Search results for "invasiveness"

showing 10 items of 192 documents

Chemokine receptor CXCR4-prognostic factor for gastrointestinal tumors

2008

To review the implication of CXCR4 for gastrointestinal cancer, a "Pubmed" analysis was performed in order to evaluate the relevance of CXCR4 and its ligands for gastrointestinal cancers. Search terms applied were "cancer, malignoma, esophageal, gastric, colon, colorectal, hepatic, pancreatic, CXCR4, SDF-1alpha, and SDF-1beta". CXCR4 expression correlated with dissemination of diverse gastrointestinal malignomas. The CXCR4 ligand SDF-1alpha might act as "chemorepellent" while SDF-1beta might act as "chemorepellent" for CTLs, inducing tumor rejection. The paracrine expression of SDF-1alpha was furthermore closely associated with neoangiogenesis. CXCR4 and its ligands influence the disseminat…

Receptors CXCR4Prognostic factorGastrointestinal tumorsBiologyLigandsCXCR4Paracrine signallingChemokine receptorBiomarkers TumormedicineAnimalsHumansNeoplasm InvasivenessGastrointestinal cancerNeoplasm MetastasisGastrointestinal NeoplasmsGastroenterologyCancerGeneral Medicinemedicine.diseaseChemokine CXCL12EditorialTreatment OutcomeSearch termsImmunologyCancer researchWorld Journal of Gastroenterology
researchProduct

Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells

2021

Triple-negative breast cancer (TNBC) is a highly aggressive disease with invasive and metastasizing properties associated with a poor prognosis. The STAT3 signaling pathway has shown a pivotal role in cancer cell migration, invasion, metastasis and drug resistance of TNBC cells. IL-6 is a main upstream activator of the JAK2/STAT3 pathway. In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments. We used a subtoxic dose of carboplatin and/or recombinant IL-6 to activate the JAK2/STAT3 signaling path…

STAT3 Transcription FactorQH301-705.5Triple Negative Breast NeoplasmsmigrationArticleCatalysisStat3 Signaling PathwayMetastasisInorganic ChemistryMiceNitroglycerinchemistry.chemical_compoundCell Movementnitric oxideIn vivoCell Line TumormedicineAnimalsHumanscancermetastasisNeoplasm InvasivenessNitric Oxide DonorsBiology (General)Physical and Theoretical ChemistrySTAT3QD1-999Molecular BiologySpectroscopyTriple-negative breast cancerMice Inbred BALB CbiologyActivator (genetics)Organic ChemistryCancerGeneral MedicineJanus Kinase 2invasionmedicine.diseaseCarboplatinComputer Science ApplicationsChemistrychemistrybiology.proteinCancer researchFemalesignalingSignal TransductionInternational Journal of Molecular Sciences
researchProduct

PARD3 Inactivation in Lung Squamous Cell Carcinomas Impairs STAT3 and Promotes Malignant Invasion.

2015

Abstract Correct apicobasal polarization and intercellular adhesions are essential for the appropriate development of normal epithelia. Here, we investigated the contribution of the cell polarity regulator PARD3 to the development of lung squamous cell carcinomas (LSCC). Tumor-specific PARD3 alterations were found in 8% of LSCCs examined, placing PARD3 among the most common tumor suppressor genes in this malignancy. Most PAR3-mutant proteins exhibited a relative reduction in the ability to mediate formation of tight junctions and actin-based protrusions, bind atypical protein kinase C, activate RAC1, and activate STAT3 at cell confluence. Thus, PARD3 alterations prevented the formation of c…

STAT3 Transcription Factorrac1 GTP-Binding ProteinCancer ResearchLung NeoplasmsCellMice NudeRAC1Cell Cycle ProteinsBiologyArticleCell MovementCell Line TumorCell polaritymedicineAnimalsHumansNeoplasm InvasivenessProtein Kinase CAdaptor Proteins Signal TransducingCell ProliferationConfluencyTight junctionBase SequenceCell growthLiver NeoplasmsMembrane ProteinsSequence Analysis DNACell biologymedicine.anatomical_structureOncologyCell cultureMutationCancer researchCarcinoma Squamous CellTranscriptomeIntracellularNeoplasm TransplantationCancer research
researchProduct

Botulinum toxin in preparation of oral cavity for microsurgical reconstruction.

2010

CONCLUSIONS: Infiltration of botulinum toxin in the major salivary glands allows a temporary reduction of salivation that begins 8 days afterwards and returns to normal within 2 months. The inhibition of salivary secretion, carried out before the oral cavity reconstructive surgery, could allow a reduction of the incidence of oro-cutaneous fistulas and local complications. OBJECTIVES: Saliva stagnation is a risk factor for patients who have to undergo reconstructive microsurgery of the oral cavity, because of fistula formation and local complications in the oral cavity. The authors suggest infiltration of botulinum toxin in the major salivary glands to reduce salivation temporarily during th…

SalivaReconstructive surgerymedicine.medical_specialtyMicrosurgeryBotulinum Toxins Type A/administration & dosage* Humans Microsurgery* Mouth Floor/surgery Mouth Neoplasms/surgery* Neck Dissection Neoplasm Invasiveness Preoperative Care* Salivary Glands/drug effects* Salivation/drug effects Surgical Flaps Tongue Neoplasms/surgeryFistulamedicine.medical_treatmentSalivary GlandsSurgical FlapsMajor Salivary GlandPreoperative CareMedicineHumansOral Cavity CarcinomaNeoplasm InvasivenessBotulinum Toxins Type AMouth Floorbusiness.industryGeneral MedicineMicrosurgerymedicine.diseaseBotulinum toxinSurgeryTongue NeoplasmsOtorhinolaryngologyNeck DissectionMouth NeoplasmsbusinessComplicationSalivationmedicine.drugActa oto-laryngologica
researchProduct

Compromised nuclear envelope integrity drives TREX1-dependent DNA damage and tumor cell invasion

2021

Although mutations leading to a compromised nuclear envelope cause diseases such as muscular dystrophies or accelerated aging, the consequences of mechanically induced nuclear envelope ruptures are less known. Here, we show that nuclear envelope ruptures induce DNA damage that promotes senescence in non-transformed cells and induces an invasive phenotype in human breast cancer cells. We find that the endoplasmic reticulum (ER)-associated exonuclease TREX1 translocates into the nucleus after nuclear envelope rupture and is required to induce DNA damage. Inside the mammary duct, cellular crowding leads to nuclear envelope ruptures that generate TREX1-dependent DNA damage, thereby driving the …

SenescenceExonucleaseDNA damageNuclear Envelope[SDV]Life Sciences [q-bio]Breast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyCell LineMicemedicineSettore MED/05 - Patologia ClinicaAnimalsHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionCellular SenescenceEndoplasmic reticulumPhosphoproteinsXenograft Model Antitumor AssaysCell biology[SDV] Life Sciences [q-bio]medicine.anatomical_structureExodeoxyribonucleasesCancer cellProteolysisbiology.proteinTREX1 nuclear envelope rupture DNA damage mammary duct carcinoma tumor invasion senescence breast cancer cGAS confinement epithelial to mesenchymal transition Animals Breast Neoplasms Cell Line Cellular Senescence Collagen Disease Progression Exodeoxyribonucleases Female Humans Mice Neoplasm InvasivenessNuclear Envelope PhosphoproteinsProteolysis Xenograft Model Antitumor Assays DNA DamageDisease ProgressionFemaleCollagenNucleusExtracellular Matrix DegradationDNA Damage
researchProduct

Dynamic Energy Budget parameters of Brachidontes pharaonis, a lessepsian bivalve in the Mediterranean Sea.

2014

Dynamic Energy Budget (DEB) models are used for describing the flow of energy through organisms. The most important and powerful aspect of DEB theory is that inter-specific differences can be captured in the same model by comparison of parameter values. However, estimation of these parameters is complicated and can often not be done with direct empirical measurements alone. Here, we present DEB parameter estimates obtained by combining both experimental and literature data for the filter feeder Brachidontes pharaonis, which is considered one among the 100 worst invasive marine species in the Mediterranean Basin. We utilize a statistical procedure based on the covariation method to obtain pa…

Settore BIO/07 - EcologiaDynamic energy budgetFilter feederAquatic ScienceBiologyOceanographyAtmospheric sciencesMediterranean BasinMarine species/dk/atira/pure/sustainabledevelopmentgoals/life_below_waterOceanographyMediterranean seaDEB ParametersInvasivenessMediterranean SeaBrachidontes pharaonisSDG 14 - Life Below WaterEcology Evolution Behavior and SystematicsJournal of sea research
researchProduct

Is immunohistochemistry more sensitive than hematoxylin-eosin staining for identifying perineural or lymphovascular invasion in oral squamous cell ca…

2021

This study aimed to analyze whether immunohistochemistry (IHC) is more sensitive than hematoxylin-eosin (H&E) staining for identifying perineural invasion (PNI) or lymphovascular invasion (LVI) in oral squamous cell carcinoma (OSCC). In this systematic review and meta-analysis (Prospective Register of Systematic Reviews ? CRD 42021256515), data were obtained from six databases (PubMed, Scopus, LILACS, Web of Science, EBSCO, LIVIVO, Embase) and the grey literature. Cross-sectional observational studies of the diagnostic sensitivity of IHC for PNI and LVI were included. Studies were selected in two phases: first collection and reference retrieval. The Quality Assessment of Diagnostic Accuracy…

Staining and LabelingSquamous Cell Carcinoma of Head and NeckneoplasmsImmunohistochemistrystomatitisCross-Sectional StudiesOtorhinolaryngologyHead and Neck NeoplasmsLymphatic MetastasisCarcinoma Squamous Cellantineoplastic agentsmicrobiotaEosine Yellowish-(YS)HumansMouth NeoplasmsNeoplasm InvasivenessSurgeryimmunotherapyHematoxylinGeneral DentistryUNESCO:CIENCIAS MÉDICASMedicina Oral Patología Oral y Cirugia Bucal
researchProduct

Intrahepatic cholangiocarcinoma: Limitations for resectability, current surgical concepts and future perspectives.

2020

Intrahepatic cholangiocarcinoma (iCCA) is the second most common hepatic malignancy and its incidence has been shown to increase significantly during the past decades. Complete surgical resection is currently acknowledged as the only curative treatment option able to provide adequate long-term outcomes. We herein review technical, functional and oncologic limitations for resectability, discuss current surgical aspects as well as highlight the fields in which future research and practice should focus on in order to ameliorate long-term outcomes in patients with iCCA.

Surgical resectionmedicine.medical_specialty030230 surgeryResectionBile duct cancerCholangiocarcinomaNeoplasms Multiple Primary03 medical and health sciences0302 clinical medicinePostoperative ComplicationsmedicineHepatectomyHepatic InsufficiencyHumansIn patientNeoplasm InvasivenessIntensive care medicineIntrahepatic Cholangiocarcinomabusiness.industryMargins of ExcisionGeneral Medicinemedicine.diseaseHepatic malignancyNeoadjuvant TherapyLiver TransplantationBile Ducts IntrahepaticOncologyBile Duct NeoplasmsCurative treatment030220 oncology & carcinogenesisBlood VesselsLymph Node ExcisionSurgeryLaparoscopyNeoplasm Recurrence LocalbusinessEuropean journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
researchProduct

Let-7d miRNA Shows Both Antioncogenic and Oncogenic Functions in Osteosarcoma-Derived 3AB-OS Cancer Stem Cells

2015

Osteosarcoma (OS), an aggressive highly invasive and metastatic bone-malignancy, shows therapy resistance and recurrence, two features that likely depend on cancer stem cells (CSCs), which hold both self-renewing and malignant potential. So, effective anticancer therapies against OS should specifically target and destroy CSCs. We previously found that the let-7d microRNA was downregulated in the 3AB-OS-CSCs, derived from the human OS-MG63 cells. Here, we aimed to assess whether let-7d modulation affected tumorigenic and stemness properties of these OS-CSCs. We found that let-7d-overexpression reduced cell proliferation by decreasing CCND2 and E2F2 cell-cycle-activators and increasing p21 an…

Time FactorsEpithelial-Mesenchymal TransitionTime FactorTranscription FactorPhysiologyClinical BiochemistryDrug ResistanceAntineoplastic AgentsApoptosisBone NeoplasmsCell Cycle ProteinsBone NeoplasmTransfectionCell LineAntineoplastic AgentCell MovementCell Line TumorCell Cycle ProteinHumansNeoplasm InvasivenessCell Self RenewalAntineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Bone Neoplasms; Cell Cycle; Cell Cycle Proteins; Cell Line Tumor; Cell Movement; Cell Self Renewal; Drug Resistance Neoplasm; Epithelial-Mesenchymal Transition; Gene Expression Regulation Neoplastic; Humans; MicroRNAs; Neoplasm Invasiveness; Neoplastic Stem Cells; Osteosarcoma; Phenotype; Signal Transduction; Time Factors; Transcription Factors; Transfection; Physiology; Medicine (all); Clinical Biochemistry; Cell BiologyNeoplasm InvasiveneNeoplasticOsteosarcomaTumorApoptosis Regulatory ProteinMedicine (all)Cell CycleApoptosiMicroRNACell BiologyGene Expression Regulation NeoplasticMicroRNAsPhenotypeGene Expression RegulationDrug Resistance NeoplasmNeoplastic Stem CellsNeoplasmNeoplastic Stem CellApoptosis Regulatory ProteinsTranscription FactorsHumanSignal Transduction
researchProduct

TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

2007

The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HN…

Transcriptional ActivationTGFβFAK; MT; Src; TGFβ; Animals; Biomarkers Tumor; Cadherins; Cell Line; Cell Transformation Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell BiologyCell LineMesodermFocal adhesionMiceTransforming Growth Factor betaBiomarkers TumorAnimalsHepatocyteNeoplasm InvasivenessNeoplasm InvasiveneEpithelial CellFocal Adhesion Protein-Tyrosine KinaseFAKbiologyAnimalCadherinLiver NeoplasmsMesenchymal stem cellEpithelial CellsCell BiologyTransforming growth factor betaTgf beta; fak; srcCadherinsUp-RegulationCell biologyEnzyme ActivationCell Transformation Neoplasticsrc-Family KinasesHepatocyte nuclear factor 4Liver NeoplasmTumor progressionMTFocal Adhesion Protein-Tyrosine KinasesCadherinHepatocytesCancer researchbiology.proteinsrc-Family KinaseSignal transductionSrcSignal TransductionProto-oncogene tyrosine-protein kinase SrcExperimental Cell Research
researchProduct