Signaling in Colorectal Carcinoma

2021

Simple Summary Colorectal cancer (CRC) belongs to the most common cancer types. It is well known that half of all CRC possess missense mutations in the TP53 tumor suppressor gene. However, the entire signaling cascade upstream and downstream of the p53 protein may also contribute to CRC development, if relevant players in this signaling cascade lost their function. Besides p53 loss-of-function by mutations, epigenetic changes (DNA methylation, post translational modifications of histones, micro-RNAs) play a vital role in CRC development. In the present review, we concentrated on the epigenetic modifications related to the entire p53 signal transduction cascade upstream and downstream of p53…

Cancer ResearchTumor suppressor genetumor suppressorUpstream and downstream (transduction)Reviewmedicine.disease_causeoncogenemicroRNAmedicineEpigeneticsneoplasmsRC254-282acetylationbiologymicro-RNANeoplasms. Tumors. Oncology. Including cancer and carcinogensMethylationdigestive system diseasesHistoneOncologyDNA methylationCancer researchbiology.proteinmethylationCarcinogenesiscarcinogenesissignal transductionCancers
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