Search results for "Gene Expression"

showing 10 items of 4085 documents

The p53 Tumor Suppressor Network Is a Key Responder to Microenvironmental Components of Chronic Inflammatory Stress

2005

Abstract Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis and may modulate cancer risk in patients afflicted with this chronic disease. Here, we describe the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO•, H2O2, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. Isogenic HCT116 and HCT116 TP53−/− colon cancer cells were exposed to the NO• donor Sper/NO, H2O2, hypoxia, or hydroxyurea, and their mRNA was analyzed using oligonucleotide microarrays. Overall, 1,396 genes changed in a p53-dependent manner (P < 0.001), wit…

Cancer ResearchTumor suppressor geneColorectal cancerInflammationBiologymedicine.disease_causeArticleGene expressionmedicineHumansNitric Oxide DonorsInflammationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleHydrogen PeroxideCell cycleHypoxia (medical)Flow CytometryHCT116 Cellsmedicine.diseaseCell HypoxiaGene expression profilingOxidative StressOncologyImmunologyNitrogen OxidesSpermineTumor Suppressor Protein p53medicine.symptomOxidative stressCancer Research
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The FHIT gene is alternatively spliced in normal kidney and renal cell carcinoma.

1997

FHIT (Fragile Histidine Triad), a putative tumor suppressor gene, was cloned from fetal brain and colon cDNA libraries. Portions of this gene are deleted in esophageal, colon, lung and breast tumors, but this gene has not been found altered in sporadic renal cell carcinomas. We report here an alternatively spliced form of this gene cloned from a kidney cDNA library. This cDNA is 1189 bp in length, and contains an additional 94 bp exon, designated exon 2a (E2a). This novel sequence is located between exon 2 and exon 3 of the FHIT gene's untranslated region and exon 2a is present in all normal kidney tissues and cell lines. Analyses performed on sporadic renal cell carcinoma (RCC) tissues and…

Cancer ResearchTumor suppressor geneMolecular Sequence DataBiologymedicine.disease_causeKidneyPolymerase Chain ReactionExonFHITComplementary DNAGene expressionGeneticsmedicineHumansGenes Tumor SuppressorAmino Acid SequenceCloning MolecularneoplasmsMolecular BiologyCarcinoma Renal CellBase SequencecDNA libraryAlternative splicingProteinsBlotting NorthernKidney NeoplasmsAcid Anhydride HydrolasesNeoplasm ProteinsAlternative SplicingCancer researchCarcinogenesisOncogene
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Heterogeneous lack of expression of the tumour suppressor PTEN protein in human neoplastic tissues.

2001

PTEN, a tumour suppressor gene located at chromosome 10q23 and commonly mutated or deleted in a variety of tumours, encodes a dual-specific/phosphatidylinositol-3,4,5-triphosphate (PIP3) phosphatase. We report the generation of an anti-PTEN monoclonal antibody (MAb) that recognises an epitope at the C-terminus of PTEN, and describe the heterogeneous lack of expression of the PTEN protein in human tumour tissues, as demonstrated by immunohistochemical methods. Our anti-PTEN MAb provides a useful tool for the study of PTEN protein expression in tumour samples, in the search for tumour prognostic molecular markers.

Cancer ResearchTumor suppressor genemedicine.drug_classMonoclonal antibodyEpitopelaw.inventionMicelawNeoplasmsGene expressionmedicineTumor Cells CulturedPTENAnimalsHumansMice Inbred BALB CbiologyTumor Suppressor ProteinsPTEN PhosphohydrolaseCancerAntibodies Monoclonalmedicine.diseaseMolecular biologyImmunohistochemistryPhosphoric Monoester HydrolasesNeoplasm ProteinsOncologybiology.proteinCancer researchSuppressorImmunohistochemistryEuropean journal of cancer (Oxford, England : 1990)
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AKT-independent signaling downstream of oncogenic PIK3CA mutations in human cancer.

2009

SummaryDysregulation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway occurs frequently in human cancer. PTEN tumor suppressor or PIK3CA oncogene mutations both direct PI3K-dependent tumorigenesis largely through activation of the AKT/PKB kinase. However, here we show through phosphoprotein profiling and functional genomic studies that many PIK3CA mutant cancer cell lines and human breast tumors exhibit only minimal AKT activation and a diminished reliance on AKT for anchorage-independent growth. Instead, these cells retain robust PDK1 activation and membrane localization and exhibit dependency on the PDK1 substrate SGK3. SGK3 undergoes PI3K- and PDK1-dependent activation in PI…

Cancer Researchanimal structuresCell SurvivalClass I Phosphatidylinositol 3-KinasesAKT1AKT2Breast NeoplasmsCELLCYCLEBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeArticle03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineCell Line TumorNeoplasmsmedicinePTENHumansProtein kinase BneoplasmsPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesGene Expression ProfilingPTEN PhosphohydrolasePyruvate Dehydrogenase Acetyl-Transferring KinaseCell Biology3. Good healthEnzyme ActivationOncology030220 oncology & carcinogenesisCancer cellMutationCancer researchbiology.proteinFemaleSignal transductionCarcinogenesisProto-Oncogene Proteins c-aktSignal TransductionCancer cell
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Unknown primary tumors

2011

An unknown primary tumor (UPT) is defined by the presence of a metastatic cancer without a known primary site of origin despite a standardized diagnostic workup. Clinically, UPTs show rapid progression and early dissemination, with signs and symptoms related to the metastatic site. The molecular bases of their biology remain largely unknown, with no evidence as to whether they represent a distinct biological entity. Immunohistochemistry remain the best diagnostic tool in term of cost-effectiveness, but the time-consuming "algorithmic process" it relies on has led to the application of new molecular techniques for the identification of the primary site of UPTs. For example, several microarra…

Cancer Researchbusiness.industryGene Expression ProfilingBiological entityMEDLINETreatment optionsSigns and symptomsBioinformaticsFunctional imagingMicroRNAsOncologyUnknown primary tumors UPTImmunologyUnknown Primary TumorsGeneticsUnknown primaryAnimalsHumansNeoplasms Unknown PrimaryMedicinebusinessSite of originBiochimica et Biophysica Acta (BBA) - Reviews on Cancer
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Oncobox, gene expression-based second opinion system for predicting response to treatment in advanced solid tumors.

2019

e13143 Background: Anticancer Targeted Drugs (ATDs) specifically target one or a few types of tumor-related molecules in a cell. More than two hundred of ATDs were approved worldwide. They have different mechanisms of action and are effective for different cohorts of patients. However, many individual cases remain poorly responsive and it is of great importance to identify predictive markers of ATD efficacy. Our aim was to develop a platform enabling smart selection of the most efficient ATD therapies. Methods: We generated a second-opinion platform for clinical oncologists termed Oncobox. It is based on the analysis of gene expression profile of a cancer sample in comparison with the corr…

Cancer Researchbusiness.industrySecond opinionCellResponse to treatment03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureOncology030220 oncology & carcinogenesisGene expressionCancer researchMedicinebusiness030215 immunologyJournal of Clinical Oncology
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Medication for Acromegaly Reduces Expression of MUC16, MACC1 and GRHL2 in Pituitary Neuroendocrine Tumour Tissue

2021

Acromegaly is a disease mainly caused by pituitary neuroendocrine tumor (PitNET) overproducing growth hormone. First-line medication for this condition is the use of somatostatin analogs (SSAs), that decrease tumor mass and induce antiproliferative effects on PitNET cells. Dopamine agonists (DAs) can also be used if SSA treatment is not effective. This study aimed to determine differences in transcriptome signatures induced by SSA/DA therapy in PitNET tissue. We selected tumor tissue from twelve patients with somatotropinomas, with half of the patients receiving SSA/DA treatment before surgery and the other half treatment naive. Transcriptome sequencing was then carried out to identify diff…

Cancer Researchbusiness.industrysomatostatin/dopamine (SSA/DA) therapynext generation sequencing (NGS)medicine.disease_causemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282TranscriptomeExtracellular matrixSomatostatinOncologyDownregulation and upregulationDopamineGene expressionAcromegalyCancer researchMedicineacromegalysomatotropinomabusinessCarcinogenesistranscriptomeOriginal Researchmedicine.drugFrontiers in Oncology
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Immune escape of AKT overexpressing ovarian cancer cells

2012

Platinum-resistance is the most crucial problem for treatment of ovarian cancer. There is a clinical need for new treatment strategies which overcome platinum resistance. As survival is strongly influenced by immunological parameters, immunotherapeutic strategies appear promising. Therefore a better understanding of the interaction between ovarian tumour cells and cells of the immune system is a necessary prerequisite. In the present study we aimed to enlighten the interactions between platinum resistant and platinum sensitive ovarian cancer cells and natural-killer (NK)-cells. Modified FATAL assay was used for determining the killing efficiency of NK-cells for the parental A2780 cells and …

Cancer Researchendocrine system diseasesUbiquitin-Protein LigasesCellApoptosisBiologymedicine.disease_causeInhibitor of Apoptosis ProteinsImmune systemCell Line TumormedicineHumansPlatinumOvarian NeoplasmsCancerCell cyclemedicine.diseaseBaculoviral IAP Repeat-Containing 3 Proteinfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticKiller Cells Naturalmedicine.anatomical_structureOncologyDrug Resistance NeoplasmCell cultureApoptosisCancer researchFemaleOvarian cancerCarcinogenesisProto-Oncogene Proteins c-aktInternational Journal of Oncology
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Histone deacetylase inhibitors: apoptotic effects and clinical implications (Review).

2008

It has been shown that epigenetic modifications play an important role in tumorigenesis. Thus, affecting epigenetic tumorigenic alterations can represent a promising strategy for anticancer targeted therapy. Among the key chromatin modifying enzymes which influence gene expression, histone acetyltransferases (HATs) and histone deacetylases (HDACs) have recently attracted interest because of their impact on tumor development and progression. Increased expression of HDACs and disrupted activities of HATs have been found in several tumor types, with a consequent hypoacetylated state of chromatin that can be strictly correlated with low expression of either tumor suppressor or pro-apoptotic gen…

Cancer Researchmedicine.drug_classAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsModels BiologicalRomidepsinEpigenesis Geneticchemistry.chemical_compoundDepsipeptidesNeoplasmsSettore BIO/10 - BiochimicamedicineHumansEpigeneticsVorinostatSulfonamidesVorinostatHistone deacetylase inhibitorHDACI apoptosisChromatinChromatinProtein Structure TertiaryGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsHistoneOncologychemistryModels ChemicalCancer researchbiology.proteinHistone deacetylaseBelinostatmedicine.drug
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Resistance factors in colon cancer tissue and the adjacent normal colon tissue: glutathione S-transferases alpha and pi, glutathione and aldehyde deh…

1998

Abstract Glutathione S -transferases (GST) α and π , glutathione (GSH) and aldehyde dehydrogenase (ADH) were determined in colorectal cancer tissue specimens and in the adjacent normal colon tissue. The median contents in normal and cancer tissue were 8.1 (2.3–30.3) (5–95% quantiles) and 15.1 (5.3–50.3) μ g/mg protein for GST π ( P =0.035), 0.0 (0.0–1.4) and 0.4 (0.0–3.5) μ g/mg protein for GST α ( P =0.019), 7.3 (1.3–22.7) and 5.6 (2.3–26.0) μ g/mg protein for GSH ( P =0.171) and 30.8 (13.0–42.0) and 23.2 (9.0–32.9) μ g/mg protein for ADH ( P =0.0017), respectively. Thus, the mean GST α and π both significantly increased in colon cancer compared to the adjacent normal tissue, which underli…

Cancer Researchmedicine.medical_specialtyColorectal cancerColonAldehyde dehydrogenaseBiologymedicine.disease_causeIsozymeGene productchemistry.chemical_compoundInternal medicineGene expressionmedicineHumansGlutathione TransferaseCancerGlutathioneAldehyde Dehydrogenasemedicine.diseaseGlutathioneEndocrinologyOncologychemistryDrug Resistance NeoplasmColonic Neoplasmsbiology.proteinCarcinogenesisCancer letters
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