Search results for "Progression"

showing 10 items of 1251 documents

An inducible mouse model of colon carcinogenesis for the analysis of sporadic and inflammation-driven tumor progression.

2007

Colorectal cancer is a life-threatening disease that can develop spontaneously or as a complication of inflammatory bowel diseases. Mouse models are essential tools for the preclinical testing of novel therapeutic options in vivo. Here, we provide a highly reliable protocol for an experimental mouse model to study the development of colon cancers. It is based on the mutagenic agent azoxymethane (AOM), which exerts colonotropic carcinogenicity. Repeated intraperitoneal administration of AOM results in the development of spontaneous tumors within 30 weeks. As an alternative option, inflammation-dependent tumor growth can be investigated by combining the administration of AOM with the inflamma…

Colorectal cancerAzoxymethaneInflammationDiseaseTumor initiationBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundMiceIn vivomedicineAnimalsCarcinogenAzoxymethaneDextran Sulfatemedicine.diseaseDisease Models AnimalchemistryTumor progressionColonic NeoplasmsCancer researchCarcinogensDisease Progressionmedicine.symptomInflammation MediatorsMutagensNature protocols
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Proliferation state and polo-like kinase1 dependence of tumorigenic colon cancer cells.

2012

Abstract Tumor-initiating cells are responsible for tumor maintenance and relapse in solid and hematologic cancers. Although tumor-initiating cells were initially believed to be mainly quiescent, rapidly proliferating tumorigenic cells were found in breast cancer. In colon cancer, the proliferative activity of the tumorigenic population has not been defined, although it represents an essential parameter for the development of more effective therapeutic strategies. Here, we show that tumorigenic colon cancer cells can be found in a rapidly proliferating state in vitro and in vivo, both in human tumors and mouse xenografts. Inhibitors of polo-like kinase1 (Plk1), a mitotic kinase essential fo…

Colorectal cancerCancer stem cellscolorectal cancercell proliferationcell cycle.Cell Cycle ProteinsMice0302 clinical medicineMice Inbred NODAC133 AntigenRNA Small Interfering0303 health scienceseducation.field_of_studyPteridinesCell CycleCell cycleImmunohistochemistry3. Good healthMitochondriaGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColonic NeoplasmsMolecular MedicineFemaleStem cellPopulationTransplantation HeterologousCell Growth ProcessesBiologyProtein Serine-Threonine KinasesPLK103 medical and health sciencesCancer stem cellAntigens CDCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumanseducationProtein Kinase Inhibitors030304 developmental biologyGlycoproteinsSettore MED/04 - Patologia GeneraleCell growthCell Biologymedicine.diseaseTumor progressionImmunologyCancer researchPeptidesDevelopmental BiologyStem cells (Dayton, Ohio)
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On a Linear Diophantine Problem of Frobenius: Extending the Basis

1998

LetXk={a1, a2, …, ak},k>1, be a subset of N such that gcd(Xk)=1. We shall say that a natural numbernisdependent(onXk) if there are nonnegative integersxisuch thatnhas a representationn=∑ki=1 xiai, elseindependent. The Frobenius numberg(Xk) ofXkis the greatest integer withnosuch representation. Selmer has raised the problem of extendingXkwithout changing the value ofg. He showed that under certain conditions it is possible to add an elementc=a+kdto the arithmetic sequencea,a+d,a+2d, …, a+(k−1) d, gcd(a, d)=1, without alteringg. In this paper, we give the setCof all independent numberscsatisfyingg(A, c)=g(A), whereAcontains the elements of the arithmetic sequence. Moreover, ifa>kthen we give …

CombinatoricsDiscrete mathematicsAlgebra and Number TheoryCardinalityIntegerDiophantine equationArithmetic progressionValue (computer science)Basis (universal algebra)Element (category theory)MathematicsJournal of Number Theory
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Metabolic disorders and gastroenteropancreatic-neuroendocrine tumors (GEP-NETs): How do they influence each other? An Italian Association of Medical …

2022

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are a heterogeneous group of malignancies derived from neuroendocrine cells that can occur anywhere along the gastrointestinal tract. GEP-NETs incidence has been steadily increasing over the past decades, in parallel with the increasing incidence of the metabolic syndrome (MetS). It is not yet fully known whether the MetS components (such as obesity, dyslipidemia and type 2 diabetes) could be involved in the etiology of GEP-NETs or could influence their outcomes. In this review, a panel of experts of the Italian Association of Medical Oncology (AIOM), Italian Association of Medical Diabetologists (AMD), Italian Society of Endocrinology…

ConsensusSettore MED/06 - Oncologia MedicaGEP-NET progressionMetabolic disordersHematologyMedical OncologyMetabolic syndromeNOGEP-NET survivalPancreatic NeoplasmsNeuroendocrine Tumorsgastroenteropancreatic neuroendocrine tumors; gep-net progression; gep-net survival; metabolic disorders; metabolic syndrome; consensus; humans; medical oncology; diabetes mellitus; type 2; intestinal neoplasms; neuroendocrine tumors; pancreatic neoplasms; stomach neoplasmsOncologyGEP-NET progression; GEP-NET survival; Gastroenteropancreatic neuroendocrine tumors; Metabolic disorders; Metabolic syndromeDiabetes Mellitus Type 2Stomach NeoplasmsIntestinal NeoplasmsDiabetes MellitusHumansLS4_3Gastroenteropancreatic neuroendocrine tumorsType 2
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Early and late clinical landmarks of corneal dystrophies

2020

Abstract Corneal dystrophies (CDs) represent a heterogenous group of genetic diseases (Lisch and Weiss, 2019). The International Committee of Classification of Corneal Dystrophies (IC3D) distinguishes between 22 distinct forms of corneal dystrophy (CD) which are predominantly autosomal dominant, although autosomal recessive and X-chromosomal dominant and recessive patterns do exist. A detailed corneal examination of as many affected family members as possible can show the phenotypic differences of the various generations. There are few publications which describe the different CDs with regard to the early and late phenotypes. According to early and late phenotype, three types of CD are gene…

Corneal Dystrophies HereditaryGeneticsTime Factorsgenetic structuresDystrophyCorneal dystrophyLate onsetBiologymedicine.diseasePhenotypeeye diseasesSensory SystemsCorneaCellular and Molecular NeuroscienceOphthalmologyPhenotypeRecessive inheritanceDisease ProgressionmedicineHumanssense organsGeneExperimental Eye Research
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Targeted Therapies for Non-Small Cell Lung Cancer

2015

The discovery of new oncogenic driver mutations and the clinical development of targeted therapies have completely changed the paradigm treatment of non-small cell lung cancer (NSCLC). Epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs), erlotinib, gefitinib, afatinib, ALK-inhibitors, crizotinib, and ceritinib, have been already approved for clinical use, benefiting many patients whose tumors harbor, respectively, EGFR or EML4-ALK molecular alterations. However, despite an initial benefit, tumor progression inevitably occurs, due to the development of acquired resistance to the targeted treatments. Several mechanisms of resistance have been identified, such as the seco…

CrizotinibbiologyCeritinibbusiness.industryAfatinibmedicine.diseaserespiratory tract diseasesGefitinibTumor progressionmedicineCancer researchbiology.proteinErlotinibEpidermal growth factor receptorLung cancerbusinessmedicine.drug
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Prognostic Value of p53, p21/WAF1, Bcl-2, Bax, Bak and Ki-67 Immunoreactivity in pT1 G3 Urothelial Bladder Carcinomas

2001

pT1 G3 bladder carcinomas are heterogeneous with respect to tumor recurrence and progression. Whereas some urologists treat these carcinomas by repeated transurethral resections often followed by intravesical chemotherapy or BCG instillation, others recommend cystectomy after tumor recurrence or early cystectomy after the initial diagnosis. Our goal was to determine the prognostic value of p53, p21/WAF1, Bcl-2, Bax, Bak, and Ki-67 immunoreactivity in these tumors. There were 30 patients with a new histopathological diagnosis of pT1 G3 urothelial carcinoma based on a transurethral resection specimen. Representative sections of these specimens were examined for the above markers. All patients…

Cyclin-Dependent Kinase Inhibitor p21medicine.medical_specialtyPathologyTime FactorsTumor suppressor genemedicine.medical_treatmentBcl 2 baxUrologyDisease-Free SurvivalCystectomyPredictive Value of TestsCyclinsProto-Oncogene ProteinsBiomarkers TumormedicineHumansNeoplasm InvasivenessRetrospective Studiesbcl-2-Associated X ProteinCarcinoma Transitional CellUrinary bladderBladder cancerbiologyMembrane ProteinsGeneral MedicinePrognosismedicine.diseaseImmunohistochemistrySurvival RateKi-67 Antigenbcl-2 Homologous Antagonist-Killer Proteinmedicine.anatomical_structureTransitional cell carcinomaProto-Oncogene Proteins c-bcl-2Urinary Bladder NeoplasmsTumor progressionKi-67biology.proteinTumor Suppressor Protein p53Follow-Up StudiesTumor Biology
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Myc Promoter-Binding Protein-1 (MBP-1) Is a Novel Potential Prognostic Marker in Invasive Ductal Breast Carcinoma

2010

BackgroundAlpha-enolase is a glycolytic enzyme that catalyses the formation of phosphoenolpyruvate in the cell cytoplasm. α-Enolase and the predominantly nuclear Myc promoter-binding protein-1 (MBP-1) originate from a single gene through the alternative use of translational starting sites. MBP-1 binds to the P2 c-myc promoter and competes with TATA-box binding protein (TBP) to suppress gene transcription. Although several studies have shown an antiproliferative effect of MBP-1 overexpression on several human cancer cells, to date detailed observations of α-enolase and MBP-1 relative expression in primary tumors versus normal tissues and their correlation with clinicopathological features ha…

CytoplasmAlpha-enolasePROGRESSIONAged 80 and overRegulation of gene expressionMultidisciplinaryQRGenetics and Genomics/Gene ExpressionMiddle AgedPrognosisPathology/Molecular PathologyNUDE-MICETransport proteinCarcinoma DuctalDNA-Binding ProteinsGene Expression Regulation NeoplasticProtein Transportmedicine.anatomical_structureGLYCOLYTIC ENZYMEOncology/Breast CancerMedicineCELL LUNG-CANCER; ALPHA-ENOLASE; PROTEOMIC ANALYSIS; GLYCOLYTIC ENZYME; NUDE-MICE; GENE; IDENTIFICATION; PROGRESSION; EXPRESSION; METASTASESFemalePROTEOMIC ANALYSISEnolase MBP-1 Breast cancer ImmunohistochemistryResearch ArticleAdultEXPRESSIONScienceCELL LUNG-CANCERBreast NeoplasmsBiologyDNA-binding proteinBiomarkers TumormedicineHumansNeoplasm InvasivenessGeneAgedCell NucleusIDENTIFICATIONBinding proteinALPHA-ENOLASEGENEMolecular biologySettore BIO/18 - GeneticaCell nucleusMETASTASESCytoplasmPhosphopyruvate Hydratasebiology.proteinPLoS ONE
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Effect of the protein kinase inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine H-7 and N-(2-[methylamino]ethyl)-5-isoquinoline-sulfonamide H…

1998

The effects of 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine H-7 (a cAMP-dependent protein kinase and protein kinase C inhibitor), n-(2-[methylamino]ethyl)-5-isoquinoline-sulfonamide H-8 (a cAMP- and cGMP-dependent protein kinase inhibitor) and indomethacin (IND, a cyclooxygenase inhibitor) on both the spontaneous metastatic ability of 3LL (Lewis lung carcinoma) tumor cells and anti-tumor host response were studied. The study of tumor progression showed that H-7 and H-8 (2 mg kg(-1) day(-1) , i.p., for 8 days) significantly reduced the mean number of metastases (0.8 +/- 0.2 and 1.0 +/- 0.7, respectively, P0.05) with respect to the number of lung metastases (4.2 +/- 2.1) observed in the con…

Cytotoxicity ImmunologicMalemedicine.medical_specialtymedicine.drug_classIndomethacinCarcinoma Lewis LungMiceInternal medicine1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinemedicineAnimalsCyclooxygenase InhibitorsLymphocytesEnzyme InhibitorsNeoplasm MetastasisCytotoxicityProtein kinase AProtein kinase CPharmacologybiologyLewis lung carcinomaProtein kinase inhibitorIsoquinolinesMice Inbred C57BLEndocrinologyEnzyme inhibitorTumor progressionbiology.proteinCancer researchDisease ProgressionLeukocytes MononuclearCyclooxygenaseCell DivisionNeoplasm TransplantationSpleenEuropean journal of pharmacology
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Nuclear expression of apurinic/apyrimidinic endonuclease increases with progression of ovarian carcinomas.

2003

Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a key enzyme in the base excision repair pathway. Besides its function in DNA repair, APE serves to maintain several transcription factors in an active reduced state such as c-Fos, c-Jun, NF-kappaB, p53 and HIF-1alpha, all of which have been shown to play a role in tumorigenesis. Because of the importance of APE in maintaining genomic stability and gene regulation, we examined whether APE expression is associated with survival and histopathological parameters of patients with ovarian cancer.Tissue sections of primary epithelial ovarian carcinomas from 141 patients were immunostained using a monoclonal antibody directed against APE.Nucl…

DNA repairvirusesBiologymedicine.disease_causestomatognathic systemOvarian carcinomamedicineBiomarkers TumorDNA-(Apurinic or Apyrimidinic Site) LyaseHumansNeoplasm StagingRegulation of gene expressionCell NucleusOvarian NeoplasmsObstetrics and Gynecologysocial sciencesBase excision repairmedicine.diseasePrognosisMolecular biologyImmunohistochemistrybody regionsSurvival RateOncologyTumor progressionCancer researchDisease ProgressionImmunohistochemistryFemaleOvarian cancerCarcinogenesisGynecologic oncology
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