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1. Montesano R, Soulié P, Eble JA, Carrozzino F: Tumour necrosis factor alpha confers an invasive, transformed phenotype on mammary epithelial cells. J Cell Sci; 2005 Aug 1;118(Pt 15):3487-500
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  • [Title] Tumour necrosis factor alpha confers an invasive, transformed phenotype on mammary epithelial cells.
  • Although loss of cell-cell adhesion and gain of invasive properties play a crucial role in the malignant progression of epithelial tumours, the molecular signals that trigger these processes have not been fully elucidated.
  • In light of the well-established relationship between chronic inflammation and cancer, we hypothesized that pro-inflammatory cytokines disrupt epithelial-cell adhesion and promote cell migration.
  • Among the several cytokines examined, tumour necrosis factor alpha (TNF-alpha) caused a pronounced 3D scattering of preformed epithelial-cell colonies and induced 31EG4-2A4 cells grown on top of a collagen gel to invade the underlying matrix.
  • In addition, TNF-alpha abolished contact-mediated inhibition of cell proliferation and stimulated cell growth both in the absence of exogenous mitogens and under anchorage-independent conditions.
  • TNF-alpha induced the expression of matrix metalloproteinase 9 (MMP-9).
  • Addition of the MMP inhibitor BB-94 abrogated TNF-alpha-induced 3D scattering.
  • TNF-alpha also enhanced the attachment of 31EG4-2A4 cells to type-I collagen and markedly increased the expression of the alpha2 integrin subunit.
  • Addition of a blocking antibody to beta1-integrin or of rhodocetin (a specific alpha2beta1 antagonist) to collagen-gel cultures abrogated 3D scattering.
  • Collectively, these results demonstrate an essential role for MMPs and alpha2beta1 integrin in the invasive response of 31EG4-2A4 cells to TNF-alpha.
  • We propose that the biological activities described in this study contribute to the ability of TNF-alpha to promote tumour progression and cancer-cell dissemination.
  • [MeSH-major] Cell Movement / drug effects. Cell Proliferation / drug effects. Epithelial Cells / drug effects. Mammary Glands, Animal / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Line. Collagen / metabolism. Extracellular Matrix / metabolism. Integrin alpha2beta1 / metabolism. Metalloproteases / antagonists & inhibitors. Metalloproteases / metabolism. Mice. Phenotype. Protease Inhibitors / pharmacology. Receptors, Tumor Necrosis Factor, Type I / metabolism

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  • (PMID = 16079290.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alpha2beta1; 0 / Protease Inhibitors; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; 9007-34-5 / Collagen; EC 3.4.- / Metalloproteases
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2. Marini P, Schmid A, Jendrossek V, Faltin H, Daniel PT, Budach W, Belka C: Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis. BMC Cancer; 2005 Jan 14;5:5
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  • [Title] Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis.
  • BACKGROUND: TRAIL (tumor necrosis factor related apoptosis inducing ligand) is an apoptosis inducing ligand with high specificity for malignant cell systems.
  • Combined treatment modalities using TRAIL and cytotoxic drugs revealed highly additive effects in different tumour cell lines.
  • Little is known about the efficacy and underlying mechanistic effects of a combined therapy using TRAIL and ionising radiation in solid tumour cell systems.
  • METHODS: Tumour cell systems derived from breast- (MDA MB231), lung--(NCI H460) colorectal--(Colo 205, HCT-15) and head and neck cancer (FaDu, SCC-4) were treated with a combination of TRAIL and irradiation using two different time schedules.
  • RESULTS: The combined treatment of TRAIL with irradiation strongly increased apoptosis induction in all treated tumour cell lines compared to treatment with TRAIL or irradiation alone.
  • Upregulation of TRAIL receptor DR5 after irradiation was observed in four of six tumour cell lines but did not correlate to tumour cell sensitisation to TRAIL.
  • TRAIL did not show toxicity in normal tissue cell systems.
  • In addition, pre-irradiation did not sensitise all nine tested human normal tissue cell cultures to TRAIL.
  • Sequential application of ionising radiation followed by TRAIL is associated with an synergistic induction of cell death in a large panel of solid tumour cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis. Membrane Glycoproteins / therapeutic use. Neoplasms / therapy. Radiation, Ionizing. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Apoptosis Regulatory Proteins. Caspase 8. Caspases / metabolism. Cell Line, Tumor. Cells, Cultured. Combined Modality Therapy. Humans. Poly(ADP-ribose) Polymerases / metabolism. Receptors, Tumor Necrosis Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 15651986.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC547906
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3. Werbowetski-Ogilvie TE, Agar NY, Waldkircher de Oliveira RM, Faury D, Antel JP, Jabado N, Del Maestro RF: Isolation of a natural inhibitor of human malignant glial cell invasion: inter alpha-trypsin inhibitor heavy chain 2. Cancer Res; 2006 Feb 1;66(3):1464-72
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  • [Title] Isolation of a natural inhibitor of human malignant glial cell invasion: inter alpha-trypsin inhibitor heavy chain 2.
  • Malignant central nervous system (CNS) tumors, such as glioblastoma multiforme, invade the brain and disrupt normal tissue architecture, making complete surgical removal virtually impossible.
  • Here, we have developed and optimized a purification strategy to isolate and identify natural inhibitors of glioma cell invasion in a three-dimensional collagen type I matrix.
  • Inter alpha-trypsin inhibitor heavy chain 2 (ITI H2) was identified from the most inhibitory fractions and its presence was confirmed both as a single protein and in a bikunin-bound form.
  • Stable overexpression in U251 glioma cells validated ITI H2's strong inhibition of human glioma cell invasion together with significant inhibition of cell proliferation and promotion of cell-cell adhesion.
  • These findings suggest that reduction of ITI H2 expression correlates with brain tumor progression and that targeting factors responsible for its loss or restoring the ITI supply exogenously may serve as potential therapeutic strategies for a variety of CNS tumors.
  • [MeSH-major] Alpha-Globulins / isolation & purification. Brain Neoplasms / chemistry. Glioma / chemistry
  • [MeSH-minor] Animals. Blotting, Western. Cell Adhesion / physiology. Cell Movement / physiology. Down-Regulation. Humans. Immunohistochemistry. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / genetics. Mice. Neoplasm Invasiveness. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Trypsin Inhibitor, Kunitz Soybean / biosynthesis. Trypsin Inhibitor, Kunitz Soybean / genetics

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  • (PMID = 16452202.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / SPINT2 protein, human; 39346-44-6 / inter-alpha-inhibitor; 9088-41-9 / Trypsin Inhibitor, Kunitz Soybean; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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4. Buritica C, Serrano M, Zuluaga A, Arrabal M, Regauer S, Nogales FF: Mixed epithelial and stromal tumour of the kidney with luteinised ovarian stroma. J Clin Pathol; 2007 Jan;60(1):98-100
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  • [Title] Mixed epithelial and stromal tumour of the kidney with luteinised ovarian stroma.
  • We report a case of a 9-cm mixed epithelial and stromal tumour of the kidney in an obese 70-year-old woman with diabetes.
  • The ovarian-type stroma had a spindle cell component that was positive for progesterone receptors and had the hitherto unreported presence of abundant foci of luteinised stromal cells with characteristic immunohistochemical positivity to alpha-inhibin, calretinin, aromatase and gonadotropin-releasing hormone (GnRH) receptors.
  • [MeSH-major] Kidney Neoplasms / pathology. Mixed Tumor, Malignant / pathology. Neoplasms, Glandular and Epithelial / pathology

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  • (PMID = 17213356.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860583
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5. Gordon GJ, Mani M, Mukhopadhyay L, Dong L, Yeap BY, Sugarbaker DJ, Bueno R: Inhibitor of apoptosis proteins are regulated by tumour necrosis factor-alpha in malignant pleural mesothelioma. J Pathol; 2007 Mar;211(4):439-46
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  • [Title] Inhibitor of apoptosis proteins are regulated by tumour necrosis factor-alpha in malignant pleural mesothelioma.
  • Inhibitor of apoptosis proteins (IAPs) are overexpressed by most neoplasms and promote tumour cell survival after a wide variety of apoptotic stimuli elicited via intrinsic (ie mitochondrial) and extrinsic (ie death receptor) pathways.
  • It has previously been reported that one of these proteins, IAP-1(MIHC/cIAP2), is overexpressed in malignant pleural mesothelioma (MPM) and is responsible for a large degree of the resistance of cultured MPM cells to cisplatin.
  • In the present study, potential regulatory mechanisms of IAP genes in MPM were investigated and it was found that tumour necrosis factor-alpha (TNF-alpha) can increase mRNA and protein levels of IAP-1, IAP-2, and XIAP, but not livin or survivin in MPM cell lines (n=4).
  • Co-incubation of MPM cells with TNF-alpha and pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor, prevented TNF-mediated up-regulation of IAP gene expression levels.
  • In survival studies, TNF-alpha was not toxic to MPM cells at any concentration examined.
  • However, MPM cells exposed to TNF-alpha were twice as resistant to cisplatin in dose response survival assays compared with unstimulated controls and were found to have a significantly greater fraction of surviving cells at multiple cisplatin concentrations (p<0.0087).
  • Finally, it was found that levels of circulating TNF-alpha were statistically significantly (p=0.031) (median 312.5 pg/ml) higher in MPM patients (n=6) prior to surgical tumour debulking compared with those after surgery (median 0 pg/ml).
  • These results when combined with previous observations by our laboratory and others strongly suggest that IAPs act synergistically with TNF family members to promote survival of MPM tumour cells after exposure to cisplatin and possibly other chemotherapeutic drugs.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / genetics. Mesothelioma / genetics. Neoplasm Proteins / genetics. Pleural Neoplasms / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / analysis. Adaptor Proteins, Signal Transducing / genetics. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cisplatin / pharmacology. Gene Expression Regulation, Neoplastic / genetics. Humans. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / genetics. NF-kappa B / genetics. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Transcription, Genetic / genetics. Up-Regulation / genetics. X-Linked Inhibitor of Apoptosis Protein / analysis. X-Linked Inhibitor of Apoptosis Protein / genetics

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland.
  • (PMID = 17253597.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-100315; United States / NCI NIH HHS / CA / CA-102591; United States / NCI NIH HHS / CA / CA-105249
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / BIRC7 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Necrosis Factor-alpha; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; Q20Q21Q62J / Cisplatin
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6. Oremek GM, Sauer-Eppel H, Bruzdziak TH: Value of tumour and inflammatory markers in lung cancer. Anticancer Res; 2007 Jul-Aug;27(4A):1911-5
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  • [Title] Value of tumour and inflammatory markers in lung cancer.
  • The aim of this study was to evaluate the individual diagnostic utility of tumour and inflammatory markers in patients with different pulmonary diseases.
  • The usefulness of neuron-specific enolase (NSE), carcino-embryonic antigen (CEA), serum pro-gastrin releasing peptide (ProGRP) and CYFRA 21-1, as tumour markers, and C-reactive protein (CRP) and tumour necrosis factor-alpha (TNFalpha) as inflammatory markers for diagnosis, treatment and monitoring of patients with different pulmonary afflictions was investigated.
  • Moreover, serum marker levels were analyzed in 139 patients with different pulmonary malignancies: 29 patients with adenocarcinoma, 30 patients with squamous cell carcinoma, 80 patients with small cell lung cancer (SCLC).
  • All tumour markers showed significantly elevated values in malignant diseases.
  • The acute phase response had a wide range in patients with malignant tumours.
  • In conclusion, when serum tumour markers are abnormally elevated in patients with lung cancer, CEA, CYFRA 21-1, NSE and ProGRP are useful clinical markers, good indicators of disease extent and may have important prognostic value.
  • [MeSH-major] Biomarkers, Tumor / blood. Inflammation / blood. Lung Neoplasms / diagnosis
  • [MeSH-minor] Antigens, Neoplasm / blood. Area Under Curve. C-Reactive Protein / analysis. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Small Cell / blood. Carcinoma, Small Cell / diagnosis. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / diagnosis. Humans. Immunoassay. Keratin-19. Keratins / blood. Lung Diseases / blood. Lung Diseases / diagnosis. Peptide Fragments / blood. Peptides / blood. Phosphopyruvate Hydratase / blood. ROC Curve. Recombinant Proteins / blood. Sensitivity and Specificity. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17649794.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / antigen CYFRA21.1; 0 / pro-gastrin-releasing peptide (31-98); 68238-35-7 / Keratins; 9007-41-4 / C-Reactive Protein; EC 4.2.1.11 / Phosphopyruvate Hydratase
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7. Nutt JE, Razak AR, O'Toole K, Black F, Quinn AE, Calvert AH, Plummer ER, Lunec J: The role of folate receptor alpha (FRalpha) in the response of malignant pleural mesothelioma to pemetrexed-containing chemotherapy. Br J Cancer; 2010 Feb 2;102(3):553-60
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  • [Title] The role of folate receptor alpha (FRalpha) in the response of malignant pleural mesothelioma to pemetrexed-containing chemotherapy.
  • BACKGROUND: The standard treatment of choice for malignant pleural mesothelioma is chemotherapy with pemetrexed and platinum, but the clinical outcome is poor.
  • This study investigates the response to pemetrexed in a panel of eight mesothelioma cell lines and the clinical outcome for patients treated with pemetrexed in relation to folate receptor alpha (FRalpha).
  • METHODS: Cell lines were treated with pemetrexed to determine the concentration that reduced growth to 50% (GI(50)).
  • RESULTS: A wide range of GI(50) values was obtained for the cell lines, H2452 cells being the most sensitive (GI(50) 22 nM) and RS5 cells having a GI(50) value greater than 10 microM.
  • No FRalpha protein was detected in any cell line, and there was no relationship between sensitivity and expression of folate transporters.
  • FRalpha was detected in 39% of tumour samples, generally in a small percentage of cells.

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  • (PMID = 20051956.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Folate Receptors, GPI-Anchored; 0 / Folic Acid Antagonists; 0 / Glutamates; 0 / Receptors, Cell Surface; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine
  • [Other-IDs] NLM/ PMC2822938
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8. Yip WK, Abdullah MA, Yusoff SM, Seow HF: Increase in tumour-infiltrating lymphocytes with regulatory T cell immunophenotypes and reduced zeta-chain expression in nasopharyngeal carcinoma patients. Clin Exp Immunol; 2009 Mar;155(3):412-22
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  • [Title] Increase in tumour-infiltrating lymphocytes with regulatory T cell immunophenotypes and reduced zeta-chain expression in nasopharyngeal carcinoma patients.
  • The pathological significance of the mechanisms of tumour immune-evasion and/or immunosuppression, such as loss of T cell signalling and increase in regulatory T cells (T(regs)), has not been well established in the nasopharyngeal carcinoma (NPC) microenvironment.
  • To evaluate the T(reg) immunophenotypes in tumour-infiltrating lymphocytes (TILs), we performed a double-enzymatic immunostaining for detection of forkhead box P3 (FoxP3) and other markers including CD4, CD8, and CD25 on 64 NPC and 36 non-malignant nasopharyngeal (NP) paraffin-embedded tissues.
  • Increased CD4(+)FoxP3(+)/CD4(+) proportion and FoxP3(+)/CD8(+) ratio were associated with keratinizing squamous cell carcinoma.
  • These data provide evidence for the imbalances of T(reg) and effector T cell phenotypes and down-regulation of signal-transducing molecules in TILs, supporting their role in suppression of immune response and immune evasion of NPC.
  • [MeSH-major] Carcinoma / immunology. Lymphocytes, Tumor-Infiltrating / immunology. Nasopharyngeal Neoplasms / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Antigens, CD3 / analysis. Biomarkers / analysis. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Carcinoma, Squamous Cell / immunology. Female. Forkhead Transcription Factors / analysis. Humans. Immunohistochemistry. Interleukin-2 Receptor alpha Subunit / analysis. Lymphocyte Count. Male. Middle Aged. Nasopharynx / immunology. Statistics, Nonparametric

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  • (PMID = 19220831.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Biomarkers; 0 / CD3 antigen, zeta chain; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
  • [Other-IDs] NLM/ PMC2669517
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9. Appetecchia M, Ferretti E, Carducci M, Izzo F, Carpanese L, Marandino F, Terzoli E: Malignant glucagonoma. New options of treatment. J Exp Clin Cancer Res; 2006 Mar;25(1):135-9
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  • [Title] Malignant glucagonoma. New options of treatment.
  • Few cases of malignant glucagonomas have been described in the literature.
  • In this paper we present a case of a 77-year-old woman with necrolytic migratory erythema and high plasma glucagon and chromogranin A levels caused by a neuroendocrine tumour.
  • An abdominal CT scan suggested a pancreatic lesion and two liver metastases.
  • The patient underwent pancreatic debulking and liver metastasectomy.
  • Histological and immunohistochemical investigations revealed a well differentiated neuroendocrine tumour with vascular invasion and scattered immunopositivity for somatostatin receptors.
  • The patient was treated with octreotide (30 mg i.m. every 28 days) and interferon-alpha (6 MU s.cc 3 times per week) plus three cycles of hepatic chemoembolisation.
  • The patient is now asymptomatic with persistent hepatic disease and normal serum glucagon levels forty months after primary treatment.
  • So far, only few immunohistochemical studies are reported on malignant glucagonoma and combined treatment schedules.
  • We demonstrated, for the first time, a scattered immunopositivity for somatostatin receptors in a malignant glucagonoma.
  • A combined antiproliferative medical treatment and the hepatic chemoembolization have been able to control tumor growth and disease symptoms for a long time after surgery.
  • [MeSH-major] Glucagonoma / therapy
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Female. Glucagon / blood. Humans. Immunohistochemistry. Interferon-alpha / metabolism. Neuroendocrine Tumors / blood. Octreotide / pharmacology. Proglucagon / metabolism. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16761630.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Interferon-alpha; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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10. Yamate J, Sakamori M, Kuwamura M, Kotani T: Neoplastic and non-neoplastic cell lines from a malignant peripheral nerve sheath tumour of the cervix of a rat. J Comp Pathol; 2007 Jul;137(1):9-21
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  • [Title] Neoplastic and non-neoplastic cell lines from a malignant peripheral nerve sheath tumour of the cervix of a rat.
  • A homotransplantable tumour (LY) and cell lines (LY-PPB6 and LY-H12) were established from a spontaneous malignant peripheral nerve sheath tumour (PNST) of the uterine cervix of an F344 rat.
  • LY-H12 cells reacted to vimentin and alpha-smooth muscle actin (alpha-SMA), and the alpha-SMA-positive cell number was increased dose-dependently by the addition of transforming growth factor (TGF)-beta1, indicating a myofibroblastic nature.
  • As TGF-beta1 mRNA expression was shown in both LY-PPB6 and LY-H12 cells by the RT-PCR, the myofibroblastic phenotype of LY-H12 cells may be mediated by paracrine or autocrine signalling in tumour tissues.
  • [MeSH-minor] Actins / genetics. Actins / metabolism. Animals. Cell Line. Cell Line, Tumor. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Neoplastic / drug effects. Nerve Growth Factor / genetics. Nerve Growth Factor / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Inbred F344. Transforming Growth Factor beta1 / pharmacology


11. Fox SA, Kusmiaty, Loh SS, Dharmarajan AM, Garlepp MJ: Cisplatin and TNF-alpha downregulate transcription of Bcl-xL in murine malignant mesothelioma cells. Biochem Biophys Res Commun; 2005 Nov 25;337(3):983-91
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  • [Title] Cisplatin and TNF-alpha downregulate transcription of Bcl-xL in murine malignant mesothelioma cells.
  • Malignant mesothelioma (MM) is an aggressive and highly chemo-resistant tumour.
  • All of the four mouse MM cell lines examined expressed Bax, Bcl-xL, c-Myc, and caspase-3 but not Bcl-2.
  • Cisplatin-induced apoptosis characterised by DNA fragmentation and cell death while caspase-3/7 was activated in 3 of 4 cell lines.
  • In the AC29 and AB1 models, both cisplatin and TNF-alpha downregulated Bcl-xL gene expression, indicating that this gene was a common transcriptional target in these cells.
  • [MeSH-major] Apoptosis / drug effects. Cisplatin / administration & dosage. Mesothelioma / metabolism. Tumor Necrosis Factor-alpha / administration & dosage. bcl-X Protein / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic. Mice. Transcription Factors / drug effects

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  • (PMID = 16225850.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bcl2l1 protein, mouse; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / bcl-X Protein; Q20Q21Q62J / Cisplatin
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12. Katori H, Nozawa A, Tsukuda M: Markers of malignant transformation of sinonasal inverted papilloma. Eur J Surg Oncol; 2005 Oct;31(8):905-11
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  • [Title] Markers of malignant transformation of sinonasal inverted papilloma.
  • AIM: To measure HPV status, epidermal growth factor receptor (EGFR) and transforming growth factor-alpha (TGF-alpha) expression and Ki-67 index in exophytic papilloma (EP), inverted papilloma (IP) with dysplasia, IP with carcinoma and invasive squamous cell carcinoma (SCC).
  • The nasal tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • RESULTS: Significant increase of EGFR and TGF-alpha was observed in IP with severe dysplasia, IP with carcinoma and invasive SCC compared to IP with mild dysplasia and control nasal mucosa.
  • Among IP, HPV 6/11-positive was present in 42% tumour and HPV 16/18-positive was present in 31% of tumours.
  • CONCLUSION: Pre-cancerous lesions of IP exhibited elevated levels of EGFR and TGF-alpha and these expression may be associated with early events in IP carcinogenesis.
  • HPV infection may be an early event in a multistep process of malignant formation of IP.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic / pathology. Nose Neoplasms / pathology. Papilloma, Inverted / pathology. Paranasal Sinus Neoplasms / pathology
  • [MeSH-minor] Antibodies, Monoclonal. Carcinoma / pathology. Carcinoma, Squamous Cell / pathology. Female. Humans. In Situ Hybridization. Ki-67 Antigen / analysis. Male. Middle Aged. Nasal Mucosa / pathology. Neoplasm Invasiveness. Papilloma / pathology. Papillomaviridae / classification. Papillomaviridae / isolation & purification. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / analysis. Transforming Growth Factor alpha / analysis

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  • (PMID = 16005600.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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13. Vasiljeva O, Korovin M, Gajda M, Brodoefel H, Bojic L, Krüger A, Schurigt U, Sevenich L, Turk B, Peters C, Reinheckel T: Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice. Oncogene; 2008 Jul 10;27(30):4191-9
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  • [Title] Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice.
  • Expression levels of the papain-like cysteine protease cathepsin B (Ctsb) have been positively correlated with mammary tumour progression and metastasis; however, its roles in the hallmark processes of malignant growth remain poorly defined.
  • Using Ctsb-deficient mice we investigated tumour cell differentiation, proliferation and apoptosis in the Tg(MMTV-PyMT) mouse mammary cancer model.
  • Mice lacking Ctsb exhibited reduced cell proliferation in mammary carcinomas and their lung metastases.
  • Notably, intravenous injection of primarily isolated, Ctsb-expressing tumour cells into congenic Ctsb-deficient mice revealed impaired cell proliferation in the resulting experimental lung metastases, providing evidence for the involvement of Ctsb in paracrine regulation of cancer cell proliferation.
  • No Ctsb genotype-dependent difference in tumour cell death was observed in vivo or by treatment of isolated PyMT cancer cells with tumour necrosis factor-alpha.
  • [MeSH-major] Carcinoma / genetics. Cathepsin B / genetics. Cell Proliferation. Immunity, Innate / genetics. Mammary Neoplasms, Animal / genetics. Tumor Burden / genetics
  • [MeSH-minor] Animals. Cell Death / genetics. Disease Progression. Female. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Mice. Mice, Knockout. Neoplasm Transplantation. Time Factors. Tumor Cells, Cultured

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  • (PMID = 18345026.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.22.1 / Cathepsin B
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14. Darra E, Lenaz G, Cavalieri E, Fato R, Mariotto S, Bergamini C, Carcereri de Prati A, Perbellini L, Leoni S, Suzuki H: Alpha-bisabolol: unexpected plant-derived weapon in the struggle against tumour survival? Ital J Biochem; 2007 Dec;56(4):323-8

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  • [Title] Alpha-bisabolol: unexpected plant-derived weapon in the struggle against tumour survival?
  • Despite enormous scientific and economic effort tumour still is one of the most terrible pathologies among human population all over the world.
  • Here, we summarize the short story of the study of an extraordinary effect of one plant compound towards transformed cells derived from highly malignant tumours.
  • Alpha-bisabolol, a sesquiterpene widely present in plants, selectively kills transformed cells by apoptosis without affecting the viability of normal cells.
  • One of its intracellular targets seems to be situated on mitochondria and is possibly identified as the permeability transition pore, as judged from rapid mitochondrial membrane potential dissipation induced by alpha-bisabolol and the failure to kill cells in the presence of cyclosporine A.
  • Preferential adsorption of alpha-bisabolol into lipid rafts, rich in tumour cells, may explain the selective action of this compounds towards tumour cells.
  • Furthermore, Surface Plasmon Resonance analysis indicates that alpha-bisabolol directly interacts with Bid protein, a member of the Bcl2 family deeply involved in apoptosis, suggesting a possibility that Bid, or similar protein(s), may be involved in a putative intracellular transport system of alpha-bisabolol from plasma membrane to mitochondria.
  • Experiments with animals indicate that alpha-bisabolol is not toxic and is accumulated, through blood flow, in every tissues examined.
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Models, Biological. Signal Transduction

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  • (PMID = 19192636.001).
  • [ISSN] 0021-2938
  • [Journal-full-title] The Italian journal of biochemistry
  • [ISO-abbreviation] Ital. J. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Sesquiterpenes; 24WE03BX2T / bisabolol
  • [Number-of-references] 15
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15. Escher N, Spies-Weisshart B, Kaatz M, Melle C, Bleul A, Driesch D, Wollina U, von Eggeling F: Identification of HNP3 as a tumour marker in CD4+ and CD4- lymphocytes of patients with cutaneous T-cell lymphoma. Eur J Cancer; 2006 Jan;42(2):249-55
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  • [Title] Identification of HNP3 as a tumour marker in CD4+ and CD4- lymphocytes of patients with cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCL) are characterized by malignant proliferation of skin homing T-cells.
  • Lymphocytes were separated in CD4+ and CD4- fractions by magnetic cell sorting (MACS).
  • For the generated combined rule base for the CD4- cell fraction, both the sensitivity and specificity for the prediction of CTCL reached 96%, while for the CD4+ fraction they were 92% and 84%, respectively, for sensitivity and specificity.
  • The most significant peak at 3489Da could be identified as HNP3, an alpha-defensin, by immunocapturing.
  • These results open up both the possibility for the use of this protein signature, especially HNP3, to more effectively monitor and screen CTCL, and the avenue to identify the other relevant peaks for a better understanding of the development of this tumour.
  • [MeSH-major] Biomarkers, Tumor / metabolism. CD4-Positive T-Lymphocytes / metabolism. Lymphoma, T-Cell, Cutaneous / diagnosis. Skin Neoplasms / diagnosis. alpha-Defensins / metabolism

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  • (PMID = 16338134.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / human neutrophil peptide 3
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16. Mathsson L, Tejde A, Carlson K, Höglund M, Nilsson B, Nilsson-Ekdahl K, Rönnelid J: Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones. Br J Haematol; 2005 Jun;129(6):830-8
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  • [Title] Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones.
  • Complement blockade resulted in increased IgG CG-induced interleukin (IL)-10 production that was inversely correlated with decreased production of tumour necrosis factor-alpha.
  • CG-induced IL-10 might be a growth factor for malignant B-lymphocytes in CG-associated lymphoproliferative diseases with constant complement consumption.
  • [MeSH-minor] Aged. Cells, Cultured. Complement Inactivator Proteins / immunology. Complement Pathway, Classical / immunology. Female. Humans. Hydrogen-Ion Concentration. Immunoglobulin G / immunology. Immunoglobulin M / immunology. Interleukin-10 / biosynthesis. Male. Middle Aged. Monocytes / immunology. Neoplastic Stem Cells / pathology. Temperature. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 15953012.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Complement Inactivator Proteins; 0 / Cryoglobulins; 0 / Cytokines; 0 / Fc gamma receptor IIA; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Receptors, IgG; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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17. Qian ZY, Miao Y, Dai CC, Xu ZK, Liu XL: [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2005 Oct;27(5):572-4
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  • [Title] [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas].
  • OBJECTIVE: To investigate the feasibility and therapeutic results of multiple organ resection in patients with tumor of the body and tail of pancreas.
  • METHODS: The clinical and pathological data were analysed in 16 consecutive patients with neoplasm of the body and tail of pancreas from 1999 to 2004 retrospectively.
  • RESULTS: Multiple organ resection was performed in 6 cases of primary pancreatic adenocarcinoma of the body and tail (3 cases of pancreatic cancer, 2 cases of malignant glucagonoma, and 1 case of well-differentiated pancreatic stromal sarcoma) and 10 cases of extrapancreatic malignancy (4 cases of gastric cancer, 2 cases of gastric leiomyosarcoma, 1 case of duodenal cancer, and 3 cases of colon cancer of hepatic flexure).
  • Patients with primary pancreatic cancer or pancreatic stromal sarcoma died within 1 year.
  • Two patients with malignant glucagonoma died 51 and 39 months later.
  • [MeSH-major] Adenocarcinoma / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16274034.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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18. Milicevic Z, Bogojevic D, Mihailovic M, Petrovic M, Krivokapic Z: Molecular characterization of hsp90 isoforms in colorectal cancer cells and its association with tumour progression. Int J Oncol; 2008 Jun;32(6):1169-78
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  • [Title] Molecular characterization of hsp90 isoforms in colorectal cancer cells and its association with tumour progression.
  • As determined by Western blot assay all hsp90 isoforms studied, alpha (84 kDa), beta (86 kDa) and hsp90N (75 kDa), were up-regulated and differentially expressed in various stages of colorectal carcinoma.
  • The expression of hsp90beta is definitely higher in poorly-differentiated carcinomas than in well-differentiated cancers, suggesting an involvement of hsp90beta in the inhibition of cancer cell differentiation.
  • Especially, the expression of cytosolic hsp90N isoform in malignant cells points to the possibility that induction or overexpression of hsp90N might be causally related to tumour formation.
  • In this way, the hsp90 would be at the crossroads of both signalling and cell migration events.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Differentiation. Cell Membrane / metabolism. Cell Movement. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Protein Isoforms. Signal Transduction

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  • (PMID = 18497978.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 0 / Protein Isoforms
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19. Daniels RA, Turley H, Kimberley FC, Liu XS, Mongkolsapaya J, Ch'En P, Xu XN, Jin BQ, Pezzella F, Screaton GR: Expression of TRAIL and TRAIL receptors in normal and malignant tissues. Cell Res; 2005 Jun;15(6):430-8
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  • [Title] Expression of TRAIL and TRAIL receptors in normal and malignant tissues.
  • TRAIL, tumor necrosis factor-related apoptosis-inducing ligand, is a member of the TNF family of proteins.
  • Tumour cells were initially found to have increased sensitivity to TRAIL compared with normal cells, raising hopes that TRAIL would prove useful as an anti-tumor agent.
  • The production of reliable monoclonal antibodies against TRAIL and its receptors that can stain fixed specimens will allow a thorough analysis of their expression on normal and malignant tissues.
  • Here we report the generation of monoclonal antibodies against TRAIL and its four membrane-bound receptors (TR1-4), which have been used to stain a range of normal and malignant cells, as routinely fixed specimens.
  • TR1 and TR2 expression increases significantly in a number of malignant tissues, but in some common malignancies their expression was low, or patchy, which may limit the therapeutic role of TRAIL.
  • [MeSH-major] Membrane Glycoproteins / biosynthesis. Neoplasms / physiopathology. Receptors, Tumor Necrosis Factor / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Antibodies, Monoclonal / biosynthesis. Apoptosis / drug effects. Apoptosis Regulatory Proteins. Female. GPI-Linked Proteins. Humans. Immunohistochemistry / methods. Jurkat Cells. Male. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor, Member 10c. Staining and Labeling / methods. TNF-Related Apoptosis-Inducing Ligand. Tissue Distribution. Tumor Necrosis Factor Decoy Receptors

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  • (PMID = 15987601.001).
  • [ISSN] 1001-0602
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0400720
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Apoptosis Regulatory Proteins; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 10c; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / Tumor Necrosis Factor-alpha
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20. Lau YS, Sabokbar A, Giele H, Cerundolo V, Hofstetter W, Athanasou NA: Malignant melanoma and bone resorption. Br J Cancer; 2006 May 22;94(10):1496-503
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  • [Title] Malignant melanoma and bone resorption.
  • The cellular and humoral mechanisms accounting for osteolysis in skeletal metastases of malignant melanoma are uncertain.
  • We isolated tumour-associated macrophages (TAMs) from metastatic (lymph node/skin) melanomas and cultured them in the presence and absence of osteoclastogenic cytokines and growth factors.
  • The effect of tumour-derived fibroblasts and melanoma cells on osteoclast formation and resorption was also analysed.
  • Tumour-associated macrophage-osteoclast differentiation also occurred via a RANKL-independent pathway when TAMs were cultured with tumour necrosis factor-alpha and interleukin (IL)-1alpha.
  • Our findings indicate that TAMs in metastatic melanomas can differentiate into osteoclasts and that melanoma fibroblasts and melanoma tumour cells can induce osteoclast formation by RANKL-dependent and RANKL-independent mechanisms, respectively.
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Carrier Proteins / metabolism. Cell Differentiation. Cells, Cultured. Culture Media, Conditioned / pharmacology. Female. Fibroblasts. Glycoproteins / pharmacology. Humans. Interleukin-1 / pharmacology. Lymphatic Metastasis. Male. Membrane Glycoproteins / metabolism. Middle Aged. Osteolysis / pathology. Osteoprotegerin. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Receptors, Cytoplasmic and Nuclear. Receptors, Tumor Necrosis Factor. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16641914.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Culture Media, Conditioned; 0 / Glycoproteins; 0 / Interleukin-1; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2361270
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21. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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22. Obi N, Katabami T, Obi R, Odanaka M, Sasano K, Tanaka Y: Primary malignant hepatic glucagonoma: an autopsy case. Endocr J; 2009;56(5):715-9
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  • [Title] Primary malignant hepatic glucagonoma: an autopsy case.
  • She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml).
  • Thus, we suspected a glucagonoma causing secondary diabetes.
  • However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma.
  • At autopsy, the only tumor detected was the liver mass.
  • This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe.
  • Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases.
  • Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
  • [MeSH-major] Diabetes Mellitus, Type 2 / etiology. Glucagonoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 19367016.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amino Acids
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23. Huang L, Verstrepen L, Heyninck K, Wullaert A, Revets H, De Baetselier P, Beyaert R: ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells. Oncogene; 2008 Oct 16;27(47):6131-40
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  • [Title] ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells.
  • The epidermal growth factor receptor (EGFR) is frequently overexpressed in various tumours of epidermal origin and is held responsible for tumourigenicity and tumour persistence.
  • Increased nuclear factor (NF)-kappaB activity has been suggested to be involved in the malignant behaviour of EGFR-overexpressing cells.
  • Moreover, EGF-induced NF-kappaB activation could be inhibited by overexpression of ABINs, which were previously identified as intracellular inhibitors of tumour necrosis factor, interleukin-1 and lipopolysaccharide-induced NF-kappaB activation.
  • Adenoviral gene transfer of ABINs reduced constitutive NF-kappaB activity as well as the proliferation of EGFR-overexpressing A431 and DU145 human carcinoma cells.
  • Altogether, these results demonstrate an important role for an ABIN-sensitive non-classical NF-kappaB signalling pathway in the proliferation of EGFR-overexpressing tumour cells, and indicate a potential use for ABIN gene therapy in the treatment of cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cyclin D1 / genetics. Epidermal Growth Factor / pharmacology. Genetic Therapy. Humans. I-kappa B Proteins / metabolism. NF-kappa B p52 Subunit / metabolism. Phosphorylation. Protein Structure, Tertiary. RNA Interference. Signal Transduction

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  • (PMID = 18622428.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / NF-kappa B p52 Subunit; 0 / TNIP1 protein, human; 0 / TNIP2 protein, human; 136601-57-5 / Cyclin D1; 139874-52-5 / NF-kappaB inhibitor alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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24. Iida H, Honda M, Kawai HF, Yamashita T, Shirota Y, Wang BC, Miao H, Kaneko S: Ephrin-A1 expression contributes to the malignant characteristics of {alpha}-fetoprotein producing hepatocellular carcinoma. Gut; 2005 Jun;54(6):843-51
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  • [Title] Ephrin-A1 expression contributes to the malignant characteristics of {alpha}-fetoprotein producing hepatocellular carcinoma.
  • BACKGROUND AND AIMS: alpha-Fetoprotein (AFP), a tumour marker for hepatocellular carcinoma (HCC), is associated with poor prognosis.
  • Using cDNA microarray analysis, we previously found that ephrin-A1, an angiogenic factor, is the most differentially overexpressed gene in AFP producing hepatoma cell lines.
  • METHODS: We examined ephrin-A1 expression and its effect on cell proliferation and gene expression in five AFP producing hepatoma cell lines, three AFP negative hepatoma cell lines, and 20 human HCC specimens.
  • Thus ephrin-A1 affects hepatoma cell growth. cDNA microarray analysis showed that ephrin-A1 induced expression of genes related to the cell cycle (p21), angiogenesis (angiopoietin 1 and thrombospondin 1), and cell-cell interactions (Rho, integrin, and matrix metalloproteinases) in cultured hepatoma cells.
  • CONCLUSION: These findings suggest that the poor prognosis of patients with AFP producing HCC is partially caused by ephrin-A1 expression, which induces expression of genes related to tumour cell growth, angiogenesis, invasion, and metastasis.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Ephrin-A1 / metabolism. Liver Neoplasms / metabolism. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. DNA, Complementary / analysis. Dose-Response Relationship, Drug. Gene Expression. Humans. Immunohistochemistry / methods. Oligonucleotide Array Sequence Analysis. Oligonucleotides, Antisense / pharmacology. Prognosis. RNA, Messenger / metabolism

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  • (PMID = 15888795.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA, Complementary; 0 / Ephrin-A1; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / alpha-Fetoproteins; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Other-IDs] NLM/ PMC1774523
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25. de Mestier L, Hammel P, Hentic O, Dove P, Lévy P, Ruszniewski P: [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency]. Gastroenterol Clin Biol; 2010 Jan;34(1):106-10
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  • [Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].
  • [Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.
  • Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.
  • We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright 2009. Published by Elsevier Masson SAS.
  • (PMID = 19875259.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil
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26. Stirewalt DL, Mhyre AJ, Marcondes M, Pogosova-Agadjanyan E, Abbasi N, Radich JP, Deeg HJ: Tumour necrosis factor-induced gene expression in human marrow stroma: clues to the pathophysiology of MDS? Br J Haematol; 2008 Feb;140(4):444-53
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  • [Title] Tumour necrosis factor-induced gene expression in human marrow stroma: clues to the pathophysiology of MDS?
  • Aberrant regulation of the tumour necrosis factor alpha gene (TNF) and stroma-derived signals are involved in the pathophysiology of myelodysplasia.
  • Therefore, KG1a, a myeloid leukaemia cell line, was exposed to Tnf in the absence or presence of either HS-5 or HS-27a cells, two human stroma cell lines.
  • DNA microarray studies found both discordant and concordant Tnf-induced expression responses in the two stroma cell lines.
  • Overall, the results suggested that Tnf induced a complex set of pro-inflammatory and pro-apoptotic signals in stroma cells that promote apoptosis in malignant myeloid clones.
  • Additional studies will be required to determine which of these signals are critical for the induction of apoptosis in the malignant clones.
  • [MeSH-major] Bone Marrow Cells / drug effects. Gene Expression Regulation / drug effects. Myelodysplastic Syndromes / physiopathology. Stromal Cells / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis Regulatory Proteins / biosynthesis. Apoptosis Regulatory Proteins / genetics. Cell Line. Coculture Techniques. Cytokines / biosynthesis. Cytokines / genetics. Humans. Inflammation Mediators / metabolism. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 18162123.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL082941; United States / NCI NIH HHS / CA / K23 CA92405
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Cytokines; 0 / Inflammation Mediators; 0 / Tumor Necrosis Factor-alpha
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27. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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28. Kelly LS, Birken S, Puett D: Determination of hyperglycosylated human chorionic gonadotropin produced by malignant gestational trophoblastic neoplasias and male germ cell tumors using a lectin-based immunoassay and surface plasmon resonance. Mol Cell Endocrinol; 2007 Jan 2;260-262:33-9

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  • [Title] Determination of hyperglycosylated human chorionic gonadotropin produced by malignant gestational trophoblastic neoplasias and male germ cell tumors using a lectin-based immunoassay and surface plasmon resonance.
  • The ability to reliably detect aberrant glycosylation of human chorionic gonadotropin (hCG) may have profound implications for the diagnosis and monitoring of malignant gestational trophoblastic neoplasia, germ cell tumors, other malignancies, and pregnancy complications.
  • Towards this end, we have developed a lectin-based sandwich-type immunoassay to compare the glycosylation patterns of hCG among urine specimens from patients presenting with a normal pregnancy, invasive mole, choriocarcinoma, and male germ cell tumors using carbohydrate-free antibody fragments as capture reagents and a panel of eight lectins, five recognizing neutral sugars and three recognizing sialic acid.
  • Three lectins, however, exhibited differential binding to urinary hCG derived from these normal pregnant controls and that from patients with malignant forms of gestational trophoblastic disease and male germ cell tumors.
  • Galanthus nivalis agglutinin and Maackia amurensis lectin, which bind terminal mannose and alpha(2-3)sialic acid, respectively, preferentially bound pregnancy-derived hCG, whereas the lectin, wheat germ agglutinin, which binds sialic acid and beta(1-4)N-acetylglucosamine, exhibited decreased binding to pregnancy-derived hCG compared to that from patients with male germ cell tumors and malignant gestational trophoblastic neoplasia.
  • The experimental paradigm also holds promise for the development of comparable assays for other glycosylated tumor markers.

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  • (PMID = 17081681.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK033973; United States / NIDDK NIH HHS / DK / DK33973; United States / NIDDK NIH HHS / DK / R01 DK033973-24
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carbohydrates; 0 / Chorionic Gonadotropin; 0 / Lectins; 0 / glycosylated HCG; GZP2782OP0 / N-Acetylneuraminic Acid
  • [Other-IDs] NLM/ NIHMS14869; NLM/ PMC1847626
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29. Klabatsa A, Sheaff MT, Steele JP, Evans MT, Rudd RM, Fennell DA: Expression and prognostic significance of hypoxia-inducible factor 1alpha (HIF-1alpha) in malignant pleural mesothelioma (MPM). Lung Cancer; 2006 Jan;51(1):53-9
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  • [Title] Expression and prognostic significance of hypoxia-inducible factor 1alpha (HIF-1alpha) in malignant pleural mesothelioma (MPM).
  • Malignant pleural mesothelioma (MPM) is a highly chemoresistant cancer with a poor prognosis.
  • Hypoxia-inducible factor 1alpha (HIF-1alpha) is a subunit of a heterodimeric transcription complex that regulates several genes associated with tumour progression and anti-apoptosis.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Mesothelioma / metabolism. Pleural Neoplasms / metabolism
  • [MeSH-minor] Antigens, CD31 / biosynthesis. Apoptosis. Cell Nucleus / metabolism. Cytoplasm / metabolism. Disease Progression. Humans. Immunohistochemistry. In Vitro Techniques. Prognosis

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  • (PMID = 16169121.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
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30. Nakabayashi H, Yawata T, Shimizu K: Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells. BMC Cancer; 2010;10:339
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  • [Title] Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells.
  • BACKGROUND: The constitutive overexpression of matrix metalloproteinases (MMPs) is frequently observed in malignant tumours.
  • In particular, MMP-2 and MMP-9 have been reported to be closely associated with invasion and angiogenesis in malignant gliomas.
  • Our study aimed to evaluate the antitumour effects of MMI-166 (Nalpha-[4-(2-Phenyl-2H- tetrazole-5-yl) phenyl sulfonyl]-D-tryptophan), a third generation MMP inhibitor, on three human glioma cell lines (T98G, U87MG, and ONS12) in vitro and in vivo.
  • The angiogenesis assay showed that MMI-166 had a suppressive effect on glioma cell-induced angiogenesis.
  • However, MMI-166 did not suppress glioma cell proliferation in the MTT assay.
  • In vivo, MMI-166 suppressed tumour growth in athymic mice implanted orthotropically with T98G cells and showed an inhibitory effect on tumour-induced angiogenesis and tumour growth.
  • This is the first report of the effect of a third generation MMP inhibitor on malignant glioma cells.
  • CONCLUSIONS: These results suggest that MMI-166 may have potentially suppressive effects on the invasion and angiogenesis of malignant gliomas.
  • [MeSH-minor] Animals. Brain Neoplasms / blood supply. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Female. Humans. Matrix Metalloproteinase Inhibitors. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasm Invasiveness. Tumor Cells, Cultured

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  • (PMID = 20587068.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Enzyme Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; 0 / N-alpha-(4-(2-phenyl-2H- tetrazole-5-yl) phenyl sulfonyl)-D-tryptophan; 0 / Sulfonamides
  • [Other-IDs] NLM/ PMC2909207
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31. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Alterations in dipeptidyl peptidase-IV (DPP-IV) enzymatic activity are characteristic of malignant transformation.
  • Through its well-characterized functionality in regulating the activity of bioactive peptides by removal of the N-terminal dipeptide, DPP-IV activity may have profound effects upon metastatic potential and cell growth.
  • Although DPP-IV/CD26 (EC 3.4.14.5) is the canonical representative of the group, a number of other proteins including DPP-7, 8, 9, and seprase/fibroblast activation protein-alpha (FAP-alpha) have been shown to have similar enzymatic activity.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • In parallel, expression of CXCR4, receptor for glioma cell growth stimulator chemokine SDF-1alpha known to be a DPP-IV substrate, was investigated.
  • This is the first report showing that non-malignant brain tissue contains a DPP-IV-like enzymatic activity attributable mostly to DPP-8/9, while the substantial part of the activity in glioma is due to increased DPP-IV/CD26, localized in both the vascular and parenchymal compartments.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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32. Patrikainen L, Porvari K, Kurkela R, Hirvikoski P, Soini Y, Vihko P: Expression profiling of PC-3 cell line variants and comparison of MIC-1 transcript levels in benign and malignant prostate. Eur J Clin Invest; 2007 Feb;37(2):126-33
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  • [Title] Expression profiling of PC-3 cell line variants and comparison of MIC-1 transcript levels in benign and malignant prostate.
  • BACKGROUND: The mechanisms behind prostate cancer progression are largely unknown, but macrophage inhibitory cytokine 1 (MIC-1) has been suggested to be involved in tumour dissemination in vivo due to its reductive effect on cell adhesion.
  • MATERIALS AND METHODS: We used two PC-3 prostate cancer epithelial cell line variants as tools to screen for gene expression differences during prostate cancer progression by cDNA microarray analysis.
  • Selected genes were further analysed by Northern blot analysis using mRNA isolated from prostatic cell lines and tissues.
  • MIC-1 expression was studied by in situ hybridization in archival patient specimens containing benign and malignant prostatic tissue.
  • RESULTS: Gene expression of human collagen type VI, basement membrane heparan sulphate proteoglycan, integrin alpha 1, and fibronectin I were remarkably decreased in suspension-adapted PC-3 (saPC-3) cells, indicating a gene expression profile of reduced cell adhesion.
  • [MeSH-major] Cytokines / metabolism. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Blotting, Northern. Cell Adhesion / physiology. Cell Line, Tumor. Epithelial Cells / metabolism. Gene Expression. Growth Differentiation Factor 15. Humans. Male. RNA, Messenger / metabolism

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  • (PMID = 17217378.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / GDF15 protein, human; 0 / Growth Differentiation Factor 15; 0 / RNA, Messenger
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33. Chen HW, Chen HW, Su DH, Shun CT, Liu KL: Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema. J Formos Med Assoc; 2005 May;104(5):363-6
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  • [Title] Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema.
  • Glucagonoma is a very rare endocrine pancreatic tumor.
  • At diagnosis, most glucagonomas are malignant and often metastatic.
  • Suspicion of glucagonoma is based on characteristic presentations known as "glucagonoma syndrome".
  • Glucagonoma is often found in the pancreatic body and/or tail and is usually large enough to be localized by computed tomography.
  • We report a case of diffuse glucagonoma necrolytic migratory erythema (NME) in a 45-year-old man with mild diabetes mellitus, mild anemia, and weight loss over 1.5 years.
  • Diffused enlarged pancreas was noted on abdominal ultrasonography incidentally during a routine health check-up.
  • No enlarged lymph node or extrapancreatic tumor mass was found by several imaging studies.
  • Total pancreatectomy was performed, and the pathology revealed glucagon-producing islet cells and intrapancreatic vascular emboli of tumor cells.
  • Presentation of diffuse malignant glucagonoma with tumor emboli but no metastasis or NME is unusual.

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  • (PMID = 15959605.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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34. Harper LJ, Costea DE, Gammon L, Fazil B, Biddle A, Mackenzie IC: Normal and malignant epithelial cells with stem-like properties have an extended G2 cell cycle phase that is associated with apoptotic resistance. BMC Cancer; 2010 Apr 28;10:166
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  • [Title] Normal and malignant epithelial cells with stem-like properties have an extended G2 cell cycle phase that is associated with apoptotic resistance.
  • BACKGROUND: Subsets of cells with stem-like properties have been previously isolated from human epithelial cancers and their resistance to apoptosis-inducing stimuli has been related to carcinoma recurrence and treatment failure.
  • The aim of this study was to investigate the mechanisms of resistance to apoptosis-inducing agents of cells with stem-like properties in both normal and malignant human epithelia.
  • METHODS: Cells isolated from fresh human head and neck carcinomas (n = 11), cell lines derived from head and neck, prostate and breast human carcinomas (n = 7), and from normal human oral mucosa (n = 5), were exposed to various apoptosis-inducing stimuli (UV, Tumour Necrosis Factor, Cisplatin, Etoposide, and Neocarzinostatin).
  • Flow cytometry for CD44 and epithelial-specific antigen (ESA) expression, colony morphology, tumour sphere formation and rapid adherence assays were used to identify the subset of cells with stem-like properties.
  • Apoptosis, cell cycle and expression of various cell cycle checkpoint proteins were assessed (Western Blot, qPCR).
  • RESULTS: In both cancer biopsies and carcinoma cell lines a subset of CD44(high) cells showed increased clonogenicity, a significantly lower rate of apoptosis, and a significantly higher proportion of cells in the G2-phase of the cell cycle.
  • Pulse-chase with iododeoxyuridine (IdU) demonstrated that CD44(high) carcinoma cells spent longer time in G2, even in un-treated controls.
  • CONCLUSIONS: These data indicate that both normal and malignant human epithelial cells with stem-like properties show greater resistance to apoptosis associated with extended G2 cell cycle phase, and that this property is not a consequence of neoplastic transformation.
  • [MeSH-minor] Antigens, CD44 / metabolism. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Shape / drug effects. Cisplatin / pharmacology. Dose-Response Relationship, Drug. Etoposide / pharmacology. Humans. Keratinocytes / drug effects. Keratinocytes / pathology. Time Factors. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology. Zinostatin / pharmacology

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  • (PMID = 20426848.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / C20349; United Kingdom / National Centre for the Replacement, Refinement and Reduction of Animals in Research / / G0900799/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Antineoplastic Agents; 0 / CD44 protein, human; 0 / Tumor Necrosis Factor-alpha; 6PLQ3CP4P3 / Etoposide; 9014-02-2 / Zinostatin; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2868812
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35. Salonen J, Leminen A, Stenman UH, Butzow R, Heikinheimo M, Heikinheimo O: Tissue AP-2gamma and Oct-3/4, and serum CA 125 as diagnostic and prognostic markers of malignant ovarian germ cell tumors. Tumour Biol; 2008;29(1):50-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue AP-2gamma and Oct-3/4, and serum CA 125 as diagnostic and prognostic markers of malignant ovarian germ cell tumors.
  • Histology, clinical stage and treatment response are used to define the prognosis of malignant ovarian germ cell tumors (MOGCTs).
  • Serum levels of alpha-fetoprotein, human chorionic gonadotropin and CA 125 were determined, and immunohistochemistry for CA 125 as well as the pluripotent stem cell markers AP-2gamma and Oct-3/4 was performed in tumor specimens and the NCC-IT human germinoma cell line.
  • Immunohistochemical evaluation revealed that in most cases the elevated CA 125 levels originated from the tumor tissue.
  • Most dysgerminomas as well as the germinoma cell line were positive for AP-2gamma and Oct-3/4, whereas the majority of yolk sac tumors and immature teratomas were negative.
  • [MeSH-major] Biomarkers, Tumor / metabolism. CA-125 Antigen / blood. Neoplasms, Germ Cell and Embryonal / metabolism. Octamer Transcription Factor-3 / metabolism. Ovarian Neoplasms / metabolism. Transcription Factor AP-2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Chorionic Gonadotropin / blood. Female. Humans. Middle Aged. Neoplasm Staging. Prognosis. alpha-Fetoproteins / metabolism

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18497549.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / Chorionic Gonadotropin; 0 / Octamer Transcription Factor-3; 0 / Transcription Factor AP-2; 0 / alpha-Fetoproteins
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36. Kasper G, Vogel A, Klaman I, Gröne J, Petersen I, Weber B, Castaños-Vélez E, Staub E, Mennerich D: The human LAPTM4b transcript is upregulated in various types of solid tumours and seems to play a dual functional role during tumour progression. Cancer Lett; 2005 Jun 16;224(1):93-103
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  • [Title] The human LAPTM4b transcript is upregulated in various types of solid tumours and seems to play a dual functional role during tumour progression.
  • LAPTM4b (lysosome associated protein transmembrane 4 beta) was recently identified as a gene overexpressed in human hepatocellular carcinoma and belongs to the mammalian LAPTM family.
  • By analysing genome-wide expression profiles of microdissected solid tumour samples by the means of Affymetrix GenChip hybridisation, we found LAPTM4b to be upregulated in 88% (23/26) of lung and in 67% (18/27) of colon carcinoma patients.
  • Other members of the LAPTM family were not overexpressed in the investigated tumour samples according to GeneChip hybridisation data.
  • Due to sequence analysis of bilaterian LAPTM proteins we suggests the presence of four transmembrane helices per protein, which are probably packed together by hydrophobic forces that are excerted by several evolutionary conserved aromatic residues within the alpha-helices.
  • We discuss an active role for LAPTM4b during disease progression of malignant cells and conclude that its putative dual functional involvement in tumour cell proliferation as well as in multidrug-resistance may represent LAPTM4b as a target suitable for development of novel therapeutic agents.
  • [MeSH-minor] Amino Acid Sequence. Blotting, Northern. Cell Proliferation. Cell Transformation, Neoplastic. Disease Progression. Female. Humans. Male. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Distribution. Up-Regulation

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  • (PMID = 15911104.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / LAPTM4B protein, human; 0 / Membrane Proteins; 0 / Oncogene Proteins
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37. Koehn H, Magan N, Isaacs RJ, Stowell KM: Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin. Anticancer Drugs; 2007 Apr;18(4):419-25
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  • [Title] Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin.
  • Radiotherapy and chemotherapy often induce DNA double-strand breaks in both normal and malignant cells.
  • The proteins involved in the repair of such lesions are central to cancer prognosis and treatment, as they can be overexpressed in many cancers, accelerating malignant transformation and increasing repair capacity, potentially leading to cellular resistance.
  • If malignant cells can be selectively targeted repair proteins could also be candidates for targeted therapy.
  • In this study, two keyplayers in eukaryotic DNA double-strand break repair, Rad51 and DNA-dependent protein kinase catalytic subunit, were analysed in noncancerous human breast cells (MCF12A) and the breast cancer cell lines (MDA MB 231 and MCF7) in response to treatment with doxorubicin.
  • A cell cycle-independent increase in Rad51 protein levels (a recombinase involved in homologous recombination repair) was observed 24 and 48 h after treatment in MDA MB 231 and MCF12A when exposed to low levels of doxorubicin, whereas MCF7 cells displayed a continuous decrease in Rad51 protein with increasing drug concentration.
  • Topoisomerase II-alpha protein, the primary target of doxorubicin, was upregulated at low concentrations of doxorubicin in all cell lines tested.
  • Here we show that Rad51 protein levels can be differentially regulated in normal and malignant breast cell lines in response to doxorubicin, independent of cell cycle state.
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA Damage. Dose-Response Relationship, Drug. Female. Flow Cytometry. Genes, p53 / genetics. Humans. Receptors, Estrogen / genetics. Receptors, Estrogen / physiology. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / physiology

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  • (PMID = 17351394.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Receptors, Estrogen; 0 / Transforming Growth Factor beta; 80168379AG / Doxorubicin; EC 2.7.7.- / Rad51 Recombinase
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38. Perrone F, Jocollè G, Pennati M, Deraco M, Baratti D, Brich S, Orsenigo M, Tarantino E, De Marco C, Bertan C, Cabras A, Bertulli R, Pierotti MA, Zaffaroni N, Pilotti S: Receptor tyrosine kinase and downstream signalling analysis in diffuse malignant peritoneal mesothelioma. Eur J Cancer; 2010 Oct;46(15):2837-48
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  • [Title] Receptor tyrosine kinase and downstream signalling analysis in diffuse malignant peritoneal mesothelioma.
  • Our aim was to assess the activation profile of EGFR, PDGFRB and PDGFRA receptor tyrosine kinases (RTK) and their downstream effectors in a series of cryopreserved diffuse malignant peritoneal mesothelioma (DMPM) surgical specimens to discover the targets for drug inhibition.
  • We also made a complementary analysis of the cytotoxic effects of some kinase inhibitors on the proliferation of the human peritoneal mesothelioma STO cell line.
  • In vitro cytotoxicity studies showed the STO cell line to be resistant to gefitinib and sensitive to sequential treatment with RAD001 and sorafenib; these findings were consistent with the presence of the KRAS mutation G12D in these cells although it was not detectable in the original tumour.
  • [MeSH-minor] Adult. Aged. Apoptosis. DNA Mutational Analysis. Female. Genes, p16. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism


39. Yamada M, Yanaba K, Hasegawa M, Matsushita Y, Horikawa M, Komura K, Matsushita T, Kawasuji A, Fujita T, Takehara K, Steeber DA, Tedder TF, Sato S: Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1. Clin Exp Immunol; 2006 Feb;143(2):216-27
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  • [Title] Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1.
  • Malignant melanoma is often accompanied by a host response of inflammatory cell infiltration that is highly regulated by multiple adhesion molecules.
  • This enhancement was associated generally with a reduced accumulation of natural killer (NK) cells, CD4+ T cells and CD8+ T cells and also with a diminished release of interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha but not interleukin (IL)-6.
  • Cytotoxicity against melanoma was not defective by the absence of ICAM-1, L-selectin or both, suggesting that the enhancement of tumour growth and metastasis caused by the loss of adhesion molecules results from an impaired migration of effector cells into the tissue rather than from a suppression of the cytotoxic response.
  • The results indicate that L-selectin and ICAM-1 contribute co-operatively to the anti-tumour reaction by regulating lymphocyte infiltration to the tumour.

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  • (PMID = 16412045.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA54464; United States / NCI NIH HHS / CA / CA81776
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin
  • [Other-IDs] NLM/ PMC1809598
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40. Eyden B: The myofibroblast: a study of normal, reactive and neoplastic tissues, with an emphasis on ultrastructure. part 2 - tumours and tumour-like lesions. J Submicrosc Cytol Pathol; 2005 Nov;37(3-4):231-96
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  • [Title] The myofibroblast: a study of normal, reactive and neoplastic tissues, with an emphasis on ultrastructure. part 2 - tumours and tumour-like lesions.
  • This paper describes the ultrastructure of the commoner myofibroblastic tumours and tumour-like lesions.
  • The objective is to complement mainstream pathology texts, which have concentrated on the clinical and light microscopy features of these lesions and which have arguably but understandably somewhat neglected electron microscopy as an ancillary diagnostic tool and a technique for investigating tumour cell biology.
  • Ultrastructural features are described of nodular fasciitis, the myofibromatoses (including Dupuytren's disease), inflammatory myofibroblastic tumour, post-operative spindle cell nodule, fibroma of tendon sheath, fibrous pseudotumour, benign fibrous histiocytoma, atypical fibroxanthoma, dermatofibrosarcoma protuberans, myofibrosarcoma (myofibroblastic sarcoma), malignant fibrous histiocytoma (pleomorphic myofibrosarcoma), epithelioid sarcoma and spindle-cell carcinoma.
  • The fibronexus is emphasised as an important marker for the most confident diagnosis of myofibrosarcoma.
  • Some pathologists accept a light microscope definition, which includes alpha-smooth-muscle actin positivity, h-caldesmon negativity and, in some cases, desmin positivity.
  • Myofibroblastoma and angiomyofibroblastoma are examples of tumours argued on the basis of ultrastructural findings (sometimes in combination with desmin staining) to be primitively differentiated smooth-muscle cell rather than myofibroblastic proliferations.

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  • (PMID = 16612972.001).
  • [ISSN] 1122-9497
  • [Journal-full-title] Journal of submicroscopic cytology and pathology
  • [ISO-abbreviation] J. Submicrosc. Cytol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 344
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41. Franz M, Wolheim A, Richter P, Umbreit C, Dahse R, Driemel O, Hyckel P, Virtanen I, Kosmehl H, Berndt A: Stromal laminin chain distribution in normal, hyperplastic and malignant oral mucosa: relation to myofibroblast occurrence and vessel formation. J Oral Pathol Med; 2010 Apr;39(4):290-8
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  • [Title] Stromal laminin chain distribution in normal, hyperplastic and malignant oral mucosa: relation to myofibroblast occurrence and vessel formation.
  • BACKGROUND: The contribution of stromal laminin chain expression to malignant potential, tumour stroma reorganization and vessel formation in oral squamous cell carcinoma (OSCC) is not fully understood.
  • METHODS: Frozen tissue of OSCC (9x G1, 24x G2, 8x G3) and normal (2x)/hyperplastic (11x) oral mucosa was subjected to laminin chain and alpha-smooth muscle actin (ASMA) immunohistochemistry.
  • Results were correlated to tumour grade.
  • A vascular basement membrane reorganization concerning alpha3 and gamma2 chain laminins during tumour angioneogenesis is suggested.
  • [MeSH-minor] Actins / analysis. Antigens, CD31 / analysis. Basement Membrane / pathology. Cell Transformation, Neoplastic / pathology. Connective Tissue / blood supply. Connective Tissue / pathology. Endothelial Cells / pathology. Endothelium, Vascular / pathology. Fluorescent Antibody Technique. Humans. Hyperplasia. Up-Regulation

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  • (PMID = 19889153.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, CD31; 0 / LAMA4 protein, human; 0 / LAMC2 protein, human; 0 / Laminin; 0 / laminin alpha 2; 0 / laminin alpha5; 170834-93-2 / laminin alpha 3
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42. Humphreys EH, Williams KT, Adams DH, Afford SC: Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent apoptosis, but are insensitive to direct activation with exogenous Fas ligand. PLoS One; 2010 Nov 17;5(11):e14037
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  • [Title] Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent apoptosis, but are insensitive to direct activation with exogenous Fas ligand.
  • We have shown that primary human cholangiocyte and hepatocyte survival is tightly regulated via co-operative interactions between two tumour necrosis family (TNF) receptor family members; CD40 and Fas (CD95).
  • AIMS: To determine whether malignant cholangiocytes display defects in CD40 mediated apoptosis.
  • By comparing CD40 and Fas-mediated apoptosis and intracellular signalling in primary human cholangiocytes and three cholangiocyte cell lines.
  • RESULTS: Primary cholangiocytes and cholangiocyte cell lines were relatively insensitive to direct Fas-mediated killing with exogenous FasL when compared with Jurkat cells, which readily underwent Fas-mediated apoptosis, but were extremely sensitive to CD154 stimulation.
  • The sensitivity of cells to CD40 activation was similar in magnitude in both primary and malignant cells and was STAT-3 and AP-1 dependent in both. CONCLUSIONS:.
  • 1) Both primary and malignant cholangiocytes are relatively resistant to Fas-mediated killing but show exquisite sensitivity to CD154, suggesting that the CD40 pathway is intact and fully functional in both primary and malignant cholangiocytes 2) The relative insensitivity of cholangiocytes to Fas activation demonstrates the importance of CD40 augmentation of Fas dependent death in these cells.
  • Agonistic therapies which target CD40 and associated intracellular signalling pathways may be effective in promoting apoptosis of malignant cholangiocytes.

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  • (PMID = 21103345.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E017096/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / STAT3 Transcription Factor; 0 / Transcription Factor AP-1; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 147205-72-9 / CD40 Ligand
  • [Other-IDs] NLM/ PMC2984448
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43. Charalambous MP, Lightfoot T, Speirs V, Horgan K, Gooderham NJ: Expression of COX-2, NF-kappaB-p65, NF-kappaB-p50 and IKKalpha in malignant and adjacent normal human colorectal tissue. Br J Cancer; 2009 Jul 7;101(1):106-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of COX-2, NF-kappaB-p65, NF-kappaB-p50 and IKKalpha in malignant and adjacent normal human colorectal tissue.
  • We hypothesised an association between COX-2 expression and NF-kappaB-p65, NF-kappaB-p50 and IkappaB-kinase-alpha (IKKalpha) in both epithelial and stromal cells in human colorectal cancer.
  • METHODS: Using immunohistochemistry, we measured COX-2, NF-kappaB-p65, NF-kappaB-p65 nuclear localisation sequence (NLS), NF-kappaB-p50, NF-kappaB-p50 NLS and IKKalpha protein expression in matched colorectal biopsy samples comprising both non-tumour and adjacent tumour tissue from 32 patients with colorectal cancer.
  • RESULTS: We have shown that stromal cells of malignant and surrounding normal colorectal tissue express COX-2.
  • In all cell types of malignant tissue, and in vascular endothelial cells (VECs) of neighbouring normal tissue, COX-2 expression was strongly associated with NF-kappaB-p65 expression (Pearson's correlation, P=0.019 for macrophages, P=0.001 for VECs, P=0.002 for fibroblasts (malignant tissue), and P=0.011 for VECs (non-malignant tissue)) but not NF-kappaB-p50 or IKKalpha.
  • Finally, the lack of association between COX-2, NF-kappaB-p65 or IKKalpha in stromal cells with the clinical severity of colorectal cancer as determined by Duke's stage, suggests that COX-2, NF-kappaB-p65 and IKKalpha expression are possibly early post-initiation events, which could be involved in tumour progression.

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  • (PMID = 19513071.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B p50 Subunit; 0 / Transcription Factor RelA; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.10 / I-kappa B Kinase
  • [Other-IDs] NLM/ PMC2713702
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44. Monteagudo C, Martin JM, Jorda E, Llombart-Bosch A: CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors. J Clin Pathol; 2007 Jun;60(6):596-9
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  • [Title] CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors.
  • BACKGROUND: A role for CXCR3, the receptor for chemokines Mig, IP-10 and interferon-inducible T cell alpha-chemoattractant, in tumour cell migration during melanoma progression has been proposed.
  • AIMS: To analyse CXCR3 expression in primary cutaneous malignant melanomas and its comparison with clinicopathological and prognostic factors.
  • Melanomas were categorised by age, sex, primary site, tumour thickness, growth phase, ulceration, lymphocytic infiltration, recurrence, lymph node and distant metastasis, and survival.
  • In univariate analysis, a significant association of CXCR3-positive tumour cell immunostaining with tumour thickness >1 mm (p = 0.003), absence of lymphocytic infiltration (p = 0.04) and the presence of distant metastasis (p = 0.048) was found.
  • Multivariate analysis found tumour thickness as the only independent factor with considerable association with distant metastases.
  • CONCLUSIONS: Our findings of a positive correlation of CXCR3 tumour cell immunoreactivity in human primary cutaneous melanoma with tumour thickness >1 mm and absence of intratumoral lymphocytic infiltration support the biological implication of CXCR3 in the tumour progression of cutaneous malignant melanoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Melanoma / metabolism. Receptors, Chemokine / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 16522748.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCR3 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, CXCR3; 0 / Receptors, Chemokine
  • [Other-IDs] NLM/ PMC1955073
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45. Ardon H, Verbinnen B, Maes W, Beez T, Van Gool S, De Vleeschouwer S: Technical advancement in regulatory T cell isolation and characterization using CD127 expression in patients with malignant glioma treated with autologous dendritic cell vaccination. J Immunol Methods; 2010 Jan 31;352(1-2):169-73
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  • [Title] Technical advancement in regulatory T cell isolation and characterization using CD127 expression in patients with malignant glioma treated with autologous dendritic cell vaccination.
  • We have successfully treated over two hundred high-grade glioma (HGG) patients with immunotherapy consisting of vaccination with autologous dendritic cells (DCs) loaded with autologous tumour lysate.
  • It has been documented that regulatory T cells (Treg) can counteract anti-tumour immune responses.
  • Here, we validated IL-7 receptor alpha subunit (CD127)dim expression as a marker for human Treg within HGG patients, as a less laborious assay for routine use in tumour vaccination trials.
  • [MeSH-major] Biomarkers / metabolism. Cancer Vaccines. Central Nervous System Neoplasms / immunology. Glioma / immunology. Interleukin-7 Receptor alpha Subunit / metabolism. T-Lymphocyte Subsets / metabolism. T-Lymphocytes, Regulatory / metabolism
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Antigens, Neoplasm / immunology. Antigens, Neoplasm / metabolism. Cells, Cultured. Dendritic Cells / immunology. Dendritic Cells / metabolism. Forkhead Transcription Factors / biosynthesis. Humans. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lymphocyte Culture Test, Mixed. Monitoring, Physiologic. Transplantation, Autologous

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  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19874827.001).
  • [ISSN] 1872-7905
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, Neoplasm; 0 / Biomarkers; 0 / Cancer Vaccines; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Interleukin-7 Receptor alpha Subunit
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46. Kang KP, Kim DH, Jung YJ, Lee AS, Lee S, Lee SY, Jang KY, Sung MJ, Park SK, Kim W: Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation. Nephrol Dial Transplant; 2009 Oct;24(10):3012-20
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  • [Title] Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation.
  • BACKGROUND: Cisplatin is a chemotherapeutic agent used in treatment of malignant tumours.
  • Alpha-lipoic acid (alpha-LA) has anti-inflammatory effects that inhibit both adhesion molecule expression in human endothelial cells and monocyte adhesion by suppressing the nuclear factor-kappaB (NF-kappaB) signalling pathway.
  • The goals of this study were to investigate the anti-inflammatory effects of alpha-LA during cisplatin-induced renal injury and to examine the mechanisms of protection.
  • METHODS: C57BL/6 mice were given cisplatin (20 mg/kg) with or without alpha-LA treatment (100 mg/kg for 3 days).
  • Renal function, histological changes, adhesion molecule expression and inflammatory cell infiltration were examined.
  • The effect of alpha-LA on NF-kappaB activity was evaluated by examining nuclear translocation and phosphorylation of NF-kappaB p65 subunits in kidney tissue.
  • RESULTS: Cisplatin-induced decreases in renal function, measured by blood urea nitrogen, serum creatinine level and renal tubular injury scores, were attenuated by alpha-LA treatment. alpha-LA decreased the tissue levels of tumour necrosis factor-alpha, the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), and suppressed the infiltration of CD11b-positive macrophages. alpha-LA also attenuated the cisplatin-induced increases in the phosphorylation and nuclear translocation of NF- kappaB p65 subunits in kidney tissue.
  • CONCLUSIONS: These results suggest that alpha-LA treatment ameliorates cisplatin-induced acute kidney injury by reducing inflammatory adhesion molecule expression and NF-kappaB activity.

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  • (PMID = 19474282.001).
  • [ISSN] 1460-2385
  • [Journal-full-title] Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • [ISO-abbreviation] Nephrol. Dial. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 73Y7P0K73Y / Thioctic Acid; Q20Q21Q62J / Cisplatin
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47. Przybyło M, Lityńska A, Pocheć E: Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation. Biochimie; 2005 Feb;87(2):133-42
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  • [Title] Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation.
  • In tumour cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • This study used cell lines having very different behaviour in vivo: HCV29 non-malignant transitional epithelium and T24 bladder transitional cell carcinoma.
  • The functional role of carbohydrates was studied by treating these cells with swainsonine, an inhibitor of Golgi alpha-mannosidase II, and in vitro adhesion and migration assays.
  • Swainsonine treatment reduced the rate of T24 cell migration by 20%.
  • We concluded that beta1-6 branched tri- and tetraantennary complex-type glycans have an important function in adhesion and migration in the studied cell lines.
  • [MeSH-major] Cell Movement. Epithelial Cells / metabolism. Polysaccharides / biosynthesis. Ureter / metabolism. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Glycosylation / drug effects. Humans. Male. Species Specificity. Swainsonine / pharmacology

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  • (PMID = 15760705.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Polysaccharides; RSY4RK37KQ / Swainsonine
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48. Muinelo-Romay L, Vázquez-Martín C, Villar-Portela S, Cuevas E, Gil-Martín E, Fernández-Briera A: Expression and enzyme activity of alpha(1,6)fucosyltransferase in human colorectal cancer. Int J Cancer; 2008 Aug 1;123(3):641-6
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  • [Title] Expression and enzyme activity of alpha(1,6)fucosyltransferase in human colorectal cancer.
  • Changes in enzyme activity and the expression levels of alpha(1,6)fucosyltransferase [alpha(1,6)FT] have been reported in certain types of malignant transformations.
  • To develop a better understanding of the role of alpha(1,6)FT in human colorectal carcinoma (CRC), we analysed the enzyme activity in healthy and tumour tissues. alpha(1,6)FT activity was considerably higher in tumour tissue than in healthy tissue and was related to gender, lymph node metastasis, type of growth and tumour stage.
  • We also observed a significant increase in the alpha(1,6)FT expression in tumour tissues as compared to healthy and transitional tissues, inflammatory lesions and adenomas.
  • The immunohistochemical expression in tumour tissues was correlated with the degree of infiltration through the intestinal wall.
  • All these findings demonstrate an alteration of alpha(1,6)FT activity and expression in CRC.
  • [MeSH-major] Adenocarcinoma / enzymology. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / enzymology. Fucosyltransferases / metabolism
  • [MeSH-minor] Adenoma / enzymology. Aged. Blotting, Western. Cell Transformation, Neoplastic. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male

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  • (PMID = 18491404.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase
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49. Yuan K, Kucik D, Singh RK, Listinsky CM, Listinsky JJ, Siegal GP: Alterations in human breast cancer adhesion-motility in response to changes in cell surface glycoproteins displaying alpha-L-fucose moieties. Int J Oncol; 2008 Apr;32(4):797-807
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  • [Title] Alterations in human breast cancer adhesion-motility in response to changes in cell surface glycoproteins displaying alpha-L-fucose moieties.
  • Glycosylation of proteins plays multiple roles in cell-cell and cell-matrix interactions.
  • Fucose is a monosaccharide associated with glycosylation events and is known to be over-expressed in many malignant tumors.
  • By using alpha-L-fucosidase (alpha-L-fase), a glycosidase that specifically removes alpha-L-fucose (alpha-L-f), we have examined the potential effects of defucosylation on tumor functions, focusing on tumor progression in the context of the interaction of tumor cells with the extracellular microenvironment.
  • In this submission, we report that alpha-L-fase treatment decreases, in static assays, tumor cell adhesion to a wide variety of ECM components including fibronectin, laminin, collagen I, hyaluronic acid and the complex human biomatrix, HuBiogel(R).
  • By immunofluorescence, co-localization of beta1 integrin and alpha-L-f was found to decrease accordingly.
  • Sialyl Lewis X, an alpha-L-f-containing tetrasaccharide, which modulates the rolling of leukocytes and tumor cells on endothelium, was found to be diminished on human breast cancer cells after alpha-L-fase treatment.
  • Further, the rolling capability of these defucosylated tumor cells was also impaired on purified E and P-selectin matrices.
  • Based on these data, we hypothesize that decreased fucosylation impairs the interaction between tumor cells and their external milieu, which in turn, affects key cell functions modulating tumor progression.
  • Building on our previous studies which demonstrated alpha-L-fase decreased tumor cell invasion while significantly reducing MMP-9 activity, when added to the fact that decreased adhesion on HUVEC occurs in the presence of alpha-L-fase also leads us to propose that defucosylation may modulate metastasis, and thus provides a promising additional glycobiotic target for novel therapies.

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  • (PMID = 18360707.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL62736; United States / PHS HHS / / HHSN2-61200566001C; United States / NCCIH NIH HHS / AT / R21 AT001636; United States / NCCIH NIH HHS / AT / R21 AT001636-02; United States / NHLBI NIH HHS / HL / R43 HL062736; United States / NCI NIH HHS / CA / P50 CA089019; United States / NCCIH NIH HHS / AT / AT001636-02; United States / NCI NIH HHS / CA / P50 CA089019-04; United States / NCI NIH HHS / CA / P50 CA89019; United States / NCI NIH HHS / CA / CA108118-02; United States / NCI NIH HHS / CA / R43 CA108118-02; United States / NCI NIH HHS / CA / CA089019-04; United States / NHLBI NIH HHS / HL / R44 HL062736
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine; 0 / E-Selectin; 0 / Glycoproteins; 0 / Oligosaccharides; 0 / P-Selectin; 126547-89-5 / Intercellular Adhesion Molecule-1; 3713-31-3 / Fucose; EC 3.2.1.51 / alpha-L-Fucosidase
  • [Other-IDs] NLM/ NIHMS101148; NLM/ PMC2671470
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50. Tomasetti M, Andera L, Alleva R, Borghi B, Neuzil J, Procopio A: Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis. FEBS Lett; 2006 Apr 3;580(8):1925-31
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  • [Title] Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis.
  • We evaluated the ability of alpha-tocopheryl succinate (alpha-TOS) to sensitise TRAIL-resistant malignant mesothelioma (MM) cells to TRAIL-induced apoptosis.
  • We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.
  • MM cells selected for TRAIL resistance expressed low cell surface levels of DR4 and DR5.
  • Treatment with sub-lethal doses of alpha-TOS restored expression of DR4 and DR5.
  • The ability of alpha-TOS to modulate expression of pro-apoptotic genes may play a role in sensitisation of tumour cells to immunological stimuli.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / pharmacology. Drug Resistance, Neoplasm / drug effects. Membrane Glycoproteins / pharmacology. Receptors, Tumor Necrosis Factor / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Protein p53 / metabolism. Vitamin E / analogs & derivatives
  • [MeSH-minor] Cytoplasm / metabolism. Humans. Neoplasms / metabolism. Neoplasms / pathology. Receptors, Cell Surface / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand. Recombinant Proteins / metabolism. TNF-Related Apoptosis-Inducing Ligand. Tocopherols. Tumor Cells, Cultured

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  • (PMID = 16529749.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols
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51. Vázquez SM, Mladovan AG, Pérez C, Bruzzone A, Baldi A, Lüthy IA: Human breast cell lines exhibit functional alpha2-adrenoceptors. Cancer Chemother Pharmacol; 2006 Jul;58(1):50-61
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  • [Title] Human breast cell lines exhibit functional alpha2-adrenoceptors.
  • However, alpha(2)-adrenoceptors have not yet been described in either normal or tumour human breast tissue.
  • The aim of this work was to describe and characterize these receptors in several tumour and non-tumour human cell lines.
  • The expression of alpha(2)-adrenoceptors was analyzed at the RNA (RT-PCR) and protein ([(3)H]-rauwolscine binding and immunocytochemistry) levels in different human breast cell lines, and the biological activity assessed by [(3)H]-thymidine incorporation.
  • The cancer IBH-6, IBH-7 and MCF-7 and the non-tumour HBL-100 cells line, expressed both alpha(2B)- and alpha(2C)-adrenoceptor-subtypes.
  • A single subtype was expressed in malignant HS-578T (alpha(2A)) and MDA-MB-231 and non-tumour MCF-10A cells (alpha(2B)).
  • All cell lines exhibited significant binding for the specific antagonist [(3)H]-rauwolscine.
  • The alpha-, alpha(2)-, and the alpha(1)-compounds with known affinity for alpha(2)-adrenoceptors, including epinephrine, norepinephrine, yohimbine, clonidine, rauwolscine and prazosin, competed significantly with binding in MCF-7 cells.
  • In addition, IBH-6, IBH-7 and MCF-7 cells showed significant staining with specific antibodies against alpha(2B)- and alpha(2C)-adrenoceptor-subtypes, when tested by immunocytochemistry.
  • In all cell lines, the specific agonist clonidine or oxymetazoline stimulated [(3)H]-thymidine incorporation.
  • The specific alpha(2)-adrenergic antagonist rauwolscine always reversed this stimulation at 0.1 nM.
  • In conclusion, this study describes for the first time, the presence of alpha(2)-adrenoceptors in human epithelial breast cell lines.
  • Moreover, activation of these receptors was associated with an enhancement of cell proliferation.
  • [MeSH-major] Breast / metabolism. Breast Neoplasms / metabolism. Cell Line / metabolism. Cell Line, Tumor / metabolism. Receptors, Adrenergic, alpha-2 / metabolism
  • [MeSH-minor] Adrenergic alpha-Agonists / pharmacology. Binding, Competitive. Cell Proliferation / drug effects. Gene Expression. Humans. RNA / metabolism. Thymidine / metabolism

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  • (PMID = 16292538.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ADRA2A protein, human; 0 / ADRA2B protein, human; 0 / ADRA2C protein, human; 0 / Adrenergic alpha-Agonists; 0 / Receptors, Adrenergic, alpha-2; 63231-63-0 / RNA; VC2W18DGKR / Thymidine
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52. Szlosarek PW, Grimshaw MJ, Wilbanks GD, Hagemann T, Wilson JL, Burke F, Stamp G, Balkwill FR: Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer. Int J Cancer; 2007 Jul 01;121(1):6-11
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  • [Title] Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer.
  • The pro-inflammatory cytokine, tumour necrosis factor-alpha, TNF-alpha, is dysregulated in malignant compared with normal ovarian surface epithelium (OSE).
  • Several epidemiological studies have associated inflammation with ovarian tumorigenesis, with TNF-alpha playing a key role in modulating invasion, angiogenesis and metastasis.
  • Here, we show that TNF-alpha also induces expression of arate-limiting enzyme in arginine synthesis, argininosuccinate synthetase (AS), thereby linking inflammation with several arginine-dependent metabolic pathways, implicated in accelerated carcinogenesis and tumour progression.
  • Having identified AS mRNA induction in TNF-alpha-treated IGROV-1 ovarian cancer cells, using RNA-arbitrarily primed-PCR, we then observed differential regulation of AS mRNA and protein in malignant, compared with normal, OSE cells.
  • A cDNA cancer profiling array with matched normal ovarian and ovarian tumour samples revealed increased expression of AS mRNA in the latter.
  • Moreover, AS protein co-localised with TNF-alpha in ovarian cancer cells, with significantly higher levels of AS in malignant compared with normal ovarian tissue.
  • Increased co-expression of AS and TNF-alpha mRNA was also observed in 2 other epithelial tumours, non-small cell lung and stomach cancer, compared with normal corresponding tissues.
  • In summary, high levels of AS expression, which may be required for several arginine-dependent processes in cancer, including the production of nitric oxide, proline, pyrimidines and polyamines, is regulated by TNF-alpha and may provide an important molecular pathway linking inflammation and metabolism to ovarian tumorigenesis.
  • [MeSH-major] Argininosuccinate Synthase / metabolism. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Ovarian Neoplasms / enzymology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Female. Health. Humans. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 17354225.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974; United Kingdom / Medical Research Council / / G0601867
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 6.3.4.5 / Argininosuccinate Synthase
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53. Fillies T, Werkmeister R, van Diest PJ, Brandt B, Joos U, Buerger H: HIF1-alpha overexpression indicates a good prognosis in early stage squamous cell carcinomas of the oral floor. BMC Cancer; 2005;5:84
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  • [Title] HIF1-alpha overexpression indicates a good prognosis in early stage squamous cell carcinomas of the oral floor.
  • BACKGROUND: Hypoxia-inducible factor 1 (HIF-1) is a transcription factor, which plays a central role in biologic processes under hypoxic conditions, especially concerning tumour angiogenesis.
  • HIF-1alpha is the relevant, oxygen-dependent subunit and its overexpression has been associated with a poor prognosis in a variety of malignant tumours.
  • METHODS: 85 patients with histologically proven surgically treated T1/2 squamous cell carcinoma (SCC) of the oral floor were eligible for the study.
  • Tumor specimens were investigated by means of tissue micro arrays (TMAs) and immunohistochemistry for the expression of HIF-1.
  • The expression of HIF-1alpha was related with a significantly improved 5-year survival rate (p < 0.01) and a significantly increased disease free period (p = 0.01) independent from nodal status and tumour size.
  • [MeSH-major] Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / metabolism. Gene Expression Regulation, Neoplastic. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Mouth Neoplasms / diagnosis. Mouth Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anoxia. Biomarkers, Tumor / biosynthesis. Disease-Free Survival. Female. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models. Regression Analysis. Treatment Outcome

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  • (PMID = 16035955.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
  • [Other-IDs] NLM/ PMC1190162
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54. Baumeister P, Schwenk-Zieger S, Reiter M, Welz C, Harréus U: Transforming Growth Factor-alpha reduces carcinogen-induced DNA damage in mini-organ cultures from head-and-neck cancer patients. Mutat Res; 2009 Jun-Jul;677(1-2):42-5
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  • [Title] Transforming Growth Factor-alpha reduces carcinogen-induced DNA damage in mini-organ cultures from head-and-neck cancer patients.
  • EGFR is over-expressed in up to 90-100% of head-and-neck squamous cell carcinomas (HNSCC), and increased expression of EGFR and its ligand Transforming Growth Factor-alpha (TGF-alpha) is not limited to malignant cells, but also detected in histologically normal mucosa of HNSCC patients, supporting the hypothesis of field carcinogenesis.
  • Our study evaluates the impact of stimulation by TGF-alpha on carcinogen-induced and oxidative DNA damage in mucosa tissue cultures of macroscopically normal biopsies from tumour patients and controls.
  • Effects of TGF-alpha on DNA-repair capacity were investigated.
  • To assess DNA fragmentation, alkaline single-cell gel electrophoresis (comet assay) was used.
  • Stimulation of cultures during 24 h with TGF-alpha decreased benzo(a)pyrene diolepoxide (BPDE)-induced DNA damage by 36% in the tumour group (p < 0.001) and by 7% in controls (n = 30).
  • The exact mechanism by which TGF-alpha stimulation reduces BPDE-induced DNA fragmentation remains unclear.
  • However, our results show a strong DNA-stabilizing effect of stimulation by TGF-alpha in mucosa tissue cultures of tumour patients and may therefore be seen as a physiological response to continued carcinogenic impact on the epithelium of the upper aerodigestive tract.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. DNA Damage / drug effects. Head and Neck Neoplasms / genetics. Transforming Growth Factor alpha / pharmacology

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  • (PMID = 19539778.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Transforming Growth Factor alpha; 55097-80-8 / 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide; BBX060AN9V / Hydrogen Peroxide
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55. Orii T, Takeda H, Kawata S, Maeda K, Yamakawa M: Differential immunophenotypic analysis of dendritic cell tumours. J Clin Pathol; 2010 Jun;63(6):497-503
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  • [Title] Differential immunophenotypic analysis of dendritic cell tumours.
  • AIMS: The phenotypic and biological characteristics of dendritic cell (DC) tumours have not been fully elucidated.
  • The aim of this study was to compare the immunophenotypic characteristics of DC-related markers and cell-cycle-associated markers among DC tumours and finally to utilise them for differential diagnosis of DC tumours.
  • METHODS: Tissue sections from 28 patients with DC tumours were immunohistochemically examined using DC-related and cell-cycle-associated markers.
  • RESULTS: The Langerhans cell histiocytosis (LCH) and Langerhans cell sarcoma (LCS) samples were positive for S-100 protein, CD1a, Langerin, fascin, DEC-205 and DC-SIGN.
  • Interdigitating dendritic cell sarcoma (IDCS) was positive for S-100 protein and fascin and negative for Langerin.
  • Follicular dendritic cell sarcoma was distinguished from other DC tumours by the lack of DC-SIGN, Langerin and DCE-205.
  • CONCLUSIONS: These results suggest that Langerin can be used to distinguish LCS from IDCS, and DC-SIGN and DEC-205 can be used to identify DC tumour cells.
  • The frequency of cell-cycle-associated markers can be used for the differential diagnosis of malignant and benign DC tumours.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dendritic Cell Sarcoma, Interdigitating / diagnosis. Histiocytosis, Langerhans-Cell / diagnosis. Langerhans Cell Sarcoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Cycle Proteins / metabolism. Child. Dendritic Cells / immunology. Diagnosis, Differential. Female. Forkhead Transcription Factors / analysis. Histones / metabolism. Humans. Immunophenotyping. Interleukin-3 Receptor alpha Subunit / analysis. Male. Middle Aged. Neoplasm Proteins / metabolism. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 20439325.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Histones; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
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56. Ko CW, Cuthbert RJ, Orsi NM, Brooke DA, Perry SL, Markham AF, Coletta PL, Hull MA: Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice. J Pathol; 2008 Apr;214(5):603-9
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  • [Title] Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice.
  • Interleukin (IL)-4 receptor (IL-4R) alpha chain-dependent signalling by IL-4 and IL-13 promotes tumour growth and metastasis in mouse models of colorectal cancer.
  • However, the role of IL-4R alpha-dependent signalling during the early, pre-malignant stages of colorectal carcinogenesis has not been investigated.
  • Therefore, we investigated the effect of deletion of the IL-4R alpha gene on azoxymethane-induced colorectal aberrant crypt focus (ACF) multiplicity and size in Balb/c mice.
  • IL-4R alpha(-/-) mice developed significantly more ACFs [median 8, inter-quartile range (IQR) 4-11.5; n = 9] than wild-type (WT) animals (median 4, IQR 1-6; n = 9; p = 0.04, Mann-Whitney U-test).
  • There were significantly higher levels of IL-4 in serum from azoxymethane- and sham-treated IL-4R alpha(-/-) mice than WT animals, but no difference in serum IL-13 levels.
  • We found that mucosal TGFbeta mRNA levels and intestinal epithelial cell TGFbeta immunoreactivity were significantly higher in IL-4R alpha(-/-) mice than in WT animals.
  • In summary, IL-4R alpha-dependent signalling has a protective, anti-neoplastic role during the post-initiation phase of azoxymethane-induced colorectal carcinogenesis in Balb/c mice.
  • Our data should prompt thorough investigation of the role of IL-4R alpha-dependent signalling during human colorectal carcinogenesis, particularly as antagonism of IL-4R signalling represents a therapeutic strategy for asthma and other allergic diseases.
  • [MeSH-major] Colorectal Neoplasms / immunology. Precancerous Conditions / immunology. Receptors, Cell Surface / immunology
  • [MeSH-minor] Animals. Azoxymethane. Carcinogens. Cell Transformation, Neoplastic / immunology. Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Female. Interleukin-13 / blood. Interleukin-4 / blood. Intestinal Mucosa / immunology. Intestinal Mucosa / pathology. Mice. Mice, Inbred BALB C. Mice, Knockout. Signal Transduction / immunology. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / blood

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  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland
  • (PMID = 18220315.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/146; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; MO0N1J0SEN / Azoxymethane
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57. Sulkowska M, Wincewicz A, Sulkowski S, Koda M, Kanczuga-Koda L: Relations of TGF-beta1 with HIF-1 alpha, GLUT-1 and longer survival of colorectal cancer patients. Pathology; 2009;41(3):254-60
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  • [Title] Relations of TGF-beta1 with HIF-1 alpha, GLUT-1 and longer survival of colorectal cancer patients.
  • AIMS AND METHODS: During colorectal carcinogenesis, transforming growth factor beta 1 (TGF-beta1) undergoes a functional change from suppression of cancer cell proliferation to inhibition of T cell mediated anti-cancer immunity.
  • We aimed to evaluate relations among TGF-beta1 and cancer cell survival factors hypoxia inducible factor-1 alpha (HIF-1 alpha) and glucose transporter 1 (GLUT-1) by immunohistochemistry in 108 colorectal cancers.
  • RESULTS: TGF-beta1 was detected in 87% (94/108), HIF-1 alpha in 85% (92/108), and GLUT-1 in 65% (70/108) of colorectal cancers.
  • GLUT-1 was visualised in a membranous fashion while HIF-1 was expressed in a paranuclear pattern and occasionally in nuclei of malignant cells.
  • Cancer immunoreactivities to TGF-beta1 correlated with HIF-1 alpha (p < 0.001, r = 0.516) and GLUT-1 (p < [corrected] 0.001, r = 0.355) in general and subgroups of different clinicopathological traits.
  • TGF-beta1 expressions of inflammatory infiltrates correlated with longer patient survival (p = 0.05, r = 0.449) and immunoreactivities to HIF-1 alpha of cancer cells (p = 0.008, r = 0.254) particularly in node positive and deeply invading cancers but failed to associate significantly with GLUT-1.
  • CONCLUSIONS: HIF-1 alpha and GLUT-1 could cooperate with TGF-beta1, and TGF-beta1 might mediate cross-talk between the inflammatory environment and tumour with a favourable impact on patient survival.
  • [MeSH-major] Colorectal Neoplasms / metabolism. Colorectal Neoplasms / mortality. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Transforming Growth Factor beta1 / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Receptor Cross-Talk / physiology

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  • [ErratumIn] Pathology. 2009;41(6):612
  • (PMID = 19142800.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transforming Growth Factor beta1
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58. Lopes N, Sousa B, Martins D, Gomes M, Vieira D, Veronese LA, Milanezi F, Paredes J, Costa JL, Schmitt F: Alterations in Vitamin D signalling and metabolic pathways in breast cancer progression: a study of VDR, CYP27B1 and CYP24A1 expression in benign and malignant breast lesions. BMC Cancer; 2010;10:483
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  • [Title] Alterations in Vitamin D signalling and metabolic pathways in breast cancer progression: a study of VDR, CYP27B1 and CYP24A1 expression in benign and malignant breast lesions.
  • CONCLUSIONS: From this study, we conclude that there is a deregulation of the Vitamin D signalling and metabolic pathways in breast cancer, favouring tumour progression.
  • Thus, during mammary malignant transformation, tumour cells lose their ability to synthesize the active form of Vitamin D and respond to VDR-mediated Vitamin D effects, while increasing their ability to degrade this hormone.
  • [MeSH-major] 25-Hydroxyvitamin D3 1-alpha-Hydroxylase / metabolism. Breast / metabolism. Breast Neoplasms / metabolism. Receptors, Calcitriol / metabolism. Steroid Hydroxylases / metabolism. Vitamin D / metabolism
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Cohort Studies. Disease Progression. Female. Gene Expression Profiling. Humans. Immunoenzyme Techniques. Metabolic Networks and Pathways. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Vitamin D3 24-Hydroxylase

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  • (PMID = 20831823.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D; EC 1.14.- / 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / CYP24A1 protein, human; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase
  • [Other-IDs] NLM/ PMC2945944
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59. Willenbrock K, Renné C, Gaulard P, Hansmann ML: In angioimmunoblastic T-cell lymphoma, neoplastic T cells may be a minor cell population. A molecular single-cell and immunohistochemical study. Virchows Arch; 2005 Jan;446(1):15-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In angioimmunoblastic T-cell lymphoma, neoplastic T cells may be a minor cell population. A molecular single-cell and immunohistochemical study.
  • The significance of T-cell proliferations in angioimmunoblastic lymphoma (AILD) is still enigmatic.
  • Although classified as a malignant T-cell lymphoma in the World Health Organisation lymphoma classification, some cases of AILD lack dominant T-cell clones.
  • In a previous study, based on single-cell polymerase chain reaction (PCR), we obtained similar results as studies of AILD using Southern blot or conventional PCR: some cases of AILD contained large T-cell clones, and, in other cases, T-cell clones were undetectable.
  • As in single-cell studies, only a limited number of cells could be investigated; thus, we wanted to gain more insight into the amount and distribution of tumour cells.
  • By applying triple immunofluorescent staining with antibodies directed against T-cell receptor Vbeta-family-specific epitopes, we investigated T-cell populations in AILD and their localisation in the tissue in relation to B cells (CD20) and follicular dendritic cells (CD21).
  • In two of five cases investigated, only a minority of the T-cells compartment belonged to the tumour clone.
  • [MeSH-major] Immunoblastic Lymphadenopathy / immunology. Lymphoma, T-Cell / immunology. T-Lymphocytes / pathology
  • [MeSH-minor] Antigens, CD20 / analysis. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Polymerase Chain Reaction. Receptors, Antigen, T-Cell, alpha-beta / analysis. Receptors, Complement 3d / analysis

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  • (PMID = 15480765.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Complement 3d
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60. Hadar T, Shvero J, Yaniv E, Shvili I, Leabu M, Koren R: Human topoisomerase II-alpha is highly expressed in sinonasal-inverted papilloma, but not in inflammatory polyp. J Cell Mol Med; 2008 Sep-Oct;12(5A):1551-8
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  • [Title] Human topoisomerase II-alpha is highly expressed in sinonasal-inverted papilloma, but not in inflammatory polyp.
  • Sinonasal-inverted papilloma is a benign tumour with a high rate of recurrence, but possible malignant transformation.
  • Therefore, investigation of predisposition to malignant transformation of sinonasal-inverted papilloma gives clinicians the opportunity for adequate treatment.
  • Topoisomerase II-alpha (topoII-alpha) and Ki67 are markers of cell proliferation in both normal and neoplastic tissues and its level o expression could be used as a predictive parameter.
  • TopoI alpha nuclear immunostaining showed a differential positivity in the investigated cases.
  • The topoII-alpha index was 30.6 +/- 12.8 in inverte papilloma, 10.7 +/- 6.6 in the adjacent epithelium of inverted papilloma, but only 2.3 +/- 2.0 in the normal sinonasal epithelium.
  • The differences in topoII-alpha expression between inverted papilloma and normal sinonasal epithelia were statistically significant.
  • In inflammatory nasal polyp group, topoII-alpha index was 2.4 +/- 2.1, and the difference in the topoII-alpha index between inverted papilloma and inflammatory polyp group was also statistically significant.
  • Significant correlation coefficients were found between topoII-alpha and epithelial thickness (r = 0.70, P > 0.0001), and between Ki67 index and epithelial thickness (r = 0.71, P> 0.0001).
  • Significant correlation coefficient was found between topoII-alpha index and Ki67 index in inverted papilloma (r = 0.42, P > 0.05).
  • These results suggest that the inverte papilloma contains a significantly higher cell population with proliferative activity by comparison with normal sinonasal and inflammatory polyp epithelia, showing a significant correlation between topoII-alpha and Ki67 expression, and indicating that topoII-alpha could be a independent prognostic factor for a putative malignant transformation.

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  • (PMID = 18544048.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC3918071
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61. Aggelis V, Craven RA, Peng J, Harnden P, Cairns DA, Maher ER, Tonge R, Selby PJ, Banks RE: Proteomic identification of differentially expressed plasma membrane proteins in renal cell carcinoma by stable isotope labelling of a von Hippel-Lindau transfectant cell line model. Proteomics; 2009 Apr;9(8):2118-30
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  • [Title] Proteomic identification of differentially expressed plasma membrane proteins in renal cell carcinoma by stable isotope labelling of a von Hippel-Lindau transfectant cell line model.
  • The von Hippel-Lindau (VHL) tumour suppressor gene plays a central role in development of clear cell renal cell carcinoma (RCC).
  • Using a cell line pair generated from the VHL-defective RCC cell line UMRC2 by transfection with vector control or VHL (-/+VHL) and stable isotope labelling with amino acids in cell culture (SILAC) followed by enrichment of plasma membrane proteins by cell surface biotinylation/avidin-affinity chromatography and analysis by GeLC-MS/MS, VHL-associated changes in plasma membrane proteins were analysed.
  • These included several proteins previously reported to be VHL targets, such as transferrin receptor 1 and the alpha 3 and beta1 integrin subunits and novel findings including upregulation of CD166 and CD147 in VHL-defective cells.
  • Analysis of patient-matched normal and malignant renal tissues confirmed these differences were also present in vivo in a subset of clear cell RCCs.
  • [MeSH-major] Carcinoma, Renal Cell / metabolism. Membrane Proteins / biosynthesis. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Antigens, CD / biosynthesis. Antigens, CD147 / biosynthesis. Biomarkers / metabolism. Cell Adhesion Molecules, Neuronal / biosynthesis. Cell Line, Tumor. Fetal Proteins / biosynthesis. Glycosylation. Humans. Isotope Labeling. Kidney Neoplasms / chemistry. Kidney Neoplasms / metabolism. Kidney Neoplasms / ultrastructure. Mass Spectrometry. Proteomics. Transfection. Up-Regulation

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  • (PMID = 19337990.001).
  • [ISSN] 1615-9861
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ALCAM protein, human; 0 / Antigens, CD; 0 / Biomarkers; 0 / Cell Adhesion Molecules, Neuronal; 0 / Fetal Proteins; 0 / Membrane Proteins; 136894-56-9 / Antigens, CD147; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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62. Lansigan F, Foss FM: Current and emerging treatment strategies for cutaneous T-cell lymphoma. Drugs; 2010 Feb 12;70(3):273-86
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  • [Title] Current and emerging treatment strategies for cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCLs) are a rare group of mature T-cell lymphomas presenting primarily in the skin.
  • Other than an allogeneic stem cell transplant, there are no curative therapies for this disease.
  • These therapies include biological immune enhancers such as interferon alpha and extracorporeal photopheresis that exert their effect by stimulating an immune response to the tumour cells.
  • The fusion toxin denileukin diftitox targets the interleukin-2 receptor expressed on malignant T cells.
  • Forodesine is a novel inhibitor of purine nucleoside phosphorylase and leads to apoptosis of malignant T cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Lymphoma, T-Cell, Cutaneous / drug therapy. Lymphoma, T-Cell, Cutaneous / therapy. Skin Neoplasms / drug therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Clinical Protocols. Drug Administration Routes. Hematopoietic Stem Cell Transplantation / methods. Humans

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  • (PMID = 20166766.001).
  • [ISSN] 1179-1950
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 90
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63. Postema EJ, McEwan AJ, Riauka TA, Kumar P, Richmond DA, Abrams DN, Wiebe LI: Initial results of hypoxia imaging using 1-alpha-D: -(5-deoxy-5-[18F]-fluoroarabinofuranosyl)-2-nitroimidazole ( 18F-FAZA). Eur J Nucl Med Mol Imaging; 2009 Oct;36(10):1565-73
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  • [Title] Initial results of hypoxia imaging using 1-alpha-D: -(5-deoxy-5-[18F]-fluoroarabinofuranosyl)-2-nitroimidazole ( 18F-FAZA).
  • PURPOSE: Tumour hypoxia is thought to play a significant role in the outcome of solid tumour therapy.
  • The locally developed PET tracer for imaging hypoxia, 1-alpha-D: -(5-deoxy-5-[(18)F]-fluoroarabinofuranosyl)-2-nitroimidazole ((18)F-FAZA), has been shown to accumulate in experimental models of tumour hypoxia and to clear rapidly from the circulation and nonhypoxic tissues.
  • The safety and general biodistribution patterns of this radiopharmaceutical in patients with squamous cell carcinoma of the head and neck (HNSCC), small-cell lung cancer (SCLC) or non-small-cell lung cancer (NSCLC), malignant lymphoma, and high-grade gliomas, were demonstrated in this study.
  • METHODS: Patients with known primary or suspected metastatic HNSCC, SCLC or NSCLC, malignant lymphoma or high-grade gliomas were dosed with 5.2 MBq/kg of (18)F-FAZA, then scanned 2-3 h after injection using a PET or PET/CT scanner.
  • The location and relative uptake scores (graded 0 to 4) of normal and abnormal (18)F-FAZA biodistribution patterns, the calculated tumour-to-background (T/B) ratio, and the maximum standardized uptake value were recorded.
  • All seven patients with high-grade gliomas showed very high uptake of (18)F-FAZA in the primary tumour.
  • In six out of nine patients with HNSCC, clear uptake of (18)F-FAZA was observed in the primary tumour and/or the lymph nodes in the neck.
  • Of the 13 lung cancer patients (12 NSCLC, 1 SCLC), 7 had increased (18)F-FAZA uptake in the primary lung tumour.
  • CONCLUSION: This study suggests that (18)F-FAZA may be a very useful radiopharmaceutical to image hypoxia in the tumour types selected.
  • Given the good imaging properties, including acceptable T/B ratios in the tumour categories studied, (18)F-FAZA could be considered as a very promising agent for assessing the hypoxic fraction of these tumour types.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Non-Small-Cell Lung / diagnostic imaging. Carcinoma, Small Cell / diagnostic imaging. Carcinoma, Squamous Cell / diagnostic imaging. Female. Fluorine Radioisotopes. Glioma / diagnostic imaging. Head and Neck Neoplasms / diagnostic imaging. Humans. Lung Neoplasms / diagnostic imaging. Lymphoma / diagnostic imaging. Male. Middle Aged. Positron-Emission Tomography. Young Adult

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  • (PMID = 19430784.001).
  • [ISSN] 1619-7089
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / Nitroimidazoles; 0 / Radiopharmaceuticals; 0 / fluoroazomycin arabinoside
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64. Lee TH, Cho HK, Cho YH, Lee MG: Development of an effective method for dendritic cell immunotherapy of mouse melanoma. Scand J Immunol; 2009 Aug;70(2):85-92
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  • [Title] Development of an effective method for dendritic cell immunotherapy of mouse melanoma.
  • Dendritic cell (DC) immunotherapy is a strong candidate for the treatment of incurable cancers especially malignant melanoma.
  • So we conducted this study in order to develop an effective DC preparation method for immunotherapy in mouse malignant melanoma.
  • Mouse bone marrow-derived DC were stimulated with tumour antigen alone or tumour antigen plus a cocktail (anti-CD40 antibody +TNF-alpha+ IL-1beta) for 8, 24 or 48 h and the characteristics of these DC, such as surface molecules (CD40, CD80, CD86, MHC class II, CCR7), cytokines(IL-12, IFN-gamma, and IL-10), DC-induced T cell proliferation in vitro, and the production of IFN-gamma by those cells, were evaluated.
  • Mice with melanoma were then treated with DC stimulated with tumour antigen alone and tumour antigen plus cocktail for 8 or 48 h.
  • The tumour size and survival rate of these mice were then evaluated. (1) Beneficial clinical effects such as a reduction of tumour size and an increased survival rate were best observed in the group treated with DC stimulated for 8 h with tumour antigen plus cocktail. (2) The single prominent characteristic of DC stimulated for 8 h with tumour antigen plus cocktail was an elevated IL-12 secretion.
  • [MeSH-minor] Animals. Antigens, CD40 / immunology. Antigens, CD40 / metabolism. Cell Proliferation. Female. Interferon-gamma / immunology. Interferon-gamma / metabolism. Interleukin-10 / immunology. Interleukin-10 / metabolism. Interleukin-12 / immunology. Interleukin-12 / metabolism. Interleukin-1beta / immunology. Interleukin-1beta / metabolism. Mice. Mice, Inbred C57BL. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19630913.001).
  • [ISSN] 1365-3083
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / IL10 protein, human; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma
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65. Ohnishi H, Abe M, Hamada H, Yokoyama A, Hirayama T, Ito R, Nishimura K, Higaki J: Metastatic renal cell carcinoma presenting as multiple pleural tumours. Respirology; 2005 Jan;10(1):128-31
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  • [Title] Metastatic renal cell carcinoma presenting as multiple pleural tumours.
  • Chest X-ray and chest computed tomography (CT) demonstrated a left-sided pleural effusion and multiple tumours, suggesting malignant mesothelioma in the left pleural space, but there were no pulmonary lesions.
  • However, abdominal CT revealed a right renal tumour.
  • An ultrasonography-guided needle biopsy of the pleural mass provided evidence of metastatic renal cell carcinoma (RCC).
  • The pleural lesions dramatically decreased in size following right radical nephrectomy and subsequent interferon-alpha treatment.
  • While the thorax is a frequently affected site of RCC, sole pleural metastases are rare and are often secondary to lung involvement.
  • [MeSH-major] Carcinoma, Renal Cell / secondary. Kidney Neoplasms / pathology. Pleural Neoplasms / secondary
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Male. Mesothelioma / diagnosis. Pleural Effusion, Malignant / pathology

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  • (PMID = 15691252.001).
  • [ISSN] 1323-7799
  • [Journal-full-title] Respirology (Carlton, Vic.)
  • [ISO-abbreviation] Respirology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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66. Kang KB, Zhu C, Yong SK, Gao Q, Wong MC: Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy. Mol Cancer; 2009;8:66
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  • [Title] Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy.
  • BACKGROUND: Selective cyclooxygenase (COX)-2 inhibitors elicit anti-proliferative responses in various tumours, however the underlying anti-tumour mechanisms are unclear.
  • Mutational inactivation of the tumour suppressor p53 gene is frequent in malignant gliomas.
  • The role of p53 mutation in the anti-tumour responses of the selective COX-2 inhibitor celecoxib in human glioblastoma cells is unknown.
  • Inhibition of p53 was achieved in U87MG cells transfected with E6 oncoprotein (U87MG-E6) and treated with pifithrin-alpha, a reversible inhibitor of p53 (U87MG-PFT).
  • We investigated whether the anti-glioblastoma responses of celecoxib were p53-dependent, and whether celecoxib induced DNA damage leading to p53-dependent G1 cell cycle arrest, followed by autophagy or apoptosis.
  • RESULTS: Our findings demonstrated that celecoxib concentration-dependently reduced glioblastoma cell viability, following 24 and 72 hours of treatment.
  • Celecoxib induced G1-phase cell cycle arrest, accompanied with p21 activation in U87MG cells.
  • Cell cycle progression of U87MG-E6 and U87MG-PFT cells was not affected by celecoxib.
  • In parallel, celecoxib induced G1 cell cycle arrest in LN229 cells, but not in U373MG cells.
  • Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.
  • [MeSH-major] Autophagy / drug effects. DNA Damage. G1 Phase / drug effects. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Analysis of Variance. Benzothiazoles / pharmacology. Blotting, Western. Celecoxib. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Comet Assay. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase Inhibitors / pharmacology. Dose-Response Relationship, Drug. G0 Phase / drug effects. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction. Toluene / analogs & derivatives. Toluene / pharmacology

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  • (PMID = 19706164.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzothiazoles; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 3FPU23BG52 / Toluene; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC2741461
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67. Rago V, Romeo F, Giordano F, Ferraro A, Andò S, Carpino A: Identification of ERbeta1 and ERbeta2 in human seminoma, in embryonal carcinoma and in their adjacent intratubular germ cell neoplasia. Reprod Biol Endocrinol; 2009;7:56
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  • [Title] Identification of ERbeta1 and ERbeta2 in human seminoma, in embryonal carcinoma and in their adjacent intratubular germ cell neoplasia.
  • BACKGROUND: Estrogens exert a role on germ cell physiology of normal human testis through the mediation of the estrogen receptor (ER) beta subtypes.
  • Epidemiological studies evidenced an increased incidence of testicular germ cell cancer after elevated pre-natal estrogen exposure but the expression of estrogen receptors in these testicular neoplasms has not been well elucidated.
  • METHODS: Immunohistochemistry and Western blot analysis were used to investigate the expression of three distinct ER isoforms, ERalpha, ERbeta1, and ERbeta2 in paraffin-embedded tissues from seminomas and embryonal carcinomas, which are the most common testicular germ cell tumours.
  • A similar pattern of estrogen receptor immunostaining was also observed in the malignant germ cells of intratubular germ cell neoplasia, adjacent to testicular cancers.
  • Western blot analysis of tumour extracts revealed two immunoreactive bands, a 59 kDa band for ERbeta1 and a 53 kDa band for ERbeta2.
  • CONCLUSION: A variable ERbeta expression was previously reported in testicular germ cell tumours and, particularly, an ERbeta down-regulation was evidenced in seminoma and embryonal carcinoma.
  • Conversely, the current study has clearly identified ERbeta1 and ERbeta2 in the neoplastic cells of seminoma and embryonal carcinoma, as well as in the malignant cells of their common pre-invasive precursor, intratubular germ cell neoplasia.
  • [MeSH-major] Carcinoma, Embryonal / metabolism. Estrogen Receptor beta / metabolism. Neoplasms, Germ Cell and Embryonal / metabolism. Seminoma / metabolism. Testicular Neoplasms / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Down-Regulation / physiology. Estrogen Receptor alpha / metabolism. Humans. Immunohistochemistry. Male. Young Adult

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  • (PMID = 19493328.001).
  • [ISSN] 1477-7827
  • [Journal-full-title] Reproductive biology and endocrinology : RB&E
  • [ISO-abbreviation] Reprod. Biol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
  • [Other-IDs] NLM/ PMC2700117
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68. Kempkensteffen C, Hinz S, Krause H, Jager T, Köllermann J, Weikert S, Christoph F, Schostak M, Miller K, Schrader M: Expression of splicing variants of the inhibitor of apoptosis livin in testicular germ cell tumors. Tumour Biol; 2008;29(2):76-82
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  • [Title] Expression of splicing variants of the inhibitor of apoptosis livin in testicular germ cell tumors.
  • Livin has therefore been evaluated as a diagnostic and prognostic marker and recently gained much attention as a target for tumor therapy.
  • We evaluated the expression of livin splicing variants in 131 testicular germ cell tumors (TGCT) compared to 20 normal testicular tissue samples using dual-color real-time RT-PCR and Western blot analysis.
  • Expression of livin beta was detected in 51.9% and expression of the alpha-variant in 28.2% of the TGCT specimens.
  • Livin alpha was only expressed in combination with the beta-isoform, the respective expression levels being highly intercorrelated (Spearman's correlation coefficient: rho = 0.854).
  • Livin expression was strongly related to TGCT differentiation but not to clinical tumor stage and patient age.
  • The beta-variant was expressed in 67.5% of seminomas but only in 27.1% of nonseminomatous germ cell tumors (NSGCT).
  • Expression of the alpha-variant was detected in 38.5% of seminomas and in 10.4% of NSGCT.
  • Considering that livin expression is restricted to malignant testicular tissue, it appears reasonable to conduct further investigations regarding its targeted inhibition in TGCT.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Apoptosis / physiology. Gene Expression Regulation, Neoplastic / physiology. Inhibitor of Apoptosis Proteins / genetics. Neoplasm Proteins / genetics. Neoplasms, Germ Cell and Embryonal / genetics. Protein Splicing / genetics. Testicular Neoplasms / genetics
  • [MeSH-minor] Carcinoma, Embryonal / genetics. Carcinoma, Embryonal / metabolism. Carcinoma, Embryonal / pathology. Humans. Male. Protein Isoforms / genetics. Protein Isoforms / metabolism. Seminoma / genetics. Seminoma / metabolism. Seminoma / pathology. Testis / cytology. Testis / metabolism

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18515985.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BIRC7 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Neoplasm Proteins; 0 / Protein Isoforms
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69. Nakashima C, Tanioka M, Takahashi K, Miyachi Y: Diffuse large B-cell lymphoma in a patient with rheumatoid arthritis treated with infliximab and methotrexate. Clin Exp Dermatol; 2008 Jul;33(4):437-9
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  • [Title] Diffuse large B-cell lymphoma in a patient with rheumatoid arthritis treated with infliximab and methotrexate.
  • Infliximab is a tumour necrosis factor (TNF)-alpha blocking drug classified as a biological response modifier.
  • It has been suggested that the risk of malignancies, especially lymphomas, is increased in patients with rheumatoid arthritis (RA) treated with anti-TNF-alpha antibody therapy.
  • We present a case of malignant lymphoma during the treatment of RA with infliximab and methotrexate.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antirheumatic Agents / adverse effects. Arthritis, Rheumatoid / drug therapy. Lymphoma, Large B-Cell, Diffuse / chemically induced. Methotrexate / adverse effects. Skin Neoplasms / chemically induced


70. Ammirante M, Luo JL, Grivennikov S, Nedospasov S, Karin M: B-cell-derived lymphotoxin promotes castration-resistant prostate cancer. Nature; 2010 Mar 11;464(7286):302-5
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  • [Title] B-cell-derived lymphotoxin promotes castration-resistant prostate cancer.
  • Prostate cancer (CaP) progresses from prostatic intraepithelial neoplasia through locally invasive adenocarcinoma to castration-resistant metastatic carcinoma.
  • Curiously, castration-resistant CaP remains androgen-receptor dependent, and potent androgen-receptor antagonists induce tumour regression in castrated mice.
  • The inflammation-responsive IkappaB kinase (IKK)-beta and its target NF-kappaB have important tumour-promoting functions within malignant cells and inflammatory cells.
  • The latter, including macrophages and lymphocytes, are important elements of the tumour microenvironment, but the mechanisms underlying their recruitment remain obscure, although they are thought to depend on chemokine and cytokine production.
  • We found that CaP progression is associated with inflammatory infiltration and activation of IKK-alpha, which stimulates metastasis by an NF-kappaB-independent, cell autonomous mechanism.
  • Here we show that androgen ablation causes infiltration of regressing androgen-dependent tumours with leukocytes, including B cells, in which IKK-beta activation results in production of cytokines that activate IKK-alpha and STAT3 in CaP cells to enhance hormone-free survival.


71. Karunakaran S, Umapathy NS, Thangaraju M, Hatanaka T, Itagaki S, Munn DH, Prasad PD, Ganapathy V: Interaction of tryptophan derivatives with SLC6A14 (ATB0,+) reveals the potential of the transporter as a drug target for cancer chemotherapy. Biochem J; 2008 Sep 15;414(3):343-55
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  • 1-Methyltryptophan is an inducer of immune surveillance against tumour cells through its ability to inhibit indoleamine dioxygenase.
  • In the present study, we investigated the role of ATB(0,+) in the uptake of 1-methyltryptophan as a potential mechanism for entry of this putative anticancer drug into tumour cells.
  • Evaluation of other derivatives of tryptophan has led to identification of alpha-methyltryptophan as a blocker, not a transportable substrate, for ATB(0,+).
  • ATB(0,+) can transport 18 of the 20 proteinogenic amino acids. alpha-Methyltryptophan blocks the transport function of ATB(0,+) with an IC(50) value of approximately 250 muM under conditions simulating normal plasma concentrations of all these 18 amino acids.
  • These results suggest that alpha-methyltryptophan may induce amino acid deprivation in cells which depend on the transporter for their amino acid nutrition.
  • Screening of several mammary epithelial cell lines shows that ATB(0,+) is expressed robustly in some cancer cell lines, but not in all; in contrast, non-malignant cell lines do not express the transporter.
  • Treatment of ATB(0,+)-positive tumour cells with alpha-methyltryptophan leads to suppression of their colony-forming ability, whereas ATB(0,+)-negative cell lines are not affected.
  • The blockade of ATB(0,+) in these cells with alpha-methyltryptophan is associated with cell cycle arrest.
  • [MeSH-minor] Amino Acid Transport Systems / metabolism. Animals. Biological Transport, Active / drug effects. Cell Line. Cell Line, Tumor. Humans. Large Neutral Amino Acid-Transporter 1 / genetics. Large Neutral Amino Acid-Transporter 1 / metabolism. Mice. Oocytes / metabolism. Plasma Membrane Neurotransmitter Transport Proteins / metabolism. Xenopus laevis

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  • (PMID = 18522536.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1-methyltryptophan; 0 / Amino Acid Transport Systems; 0 / Amino Acid Transport Systems, Neutral; 0 / Antineoplastic Agents; 0 / Large Neutral Amino Acid-Transporter 1; 0 / Plasma Membrane Neurotransmitter Transport Proteins; 0 / SLC6A14 protein, human; 0 / Slc6A14 protein, mouse; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan
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72. Bien E, Balcerska A: Serum soluble interleukin 2 receptor alpha in human cancer of adults and children: a review. Biomarkers; 2008 Feb;13(1):1-26
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  • [Title] Serum soluble interleukin 2 receptor alpha in human cancer of adults and children: a review.
  • In most haematological malignancies, including different types of leukaemias and lymphomas, sIL-2Ralpha has been found to be released directly from the surface of neoplastic cells thus reflecting the tumour bulk, turnover and activity.
  • They include malignant melanoma and carcinomas of the kidney, head and neck, oesophagus and lung.
  • It is suggested that in most malignant solid tumours, elevated levels of sIL-2Ralpha are likely to be the product of normal peripheral mononuclear cells activated in response to the neoplasm's growth or that they are released from activated lymphoid cells infiltrating neoplastic tissues.
  • This latter hypothesis has been proved by discovering the high expression of CD25 on the cell surface of most of these cells.
  • The authors review the published data on clinical applicability of soluble IL-2Ralpha determination in terms of diagnostics, prognosis and treatment monitoring of particular types of malignant disorders both in adults and in children.
  • [MeSH-major] Biomarkers, Tumor / blood. Interleukin-2 Receptor alpha Subunit / blood. Neoplasms / blood

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  • (PMID = 17906988.001).
  • [ISSN] 1354-750X
  • [Journal-full-title] Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
  • [ISO-abbreviation] Biomarkers
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-2 Receptor alpha Subunit
  • [Number-of-references] 169
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73. Sánchez Carazo JL, Mahiques Santos L, Oliver Martinez V: Safety of etanercept in psoriasis: a critical review. Drug Saf; 2006;29(8):675-85
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  • The drug is a competitive inhibitor of tumour necrosis factor-alpha (TNFalpha) that prevents interaction between this cytokine and its cell surface receptors.
  • Etanercept also modulates the activity of other inflammatory cytokines and does not induce complement-mediated cell lysis in vitro.
  • The most common adverse effect during drug administration is mild injection site reactions.
  • There are no data showing that treatment with etanercept results in an increase in the occurrence of malignant neoplasms.
  • Etanercept must be used with extreme caution in patients with heart failure because of several reports indicating a worsening or de novo occurrence of congestive heart failure while receiving the drug.
  • In patients with hepatitis C viral infection, etanercept does not increase transaminase levels or viral load and in some instances has allowed the concomitant use of interferon which had previously been discontinued because of a worsening of psoriasis.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Immunoglobulin G / adverse effects. Psoriasis / drug therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Child. Etanercept. Female. Humans. Practice Guidelines as Topic. Pregnancy. Randomized Controlled Trials as Topic. Receptors, Tumor Necrosis Factor

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  • (PMID = 16872241.001).
  • [ISSN] 0114-5916
  • [Journal-full-title] Drug safety
  • [ISO-abbreviation] Drug Saf
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  • [Number-of-references] 86
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74. Panteli C, Curry J, Kiely E, Pierro A, de Coppi P, Anderson J, Sebire N, Drake D: Ovarian germ cell tumours: a 17-year study in a single unit. Eur J Pediatr Surg; 2009 Apr;19(2):96-100
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  • [Title] Ovarian germ cell tumours: a 17-year study in a single unit.
  • BACKGROUND/PURPOSE: The aim of this study was to evaluate the clinical presentation, management and outcome in girls treated for ovarian germ cell tumours at a single unit.
  • METHODS: The records of 40 girls (median age 10.5 years) with histologically proven ovarian germ cell tumours operated upon between 1990 and 2007 were reviewed.
  • RESULTS: Twenty-nine patients had mature teratomas (MT), 5 patients had immature teratomas (IT) and 6 had malignant tumours: 4 malignant mixed germ cell tumours (MMGCT) and 2 germinomas (G).
  • The median age at presentation was 11 years for the MT and IT groups and 8.5 years for the malignant group.
  • Precocious puberty was noted at presentation in three patients with malignant tumours.
  • Tumour markers were elevated at presentation in all patients with MMGCT.
  • Of the patients with malignant tumours, 1 had stage I, 2 had stage II, 1 had stage III and 1 had stage IV disease.
  • There was one recurrence in a patient with IT, with raised tumour markers.
  • CONCLUSIONS: Ovarian germ cell tumours are uncommon in childhood.
  • Tumour markers are valuable both pre and post-operatively.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / pathology. Neoplasms, Germ Cell and Embryonal / surgery. Ovarian Neoplasms / pathology. Ovarian Neoplasms / surgery
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / blood. Biopsy. CA-125 Antigen / blood. Child. Child, Preschool. Chorionic Gonadotropin / blood. Female. Follow-Up Studies. Humans. Medical Records. Neoplasm Staging. Retrospective Studies. Teratoma / pathology. Teratoma / surgery. Treatment Outcome. alpha-Fetoproteins / metabolism

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  • (PMID = 19360543.001).
  • [ISSN] 1439-359X
  • [Journal-full-title] European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift für Kinderchirurgie
  • [ISO-abbreviation] Eur J Pediatr Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / Chorionic Gonadotropin; 0 / alpha-Fetoproteins
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75. Heidenreich O: Targeting oncogenes with siRNAs. Methods Mol Biol; 2009;487:221-42
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  • This lack of tumour cell specificity results in severe toxic side effects and may only hardly affect quiescent cancer stem cells consequently leading to relapse.
  • Since oncogenes are exclusively expressed in malignant and pre-malignant cells, they may provide unique, cancer cell specific targets for therapeutic strategies.
  • However, their role in maintaining the malignant phenotype is frequently unknown.
  • Oncogene-specific RNA interference offers here new and exciting options to analyse oncogene functions directly in the malignant environment.
  • [MeSH-minor] Core Binding Factor Alpha 2 Subunit / antagonists & inhibitors. Core Binding Factor Alpha 2 Subunit / metabolism. Humans. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / metabolism. Tumor Cells, Cultured

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  • (PMID = 19301650.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Small Interfering
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76. Eyden B, Banerjee SS, Shenjere P, Fisher C: The myofibroblast and its tumours. J Clin Pathol; 2009 Mar;62(3):236-49
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  • Tumours and tumour-like lesions of myofibroblasts may present diagnostic difficulty because of their rarity and because of uncertainties in identifying the myofibroblast.
  • The objectives of this review are to provide a definition of the myofibroblast and an account of its biology for facilitating an understanding of the cell and of myofibroblastic lesions; and to describe, in the context of common diagnostic problems, the features of benign and malignant myofibroblastic lesions.
  • The main characteristics of the myofibroblast include a spindled or stellate morphology; immunostaining for alpha-smooth muscle actin and the extra domain A variant of cellular fibronectin; and an ultrastructure of rough endoplasmic reticulum, peripheral contractile filaments and the cell-to-matrix junction known as the fibronexus.
  • [MeSH-minor] Diagnosis, Differential. Fasciitis / pathology. Humans

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  • (PMID = 18930983.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 203
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77. Tajima N, Schönherr K, Niedling S, Kaatz M, Kanno H, Schönherr R, Heinemann SH: Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1alpha and the von Hippel-Lindau protein. J Physiol; 2006 Mar 1;571(Pt 2):349-59
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  • Under chronic hypoxia, tumour cells undergo adaptive changes involving hypoxia-inducible factors (HIFs).
  • This increase involves the HIF system as confirmed by overexpression of HIF-1alpha or the von Hippel-Lindau tumour suppressor gene.
  • Hypoxia increased cell proliferation, but the K(Ca) channel blockers apamin and charybdotoxin slowed down cell growth, particularly under hypoxic conditions.
  • Similar results were obtained for the cell line IGR39 and for acutely isolated cells from a biopsy of a melanoma metastasis.
  • Thus, up-regulation of K(Ca) channels may be a novel mechanism by which HIFs can contribute to the malignant phenotype of human tumour cells.
  • [MeSH-major] Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Intermediate-Conductance Calcium-Activated Potassium Channels / metabolism. Melanoma / metabolism. Potassium Channels, Calcium-Activated / metabolism. Small-Conductance Calcium-Activated Potassium Channels / metabolism. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Apamin / pharmacology. Cell Hypoxia. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Transfection. Tumor Cells, Cultured. Up-Regulation

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  • (PMID = 16396931.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intermediate-Conductance Calcium-Activated Potassium Channels; 0 / Potassium Channels, Calcium-Activated; 0 / Small-Conductance Calcium-Activated Potassium Channels; 24345-16-2 / Apamin; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC1796787
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78. Wenghoefer M, Pantelis A, Dommisch H, Reich R, Martini M, Allam JP, Novak N, Bergé S, Jepsen S, Winter J: Decreased gene expression of human beta-defensin-1 in the development of squamous cell carcinoma of the oral cavity. Int J Oral Maxillofac Surg; 2008 Jul;37(7):660-3
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  • [Title] Decreased gene expression of human beta-defensin-1 in the development of squamous cell carcinoma of the oral cavity.
  • The aim of this study was to investigate the gene expression of human beta-defensin-1, -2, -3 (hBD-1, -2, -3), interleukin-1beta, tumour necrosis factor-alpha and cyclooxygenase-2 in oral squamous cell carcinoma (OSCC) compared to benign and premalignant lesions as well as healthy controls.
  • RNA was extracted according to standard protocols and transcripts of hBD-1, -2, -3, interleukin-1beta, tumour necrosis factor-alpha and cyclooxygenase-2 were analysed by real-time polymerase chain reaction.
  • The loss of its function might contribute to the malignant progression of these tumours.
  • [MeSH-major] Anti-Infective Agents / analysis. Carcinoma, Squamous Cell / pathology. Mouth Neoplasms / pathology. beta-Defensins / analysis
  • [MeSH-minor] Cyclooxygenase 2 / analysis. Disease Progression. Fibroma / genetics. Fibroma / pathology. Gene Expression Regulation, Neoplastic / genetics. Gingiva / anatomy & histology. Humans. Interleukin-1beta / analysis. Leukoplakia, Oral / genetics. Leukoplakia, Oral / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 18346877.001).
  • [ISSN] 0901-5027
  • [Journal-full-title] International journal of oral and maxillofacial surgery
  • [ISO-abbreviation] Int J Oral Maxillofac Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / DEFB1 protein, human; 0 / DEFB4A protein, human; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 0 / beta-Defensins; 0 / beta-defensin 3, human; EC 1.14.99.1 / Cyclooxygenase 2
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79. Greco S, Elia MG, Muscella A, Romano S, Storelli C, Marsigliante S: Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. J Endocrinol; 2005 Aug;186(2):291-301
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  • [Title] Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture.
  • We here investigated the mitogenic effects and the signalling pathways of BK in primary cultured human epithelial breast cells obtained from a tumour and from the histologically proven non-malignant tissue adjacent to the tumour.
  • BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2).
  • In conclusion, the mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression.
  • [MeSH-minor] Analysis of Variance. Calcium / analysis. Cell Proliferation / drug effects. Enzyme Activation. Female. Humans. Immunoblotting / methods. Intracellular Fluid / chemistry. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / metabolism. Receptors, Bradykinin / metabolism. Tumor Cells, Cultured

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  • (PMID = 16079255.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mitogens; 0 / Receptors, Bradykinin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
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80. Chen Y, Shu W, Chen W, Wu Q, Liu H, Cui G: Curcumin, both histone deacetylase and p300/CBP-specific inhibitor, represses the activity of nuclear factor kappa B and Notch 1 in Raji cells. Basic Clin Pharmacol Toxicol; 2007 Dec;101(6):427-33
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  • Curcumin, the active chemical of the Asian spice turmeric, exhibits anticancer activity in several human cancer cell lines.
  • We previously have proved that curcumin was a new member of the histone deacetylases (HDAC) inhibitors, while constitutive nuclear factor kappa B (NF-kappaB) is believed to be a crucial event for enhanced proliferation and survival of malignant cells.
  • Furthermore, curcumin could also prevent degradation of I kappaB alpha and inhibit nuclear translocation of the NF-kappaB/p65 subunit, as well as expression of Notch 1, induced by tumour necrosis factor-alpha.
  • [MeSH-minor] CREB-Binding Protein / antagonists & inhibitors. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. E1A-Associated p300 Protein / antagonists & inhibitors. Gene Expression Regulation / drug effects. Histone Deacetylase 1. Histone Deacetylase Inhibitors. Histone Deacetylases. Humans. I-kappa B Proteins / drug effects. I-kappa B Proteins / metabolism. Inhibitory Concentration 50. Leukemia / drug therapy. Leupeptins / pharmacology. Signal Transduction / drug effects. Transcription Factor RelA / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17927689.001).
  • [ISSN] 1742-7843
  • [Journal-full-title] Basic & clinical pharmacology & toxicology
  • [ISO-abbreviation] Basic Clin. Pharmacol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / I-kappa B Proteins; 0 / Leupeptins; 0 / NF-kappa B; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 139874-52-5 / NF-kappaB inhibitor alpha; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / E1A-Associated p300 Protein; EC 2.3.1.48 / EP300 protein, human; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3; IT942ZTH98 / Curcumin
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81. Wang HY, Yang YM, Zhuang Y, Chen HN, Wan YL, Huang YT: The effect of celecoxib on tissue factor expression in pancreatic cancer cells. Chin Med J (Engl); 2007 Oct 20;120(20):1753-6
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  • [Title] The effect of celecoxib on tissue factor expression in pancreatic cancer cells.
  • BACKGROUND: Tissue factor (TF) is overexpressed in many malignant tumours and is linked to the pathogenesis and prognosis of such malignancies.
  • In vitro studies have proved that reduced expression of TF has inhibitory effect on the angiogenesis and cell proliferation of the malignant tumour.
  • Therefore, TF suppression has been raised as a possible treatment for malignant tumours.
  • Here we investigated the effect of celecoxib on TF expression induced by tumour necrosis factor alpha (TNFalpha) in PANC-1 cells and a possible molecular mechanism underlying the celecoxib effect.
  • METHODS: Various doses of celecoxib solution were added to standard cell numbers of PANC-1 cells mixed with equal dose of TNFalpha for 6 hours.
  • [MeSH-major] Cyclooxygenase 2 Inhibitors / pharmacology. Gene Expression Regulation / drug effects. Pancreatic Neoplasms / metabolism. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Thromboplastin / genetics
  • [MeSH-minor] Celecoxib. Cell Line, Tumor. Humans. NF-kappa B / metabolism. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 18028765.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / NF-kappa B; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tumor Necrosis Factor-alpha; 9035-58-9 / Thromboplastin; JCX84Q7J1L / Celecoxib
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82. Miao R, Wei J, Zhang Q, Sajja V, Yang J, Wang Q: Redifferentiation of human hepatoma cells (SMMC-7721) induced by two new highly oxygenated bisabolane-type sesquiterpenes. J Biosci; 2008 Dec;33(5):723-30

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  • Bisabolane-type sesquiterpenes are a class of biologically active compounds that has antitumour,antifungal, antibacterial,antioxidant and antivenom properties.We investigated the effect of two new highly oxygenated bisabolane-type sesquiterpenes (HOBS)isolated from Cremanthodium discoideum (C.discoideum) on tumour cells.
  • Our results showed that HOBS induced morphological differentiation and reduced microvilli formation on the cell surface in SMMC-7721 cells.Flow cytometry analysis demonstrated that HOBS could induce cell-cycle arrest in the G1 phase.
  • Moreover,HOBS was able to increase tyrosine-alpha ketoglutarate transaminase activity,decrease alpha- foetoprotein level and gamma-glutamyl transferase activity.
  • In addition,we found that HOBS inhibited the anchorage- independent growth of SMMC-7721 cells in a dose-dependent manner.Taken together,all the above observations indicate that HOBS might be able to normalize malignant SMMC-7721 cells by inhibiting cell proliferation and inducing redifferentiation.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Hepatocellular / metabolism. Sesquiterpenes / pharmacology
  • [MeSH-minor] Asteraceae / chemistry. Cell Cycle / drug effects. Cell Differentiation / drug effects. Hepatocytes / drug effects. Humans. Molecular Structure. Structure-Activity Relationship. alpha-Fetoproteins / metabolism. gamma-Glutamyltransferase / metabolism

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  • (PMID = 19179760.001).
  • [ISSN] 0250-5991
  • [Journal-full-title] Journal of biosciences
  • [ISO-abbreviation] J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / 1beta,8-diangeloyloxy-2beta-acetoxy-4alpha-chloro-11-methoxy-3beta, 10-dihydroxybisabola-7(14)-ene; 0 / 1beta,8-diangeloyloxy-2beta-acetoxy-4alpha-chloro-3beta-hydroxy-10, 11-o,o-isopropylidenebis-aboia-7(14)-ene; 0 / Antineoplastic Agents, Phytogenic; 0 / Sesquiterpenes; 0 / alpha-Fetoproteins; EC 2.3.2.2 / gamma-Glutamyltransferase
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83. Neuzil J, Dyason JC, Freeman R, Dong LF, Prochazka L, Wang XF, Scheffler I, Ralph SJ: Mitocans as anti-cancer agents targeting mitochondria: lessons from studies with vitamin E analogues, inhibitors of complex II. J Bioenerg Biomembr; 2007 Feb;39(1):65-72
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  • Recently mitochondria in cancer cells have emerged as the Achilles heel for tumour destruction.
  • Anti-cancer agents specifically targeting cancer cell mitochondria are referred to as 'mitocans'.
  • These compounds act by destabilising these organelles, unleashing their apoptogenic potential, resulting in the efficient death of malignant cells and suppression of tumour growth.
  • Importantly, at least some mitocans are selective for cancer cells, and these are represented by the group of redox-silent vitamin E analogues, epitomised by alpha-tocopheryl succinate (alpha-TOS).
  • Moreover, alpha-TOS is selective for cancer cells with their reduced anti-oxidant defenses and lower esterase activity than the normal (non-malignant) counterparts.
  • In this mini-review we discuss the emerging significance of mitocans, as exemplified by alpha-TOS.

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  • (PMID = 17294131.001).
  • [ISSN] 0145-479X
  • [Journal-full-title] Journal of bioenergetics and biomembranes
  • [ISO-abbreviation] J. Bioenerg. Biomembr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 1406-18-4 / Vitamin E; EC 1.3.5.1 / Electron Transport Complex II
  • [Number-of-references] 73
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84. Dohi O, Ohtani H, Hatori M, Sato E, Hosaka M, Nagura H, Itoi E, Kokubun S: Histogenesis-specific expression of fibroblast activation protein and dipeptidylpeptidase-IV in human bone and soft tissue tumours. Histopathology; 2009 Oct;55(4):432-40
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  • The aim was to identify cell types that express FAP and DPP-IV in human bone and soft tissue tumours, and to determine whether there are any correlations between the expression of FAP and DPP-IV and the malignant potential of tumours.
  • METHODS AND RESULTS: This study analysed in situ expression in 25 malignant and 13 benign human bone and soft tissue tumours.
  • Immunohistochemistry using pre-fixed frozen sections revealed that FAP was positive in low-grade myofibroblastic sarcoma, the fibroblastic component of osteosarcomas, and malignant fibrous histiocytomas, but negative in Ewing's sarcomas and rhabdomyosarcomas.
  • Giant cells expressed DPP-IV in giant cell tumours.
  • CONCLUSIONS: Our data suggest that FAP and DPP-IV are consistently expressed in bone and soft tissue tumour cells that are histogenetically related to activated fibroblasts and/or myofibroblasts, irrespective of their malignancy.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Bone Neoplasms / metabolism. Bone Neoplasms / pathology. Dipeptidyl Peptidase 4 / metabolism. Gelatinases / metabolism. Membrane Proteins / metabolism. Serine Endopeptidases / metabolism. Soft Tissue Neoplasms / metabolism. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Fibroblasts / metabolism. Fibroblasts / pathology. Histiocytoma, Malignant Fibrous / metabolism. Histiocytoma, Malignant Fibrous / pathology. Humans. Macrophages / metabolism. Macrophages / pathology. Monocytes / metabolism. Monocytes / pathology. Osteosarcoma / metabolism. Osteosarcoma / pathology. Rhabdomyosarcoma / metabolism. Rhabdomyosarcoma / pathology. Sarcoma, Ewing / metabolism. Sarcoma, Ewing / pathology

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  • (PMID = 19817894.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC2784039
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85. Zisakis A, Piperi C, Themistocleous MS, Korkolopoulou P, Boviatsis EI, Sakas DE, Patsouris E, Lea RW, Kalofoutis A: Comparative analysis of peripheral and localised cytokine secretion in glioblastoma patients. Cytokine; 2007 Aug;39(2):99-105
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  • BACKGROUND: Malignant gliomas are the most common primary brain tumours of both children and adults.
  • The unique aspects of their biology and anatomic site render them refractory to conventional therapeutic strategies such as surgery and chemotherapy.
  • METHODS: To further understand the immunobiology of glioblastomas in clinical settings, we examined the secretion of four main cytokines in the peripheral blood and in primary cell cultures of 33 human glioblastoma patients.
  • An ELISPOT methodology was used for the first time to examine Th1, and Th2 cytokine secretion from both peripheral lymphocytes and glioma tumour cells.
  • RESULTS: Th1 cytokines (tumour necrosis factor (TNF-alpha), interferon (IFN-gamma) were markedly reduced compared to control levels (P=0.01 and P<0.001, respectively), whereas in contrast, Th2 (interleukin (IL)-4 and IL-10) were strongly expressed in both peripheral lymphocytes and glioma cell cultures (P=0.05 and P<0.001, respectively).
  • Furthermore, ELISPOT methodology can be used for monitoring of cytokine secretion from tumour cells, in addition to the well-established peripheral cytokine secretion.
  • [MeSH-minor] Adult. Aged. Cells, Cultured. Female. Humans. Interferon-gamma / metabolism. Interferon-gamma / secretion. Interleukin-10 / metabolism. Interleukin-10 / secretion. Interleukin-1beta / metabolism. Interleukin-1beta / secretion. Interleukin-4 / metabolism. Interleukin-4 / secretion. Male. Middle Aged. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 17697783.001).
  • [ISSN] 1043-4666
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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86. Redpath M, Marques CM, Dibden C, Waddon A, Lalla R, Macneil S: Ibuprofen and hydrogel-released ibuprofen in the reduction of inflammation-induced migration in melanoma cells. Br J Dermatol; 2009 Jul;161(1):25-33
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  • OBJECTIVES: The aims of this study were: (i) to examine the effects of ibuprofen on the major proinflammatory cytokine tumour necrosis factor (TNF)-alpha induction of migration of C8161 and HBL human melanoma cells;.
  • METHODS: Melanoma cells were exposed to 300 U mL(-1) TNF-alpha for a 24-h period prior to making a scratch wound to which ibuprofen or ibuprofen-loaded hydrogels were then added.
  • The effects of relevant concentrations of ibuprofen on cell viability and apoptosis were examined.
  • RESULTS: Ibuprofen at 10(-3) mol L(-1) significantly reduced TNF-alpha-stimulated migration of both cell types to that of nonstimulated cells (P < 0.001).
  • TNF-alpha-unstimulated cell migration was not significantly affected.
  • CONCLUSIONS: These results demonstrate that TNF-alpha upregulated malignant melanoma migration in vitro and that this could be reduced by ibuprofen both in solution and delivered from a hydrogel.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Apoptosis / drug effects. Cell Movement / drug effects. Ibuprofen / pharmacology. Melanoma / pathology. Skin Neoplasms / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Delayed-Action Preparations / pharmacology. Humans. Hydrogel / pharmacology. Inflammation / drug therapy. Tumor Cells, Cultured

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  • (PMID = 19438858.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0401428; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Delayed-Action Preparations; 0 / Tumor Necrosis Factor-alpha; 25852-47-5 / Hydrogel; WK2XYI10QM / Ibuprofen
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87. Nogales FF, Stolnicu S, Harilal KR, Mooney E, García-Galvis OF: Retiform uterine tumours resembling ovarian sex cord tumours. A comparative immunohistochemical study with retiform structures of the female genital tract. Histopathology; 2009 Mar;54(4):471-7
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  • AIMS: To analyse both the clinicopathological and immunohistochemical findings in six cases of uterine tumours resembling ovarian sex cord tumours with a predominant epithelial retiform component resembling the rete ovarii (RUTROSCT) and to compare their immunophenotype with tissues containing retiform structures such as the normal rete ovarii, retiform Wolffian adnexal tumour (RWAT) and ovarian retiform areas of Sertoli-Leydig cell tumours (ORSLCT).
  • Two cases were misdiagnosed as malignant in endometrial biopsy specimens and one in the hysterectomy specimen.
  • Histologically they had a tubulopapillary or glomeruloid formation; a sex-cord-like or endometrial stromal component was absent or comprised at most 30% of the tumour.
  • CD56 and alpha-inhibin were positive in half of the cases.
  • ORSLCT differed in its conspicuous positivity to CD56, CD10, alpha-inhibin and calretinin, but absent CK7 expression.
  • Correct diagnosis should avoid overtreatment.
  • [MeSH-minor] Adult. Aged. Antigens, CD56 / metabolism. Biomarkers, Tumor / metabolism. Calbindin 2. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Inhibins / metabolism. Keratin-7 / metabolism. Middle Aged. Mucin-1 / metabolism. Neprilysin / metabolism. S100 Calcium Binding Protein G / metabolism. Sertoli-Leydig Cell Tumor / metabolism. Sertoli-Leydig Cell Tumor / pathology

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  • [CommentIn] Histopathology. 2009 Nov;55(5):619-20; author reply 620-1 [19912370.001]
  • (PMID = 19309399.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / Keratin-7; 0 / Mucin-1; 0 / S100 Calcium Binding Protein G; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; EC 3.4.24.11 / Neprilysin
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88. Hungermann D, Buerger H, Oehlschlegel C, Herbst H, Boecker W: Adenomyoepithelial tumours and myoepithelial carcinomas of the breast--a spectrum of monophasic and biphasic tumours dominated by immature myoepithelial cells. BMC Cancer; 2005;5:92
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  • METHODS: A series of 27 adenomyoepithelial tumours of the breast was analysed immunohistochemically with antibodies directed against various cytokeratins, p63, smooth muscle alpha-actin (SMA) and vimentin.
  • With exception of one case diagnosed as myoepithelial carcinoma, all tested tumours expressed low molecular weight cytokeratin Ck18 in variable proportions of cells.
  • Double immunofluorescence revealed tumour cells exclusively staining for Ck5/Ck14 in the presence of other cell populations that co-expressed high molecular weight Ck5/Ck14 as well as either low molecular weight Ck8/18 or SMA.
  • Based on morphology, we assigned the series to three categories, benign, borderline and malignant.
  • Although categorisation of adenomyoepithelial tumours in benign, borderline and malignant was supported by results of CGH, any assessment of prognosis requires to be firmly based on morphological grounds.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma / diagnosis. Epithelial Cells / cytology. Myoepithelioma / diagnosis
  • [MeSH-minor] Actins / biosynthesis. Adult. Aged. Aged, 80 and over. Cell Proliferation. DNA-Binding Proteins. Female. Genes, Tumor Suppressor. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Immunophenotyping. Keratins / biosynthesis. Microscopy, Fluorescence. Middle Aged. Nucleic Acid Hybridization. Phosphoproteins / biosynthesis. Prognosis. Trans-Activators / biosynthesis. Transcription Factors. Tumor Suppressor Proteins. Vimentin / biosynthesis

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  • [Cites] J Pathol. 1998 Feb;184(2):197-206 [9602712.001]
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  • (PMID = 16050957.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vimentin; 68238-35-7 / Keratins
  • [Other-IDs] NLM/ PMC1187882
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89. Kourelis K, Vandoros G, Kourelis T, Goumas P, Sotiropoulou-Bonikou G: Retinoid X receptor overexpression desensitizes laryngeal epithelium to carcinogenic effects associated with epidermal growth factor receptor upregulation. J Otolaryngol Head Neck Surg; 2009 Apr;38(2):233-9
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  • OBJECTIVE: Squamous cell carcinomas (SCCs) of the larynx are sequelae of hyperplastic and dysplastic lesions.
  • Conversely, retinoid X receptor alpha (RXRalpha) mediates the reversing effects of retinoids on head and neck carcinogenesis.
  • MATERIALS: Tissue samples from 129 patients with premalignant or malignant laryngeal lesions.
  • RESULTS: EGFR was upregulated along the epithelial deterioration toward neoplasia (p < .001) but was unaffected by tumour grade.
  • In RXRalpha-positive cases, a markedly stronger induction of EGFR occurred with malignant transformation compared with the epithelia immunonegative for the nuclear receptor.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Laryngeal Mucosa / metabolism. Laryngeal Mucosa / pathology. Laryngeal Neoplasms / metabolism. Laryngeal Neoplasms / pathology. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / metabolism. Retinoid X Receptor alpha / metabolism. Up-Regulation

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  • (PMID = 19442374.001).
  • [ISSN] 1916-0216
  • [Journal-full-title] Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale
  • [ISO-abbreviation] J Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Retinoid X Receptor alpha; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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90. Nystrom ML, McCulloch D, Weinreb PH, Violette SM, Speight PM, Marshall JF, Hart IR, Thomas GJ: Cyclooxygenase-2 inhibition suppresses alphavbeta6 integrin-dependent oral squamous carcinoma invasion. Cancer Res; 2006 Nov 15;66(22):10833-42
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  • [Title] Cyclooxygenase-2 inhibition suppresses alphavbeta6 integrin-dependent oral squamous carcinoma invasion.
  • Worldwide oral squamous cell carcinoma (OSCC) represents about 5.5% of all malignancies, with approximately 30,000 new cases each year in the United States.
  • The integrin alpha(v)beta(6) and the enzyme cyclooxygenase-2 (COX-2) are implicated in OSCC progression and have been suggested as possible therapeutic targets.
  • Each protein also is reported to identify dysplasias at high risk of malignant transformation, and current clinical trials are testing the efficacy of nonsteroidal anti-inflammatory drugs (NSAID) at preventing OSCC development.
  • Given the probable increased expression of alpha(v)beta(6) and COX-2 in OSCC and the inhibition of several integrins by NSAIDs, we investigated whether NSAIDs affected alpha(v)beta(6)-dependent cell functions.
  • We found that expression of both alpha(v)beta(6) and COX-2 was significantly higher in OSCC compared with oral epithelial dysplasias.
  • Neither protein preferentially identified those dysplastic lesions that became malignant.
  • Using OSCC cell lines, modified to express varying levels of alpha(v)beta(6), we assessed the effect of COX-2 inhibition on cell invasion.
  • We found that the COX-2 inhibitor NS398 inhibited specifically alpha(v)beta(6)-dependent, but not alpha(v)beta(6)-independent, OSCC invasion in vitro and in vivo, and this effect was modulated through prostaglandin E(2) (PGE(2))-dependent activation of Rac-1.
  • Conversely, RNA interference down-regulation of Rac-1 inhibited alpha(v)beta(6)-dependent invasion.
  • These findings suggest that COX-2 and alpha(v)beta(6) interact in promoting OSCC invasion.
  • This is a novel mechanism that, given the ubiquity of alpha(v)beta(6) expression by head and neck cancers, raises the possibility that NSAIDs could protect against OSCC invasion.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Cyclooxygenase 2 Inhibitors / pharmacology. Integrins / antagonists & inhibitors. Mouth Neoplasms / drug therapy. Mouth Neoplasms / pathology
  • [MeSH-minor] Animals. Antigens, Neoplasm / biosynthesis. Antigens, Neoplasm / metabolism. Cell Line, Tumor. Cyclooxygenase 2 / biosynthesis. Cyclooxygenase 2 / metabolism. Dinoprostone / metabolism. Dinoprostone / pharmacology. Epithelial Cells / pathology. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Nitrobenzenes / pharmacology. Protein Binding. Sulfonamides / pharmacology. Xenograft Model Antitumor Assays. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 17108119.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antigens, Neoplasm; 0 / Cyclooxygenase 2 Inhibitors; 0 / Integrins; 0 / Nitrobenzenes; 0 / RAC1 protein, human; 0 / Sulfonamides; 0 / integrin alphavbeta6; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.6.5.2 / rac1 GTP-Binding Protein; K7Q1JQR04M / Dinoprostone
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91. Ludwig A, Schulte A, Schnack C, Hundhausen C, Reiss K, Brodway N, Held-Feindt J, Mentlein R: Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells. J Neurochem; 2005 Jun;93(5):1293-303
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  • In cultivated human glioma cells as well as in activated mouse astroglial cells, CXCL16 mRNA and protein is constitutively expressed and further up-regulated by tumour necrosis factor alpha (TNFalpha) and interferon-gamma (IFNgamma).
  • Thus, the transmembrane chemokine CXCL16 is expressed in the brain by malignant and inflamed astroglial cells, shed to a soluble form and targets not only activated T cells but also glial cells themselves.
  • [MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL6. Humans. Interferon-gamma / pharmacology. Metalloproteases / metabolism. Mice. Microglia / metabolism. Neuroglia / metabolism. RNA, Messenger / metabolism. Receptors, Scavenger. Recombinant Proteins / pharmacology. Solubility. Tissue Culture Techniques. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation

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  • (PMID = 15934948.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL16 protein, human; 0 / Chemokine CXCL6; 0 / Chemokines, CXC; 0 / Cxcl16 protein, mouse; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Immunologic; 0 / Receptors, Scavenger; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 3.4.- / Metalloproteases
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92. Brennan PA, Mackenzie N, Quintero M: Hypoxia-inducible factor 1alpha in oral cancer. J Oral Pathol Med; 2005 Aug;34(7):385-9
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  • It contributes to local and systemic tumour progression as well as potentially compromising radiotherapy and chemotherapy.
  • It targets the transcription of over 60 genes involved in many aspects of cancer biology including cell survival, glucose metabolism, cell invasion and angiogenesis.
  • RESULTS: Although there are a few conflicting reports of its prognostic significance, over expression of HIF-1alpha seems to play an adverse role in the malignant progression of head and neck cancer by facilitating the adaptation of cells to hypoxia as well as contributing to the invasive properties and angiogenesis in these tumours.
  • The pharmacological manipulation of HIF-1alpha has marked effects on tumour growth, and it could prove to be an important target for drug therapy, both in oral cancer and in other hypoxia-dependent disease states.
  • [MeSH-major] Cell Hypoxia / physiology. Mouth Neoplasms / metabolism. Nitric Oxide / physiology. Transcription Factors / physiology
  • [MeSH-minor] Humans. Hypoxia-Inducible Factor 1, alpha Subunit

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  • (PMID = 16011605.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 40
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93. Moriya T, Kozuka Y, Kanomata N, Tse GM, Tan PH: The role of immunohistochemistry in the differential diagnosis of breast lesions. Pathology; 2009 Jan;41(1):68-76
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  • [Title] The role of immunohistochemistry in the differential diagnosis of breast lesions.
  • Immunohistochemistry may be helpful in the diagnosis of various breast lesions.
  • It can be used to assist in distinguishing benign and malignant conditions, or to clarify the histological subtype of invasive carcinomas.
  • Myoepithelial markers (p63, alpha-SMA, smooth muscle myosin heavy chain, and others) are useful to highlight myoepithelial cells.
  • They are employed to verify myoepithelial cell lining in intraductal papillary lesions, or to recognise peripheral myoepithelial cells for non-invasive carcinoma, although their staining results are not always excellent.
  • High molecular weight cytokeratins (CK5/6, CK14, 34betaE12) typically show a mosaic-like pattern of expression in benign papillary/hyperplastic lesions, and are mostly negative in ductal in situ carcinoma, but some exceptions exist.
  • Negative E-cadherin staining is used for making confirmative diagnosis of lobular carcinoma, with a specificity and sensitivity of approximately 90%.
  • Cytokeratins, especially the antibody 34betaE12, are of value to differentiate spindle cell carcinoma from phyllodes tumour.
  • Nevertheless, for accurate diagnosis, it is essential to correlate the immmunohistochemical staining results with the histological findings.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Breast Neoplasms / diagnosis. Breast Neoplasms / metabolism. Immunohistochemistry / methods
  • [MeSH-minor] Carcinoma, Intraductal, Noninfiltrating / diagnosis. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / diagnosis. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Diagnosis, Differential. Female. Humans. Myoepithelioma / diagnosis. Myoepithelioma / metabolism. Myoepithelioma / pathology

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  • (PMID = 19089742.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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94. Bing C, Trayhurn P: New insights into adipose tissue atrophy in cancer cachexia. Proc Nutr Soc; 2009 Nov;68(4):385-92
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  • It is characterised by the tissue containing shrunken adipocytes with a major reduction in cell size and increased fibrosis in the tissue matrix.
  • The ultrastructure of 'slimmed' adipocytes has revealed severe delipidation and modifications in cell membrane conformation.
  • Both tumour and host-derived factors are implicated in adipose atrophy.
  • Zinc-alpha2-glycoprotein (ZAG), which is overexpressed by certain malignant tumours, has been identified as a novel adipokine.
  • [MeSH-minor] Animals. Cell Membrane / pathology. Fibrosis. Humans. Mice. Up-Regulation

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  • (PMID = 19719894.001).
  • [ISSN] 1475-2719
  • [Journal-full-title] The Proceedings of the Nutrition Society
  • [ISO-abbreviation] Proc Nutr Soc
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E015379/1; United Kingdom / Medical Research Council / / 87972; United Kingdom / Biotechnology and Biological Sciences Research Council / / BBE015379
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Seminal Plasma Proteins; 0 / Zn-alpha-2-glycoprotein
  • [Number-of-references] 85
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95. Mayer A, Steimel M, Wree A, Kelleher D, Vaupel P: Solid tumours arising from differently pre-oxygenated cells: comparable growth rates despite dissimilar tissue oxygenation. Int J Radiat Biol; 2009 Nov;85(11):981-8
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  • PURPOSE: The hypoxia-inducible factor (HIF)-dependent transcriptional response is often very pronounced in hypoxic microregions of solid malignant tumours, leading to secretion of pro-angiogenic factors and activation of a hypoxia-tolerant, glycolytic metabolism.
  • Here, the influence of the microenvironment of tumour-initiating cells as a factor determining intertumoural variations in the relative contributions of both processes has been examined.
  • Tumours were generated by allografting cells from either normoxic cell culture or severely hypoxic/anoxic ascites.
  • Conversely, tumour-initiating DS-cells derived from normoxic cell culture form highly angiogenic, normoxic tumours with a significantly lower expression of HIF-1alpha and GLUT-1.
  • Growth rates and the fraction of Ki-67 positive cells for both tumour groups were comparable.
  • CONCLUSIONS: The intensity of angiogenesis in this model is primarily determined by the state of metabolic adaptation of tumour-initiating cells, rather than being a function of HIF-activation during solid tumour growth, a finding which is highly relevant for the design of treatment regimens targeting the tumour vasculature.
  • [MeSH-minor] Animals. Anoxia / metabolism. Anoxia / pathology. Cell Line, Tumor. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Neovascularization, Pathologic. Oxygen / metabolism. Rats. Rats, Sprague-Dawley

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  • (PMID = 19895275.001).
  • [ISSN] 1362-3095
  • [Journal-full-title] International journal of radiation biology
  • [ISO-abbreviation] Int. J. Radiat. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucose Transporter Type 1; 0 / Hif1a protein, rat; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / Slc2a1 protein, rat; S88TT14065 / Oxygen
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96. Lee JH, Park H, Chung H, Choi S, Kim Y, Yoo H, Kim TY, Hann HJ, Seong I, Kim J, Kang KG, Han IO, Oh ES: Syndecan-2 regulates the migratory potential of melanoma cells. J Biol Chem; 2009 Oct 2;284(40):27167-75
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  • Syndecan-2, a transmembrane heparan sulfate proteoglycan, is a critical mediator in the tumorigenesis of colon carcinoma cells.
  • We explored the function of syndecan-2 in melanoma, one of the most invasive types of cancers, and found that the expression of this protein was elevated in tissue samples from both nevus and malignant human melanomas but not in melanocytes of the normal human skin tissues.
  • Similarly, elevated syndecan-2 expression was observed in various melanoma cell lines.
  • Syndecan-2 expression was enhanced by fibroblast growth factor-2, which is known to stimulate melanoma cell migration; however, alpha-melanocyte-stimulating hormone decreased syndecan-2 expression and melanoma cell migration and invasion in a melanin synthesis-independent manner.
  • Furthermore, syndecan-2 overexpression rescued the migration defects induced by alpha-melanocyte-stimulating hormone treatment.
  • [MeSH-major] Cell Movement. Melanoma / metabolism. Melanoma / pathology. Syndecan-2 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. Melanins / biosynthesis. Mice. Rats. Up-Regulation. alpha-MSH / pharmacology

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  • (PMID = 19641225.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Melanins; 149769-25-5 / Syndecan-2; 581-05-5 / alpha-MSH
  • [Other-IDs] NLM/ PMC2785644
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97. Catassi A, Paleari L, Servent D, Sessa F, Dominioni L, Ognio E, Cilli M, Vacca P, Mingari M, Gaudino G, Bertino P, Paolucci M, Calcaterra A, Cesario A, Granone P, Costa R, Ciarlo M, Alama A, Russo P: Targeting alpha7-nicotinic receptor for the treatment of pleural mesothelioma. Eur J Cancer; 2008 Oct;44(15):2296-311
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  • Human malignant pleural mesothelioma (MPM) is a dreadful disease and there is still no standard therapy available for a consistent therapeutic approach.
  • This research is aimed at the evaluation of the potential therapeutic effect of a specific nicotinic receptor (nAChR) antagonist, namely alpha-Cobratoxin (alpha-CbT).
  • Its effectiveness was tested in mesothelioma cell lines and in primary mesothelioma cells in vitro, as well as in vivo, in orthotopically xenotransplanted NOD/SCID mice.
  • Cells showed alpha7-nAChR expression and their growth was significantly inhibited by alpha-CbT.
  • Severe induction of apoptosis was observed after exposure to alpha-CbT [IC(80-90)].
  • In vivo, the alpha-CbT acute LD(50) was 0.15 mg/kg.
  • Phase II experiments with 0.12 ng/kg alpha-CbT (1/1000 of LD(10)) were done in 53 xenotransplanted mice, inhibiting tumour development as confirmed by chest X-ray examinations, autopsy and microscopical findings.
  • The growth of human proliferating T lymphocytes and of mesothelial cells in primary culture was not affected by alpha-CbT.
  • Non-immunogenic derivatives of the alpha-CbT molecule need to be developed for possible human use.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction / methods. Transplantation, Heterologous. Tumor Cells, Cultured. alpha7 Nicotinic Acetylcholine Receptor

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
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  • (PMID = 18722110.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Cobra Neurotoxin Proteins; 0 / Neoplasm Proteins; 0 / Nicotinic Antagonists; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 69344-74-7 / alpha-cobratoxin
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98. Rankin EB, Giaccia AJ: The role of hypoxia-inducible factors in tumorigenesis. Cell Death Differ; 2008 Apr;15(4):678-85
The Lens. Cited by Patents in .

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  • They are heterodimeric transcription factors consisting of an oxygen-sensitive alpha subunit (HIF-alpha) and a constitutive beta subunit (HIF-beta) that facilitate both oxygen delivery and adaptation to oxygen deprivation by regulating the expression of genes that control glucose uptake, metabolism, angiogenesis, erythropoiesis, cell proliferation, and apoptosis.
  • In most experimental models, the HIF pathway is a positive regulator of tumor growth as its inhibition often results in tumor suppression.
  • In summary, HIF regulates multiple aspects of tumorigenesis, including angiogenesis, proliferation, metabolism, metastasis, differentiation, and response to radiation therapy, making it a critical regulator of the malignant phenotype.

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