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1. Poggi G, Villani L, Bernardo G: Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma. Rare Tumors; 2009;1(1):e6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma.
  • Glucagonomas are pancreatic islet cell tumors arising from the alpha cells which belong to neuroendocrine tumors.
  • We report the case of a 52- year old man with a pancreatic glucagonoma with synchronous multiple liver metastases treated by surgery, transarterial chemoembolization, percutaneous radiofrequency thermal ablation and long-acting octreotide.
  • Our report confirms that a multimodal approach is very effective in patients with unresectable liver metastases from pancreatic endocrine tumors providing long-lasting palliation and probably prolonging survival.

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  • (PMID = 21139900.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2994425
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2. Okauchi Y, Nammo T, Iwahashi H, Kizu T, Hayashi I, Okita K, Yamagata K, Uno S, Katsube F, Matsuhisa M, Kato K, Aozasa K, Kim T, Osuga K, Nakamori S, Tamaki Y, Funahashi T, Miyagawa J, Shimomura I: Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS). Intern Med; 2009;48(12):1025-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS).
  • To identify the location of pancreatic endocrine tumors, arterial stimulation and venous sampling (ASVS) is known to be useful for insulinoma and gastrinoma, but its usefulness for glucagonoma has not been verified to date.
  • Here we report a case of glucagonoma that was diagnosed by ASVS with calcium loading, in which an approximately 6-fold increase of glucagon was observed in the splenic artery territory.
  • MEN1 gene analysis verified the presence of a mutation and the glucagonoma was confirmed after operation.
  • In conclusion, ASVS could be useful for the diagnosis of glucagonoma.
  • [MeSH-major] Glucagon / blood. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19525592.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9007-92-5 / Glucagon; SY7Q814VUP / Calcium
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3. Oguma K, Oshima H, Aoki M, Uchio R, Naka K, Nakamura S, Hirao A, Saya H, Taketo MM, Oshima M: Activated macrophages promote Wnt signalling through tumour necrosis factor-alpha in gastric tumour cells. EMBO J; 2008 Jun 18;27(12):1671-81
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  • [Title] Activated macrophages promote Wnt signalling through tumour necrosis factor-alpha in gastric tumour cells.
  • These results suggested the role of macrophages in the activation of Wnt/beta-catenin signalling, which thus leads to tumour development.
  • Importantly, the conditioned medium of activated macrophages promoted Wnt/beta-catenin signalling in gastric cancer cells, which was suppressed by the inhibition of tumour necrosis factor (TNF)-alpha.
  • Furthermore, treatment with TNF-alpha induced glycogen synthase kinase 3beta (GSK3beta) phosphorylation, which resulted in the stabilization of beta-catenin.
  • These results suggest that macrophage-derived TNF-alpha promotes Wnt/beta-catenin signalling through inhibition of GSK3beta, which may contribute to tumour development in the gastric mucosa.
  • [MeSH-major] Macrophage Activation. Signal Transduction. Stomach Neoplasms / metabolism. Tumor Necrosis Factor-alpha / metabolism. Wnt1 Protein / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Animals. Cell Line, Tumor. Cell Nucleus / metabolism. Epithelial Cells / microbiology. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Helicobacter Infections / pathology. Humans. Mice. Mice, Transgenic. Mutation / genetics. NF-kappa B / metabolism. Phosphorylation. Precancerous Conditions / enzymology. Precancerous Conditions / pathology. Stomach / microbiology. Stomach / pathology. beta Catenin / metabolism

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  • (PMID = 18511911.001).
  • [ISSN] 1460-2075
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 0 / Wnt1 Protein; 0 / beta Catenin; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2413189
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4. 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.
  • Those two would probably result in discovery of more glucagonomas and other neuroendocrine tumours without characteristic clinical syndromes.
  • [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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5. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma syndrome and necrolytic migratory erythema.
  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • The dermatologic and endocrine approach to this syndrome is discussed here.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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6. Chan DA, Giaccia AJ: PHD2 in tumour angiogenesis. Br J Cancer; 2010 Jun 29;103(1):1-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PHD2 in tumour angiogenesis.
  • However, there is conflicting evidence as to the exact role of PHD2 in tumour angiogenesis.
  • The divergence seems to be because of the contribution of stromal-derived PHD2, and in particular the involvement of endothelial cells, vs tumour-derived PHD2.
  • This review summarises our current understanding of PHD2 and tumour angiogenesis, focusing on the influences of PHD2 on vascular normalisation and neovascularisation.

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  • (PMID = 20461086.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-88480; United States / NCI NIH HHS / CA / P01 CA067166; United States / NCI NIH HHS / CA / CA-123823; United States / NCI NIH HHS / CA / F32 CA123823; United States / NCI NIH HHS / CA / CA-67166; United States / NCI NIH HHS / CA / R01 CA088480; United States / NCI NIH HHS / CA / R37 CA088480
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
  • [Number-of-references] 41
  • [Other-IDs] NLM/ PMC2905285
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7. Theis VS, Rhodes JM: Review article: minimizing tuberculosis during anti-tumour necrosis factor-alpha treatment of inflammatory bowel disease. Aliment Pharmacol Ther; 2008 Jan 1;27(1):19-30
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  • [Title] Review article: minimizing tuberculosis during anti-tumour necrosis factor-alpha treatment of inflammatory bowel disease.
  • BACKGROUND: Tumour necrosis factor (TNF)-alpha inhibitors are a major advance in the management of inflammatory bowel disease but increase the risk for tuberculosis (TB).
  • METHODS: PubMed searches were performed using search terms that included TB and each of the current anti-TNF-alpha biological agents and also TB and Crohn's disease.
  • RESULTS: Increased susceptibility to TB, often with extrapulmonary or disseminated disease, occurs following treatment with all anti-TNF-alpha biological agents and amounts to a four- to 20-fold increased risk with infliximab.
  • TB usually occurs shortly after anti-TNF-alpha initiation suggesting reactivation of latent infection.
  • Animal studies show that TNF-alpha inhibition impairs inflammatory cell trafficking and granuloma formation.
  • Currently recommended screening for latent TB typically, risk assessment, tuberculin skin testing and chest radiograph used prior to anti-TNF-alpha treatment can reduce TB rates by up to 90% but newer screening interferon gamma assays may enhance screening efficacy.
  • Patients positive on screening who are treated with isoniazid and subsequently receive anti-TNF-alpha treatment still have approximately 19% risk for TB.
  • CONCLUSIONS: Tuberculosis following treatment with TNF-alpha inhibitors usually results from reactivation of latent disease.
  • [MeSH-major] Inflammatory Bowel Diseases / drug therapy. Tuberculosis / prevention & control. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • [CommentIn] Aliment Pharmacol Ther. 2008 Apr 1;27(7):619 [18194496.001]
  • (PMID = 17944997.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 86
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8. Duncan DJ, Hopkins PM, Harrison SM: Negative inotropic effects of tumour necrosis factor-alpha and interleukin-1beta are ameliorated by alfentanil in rat ventricular myocytes. Br J Pharmacol; 2007 Mar;150(6):720-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Negative inotropic effects of tumour necrosis factor-alpha and interleukin-1beta are ameliorated by alfentanil in rat ventricular myocytes.
  • BACKGROUND AND PURPOSE: Serum levels of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) increase during an inflammatory response and have been reported to induce a negative inotropic effect on the myocardium.
  • This study characterised the effects of TNF-alpha and IL-1beta on contraction and the Ca(2+) transient and investigated whether depressed ventricular function was ameliorated by alfentanil.
  • Contraction and Ca(2+) transients were measured after 60, 120 and 180 min incubations in TNF-alpha (0.05 ng ml(-1)) and IL-1beta (2 ng ml(-1)).
  • The effects of 10 microM alfentanil on contractility and Ca(2+) transients of TNF-alpha and IL-1beta treated cells were determined.
  • KEY RESULTS: After 180 min of TNF-alpha and IL-1beta treatment, the amplitude of contraction, the Ca(2+) transient and sarcoplasmic reticulum (SR) Ca(2+) content were significantly reduced.
  • Alfentanil significantly increased contraction of TNF-alpha and IL-1beta treated cells via a small increase in the Ca(2+) transient and a larger increase in myofilament Ca(2+) sensitivity, effects that were not blocked by 10 microM naloxone, a broad spectrum opioid receptor antagonist.
  • CONCLUSIONS AND IMPLICATIONS: TNF-alpha and IL-1beta induce a significant negative inotropic effect on ventricular myocytes in a time dependent manner through disruption of SR Ca(2+) handling and the Ca(2+) transient.
  • [MeSH-major] Alfentanil / pharmacology. Interleukin-1beta / pharmacology. Myocardial Contraction / drug effects. Myocytes, Cardiac / drug effects. Myocytes, Cardiac / physiology. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 17279089.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 1N74HM2BS7 / Alfentanil; 36B82AMQ7N / Naloxone
  • [Other-IDs] NLM/ PMC2013863
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9. Yoshida M, Hayashi K, Ohara H, Miyabe K, Okumura F, Naitoh I, Tanaka H, Ando T, Nakazawa T, Takahashi S, Joh T: A case of pancreatic glucagonoma with erythema. Nihon Shokakibyo Gakkai Zasshi; 2010 Jun;107(6):930-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of pancreatic glucagonoma with erythema.
  • Full-body computed tomography (CT) scanning revealed a tumor mass in the tail of the pancreas; CT and magnetic resonance imaging (MRI) scans confirmed the presence of a spherical mass.
  • In contrast CT scans, although the contrast was gradually increased, no strong contrast differences were observed between the tumor and the surrounding tissue.
  • Blood test results revealed that the patient had a high glucagon level.
  • We diagnosed glucagonoma syndrome on the basis of the above results and resected the tail of the pancreas.
  • Pathological analysis revealed that the tumor cells had proliferated in ribbon-like, cord-like structures.
  • Immunostaining results were positive for glucagon, which confirmed our diagnosis.
  • [MeSH-major] Erythema / etiology. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20530930.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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10. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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11. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications


12. Székelyhidi Z, Pató J, Hegymegi-Barakonyi B, Bánhegyi P, Mészáros G, Kéri G, Orfi L: [Synthesis of thiophene and alpha-terthiophene derivatives with antiproliferative activity]. Acta Pharm Hung; 2005;75(4):185-93
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Synthesis of thiophene and alpha-terthiophene derivatives with antiproliferative activity].
  • [Transliterated title] Antiproliferatív hatású tiofén es alpha-tertiofénszármazékok eloállítása.
  • We have synthesised a series of known alpha-terthiophene lead molecules with PKC (protein kinase C) inhibitory activity and the compounds were tested in cell proliferation assay on EGF-RTK (epidermal growth factor receptor protein tyrosine kinase) over-expressing tumour cell line (A431).
  • We prepared a focused molecule library around the thiophene and the terthiophene scaffold and examined these compounds in cell proliferation assay on A431.
  • [MeSH-major] Anti-Infective Agents / pharmacology. Cell Division / drug effects. Thiophenes / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Humans. Protein Kinase C / antagonists & inhibitors. Receptor, Epidermal Growth Factor / antagonists & inhibitors

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  • (PMID = 16711395.001).
  • [ISSN] 0001-6659
  • [Journal-full-title] Acta pharmaceutica Hungarica
  • [ISO-abbreviation] Acta Pharm Hung
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Enzyme Inhibitors; 0 / Thiophenes; 0P77RAU2RR / alpha-terthienyl; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.13 / Protein Kinase C
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13. Cruz-Bautista I, Lerman I, Perez-Enriquez B, Padilla LS, Torres CL, Lopez A, Cabrera T, Mehta RP, Gómez-Pérez FJ, Rull JA, Orozco-Topete R: Diagnostic challenge of glucagonoma: case report and literature review. Endocr Pract; 2006 Jul-Aug;12(4):422-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic challenge of glucagonoma: case report and literature review.
  • OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.
  • METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.
  • The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.
  • Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.
  • After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.
  • The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.
  • Subsequently, all related symptoms resolved, and the glucagon levels normalized.
  • CONCLUSION: The diagnosis of glucagonoma is often delayed.
  • Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / diagnosis
  • [MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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  • (PMID = 16901799.001).
  • [ISSN] 1530-891X
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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14. Mutschler J, Steinbach G, Bunjes D, Reske SN, Buchmann I: [Myeloablative radioimmunotherapy with 188Re-CD66mAb before stem cell transplantation. No increase of proinflammatory cytokine levels of TNF-alpha]. Nuklearmedizin; 2009;48(1):30-6
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  • [Title] [Myeloablative radioimmunotherapy with 188Re-CD66mAb before stem cell transplantation. No increase of proinflammatory cytokine levels of TNF-alpha].
  • [Transliterated title] Myeloablative Radioimmuntherapie mit 188Re-CD66mAb vor Stammzelltransplantation: Kein Anstieg proinflammatorischer Zytokinspiegel von TNF-alpha.
  • AIM: Tumour necrosis factor-alpha (TNF-alpha) serum levels may increase due to intensive conditioning regimes with high-dose-chemotherapy and total body irradiation (TBI) before stem cell transplantation.
  • This increases the risk for developing acute graft versus host disease (aGvHD) after stem cell transplantation.
  • In this prospective study we investigated the influence of radioimmunotherapy with 188Re-CD-66-mAb on changes on TNF-alpha serum levels.
  • PATIENTS, METHODS: In 18 patients we measured TNF-alpha before and up to 96 hours after radioimmunotherapy, in 2 patients in addition following TBI, in 9 patients also following chemotherapy.
  • For measuring TNF-alpha we used an automated immunochemiluminescence assay (Immulite 1000 DPC Biermann, Bad Nauheim).
  • The mean follow up period to record incidence of aGVHD was 100 days after stem cell transplantation.
  • RESULTS: Compared to the basal levels before, the levels of TNF-alpha after conditioning with 188Re-CD-66-mAb did not increase significantly and remained in the physiological range.
  • CONCLUSION: These results demonstrate that additional conditioning therapy with 188Re-CD-66-mAb does not increase proinflammatory cytokine levels of TNF-alpha.
  • This finding may indicate that additive radioimmunotherapy may not be a significant factor for increasing the rate of conditioning-associated aGvHD.
  • [MeSH-major] Leukemia, Myeloid, Acute / radiotherapy. Myelodysplastic Syndromes / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Radioimmunotherapy / methods. Radioisotopes / therapeutic use. Rhenium / therapeutic use. Stem Cell Transplantation / methods. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. Cell Adhesion Molecules / immunology. Child. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19212609.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CD66 antigens; 0 / Cell Adhesion Molecules; 0 / Radioisotopes; 0 / Tumor Necrosis Factor-alpha; 7440-15-5 / Rhenium
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15. Oberkirchner U, Linder KE, Zadrozny L, Olivry T: Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide. Vet Dermatol; 2010 Oct;21(5):510-6
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  • [Title] Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide.
  • Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas.
  • In humans with glucagonoma-associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release.
  • In this report an 11-year-old golden retriever dog with pancreatic glucagonoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME.
  • The dog was later euthanized because of progressive metastatic disease.
  • In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma-associated NME.
  • This somatostatin analogue could be a valuable option to treat canine patients with non-resectable or relapsing pancreatic glucagonoma-associated NME.
  • [MeSH-major] Dog Diseases / drug therapy. Glucagonoma / veterinary. Necrolytic Migratory Erythema / veterinary. Octreotide / therapeutic use. Pancreatic Neoplasms / veterinary
  • [MeSH-minor] Animals. Anorexia / chemically induced. Anorexia / veterinary. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Dogs. Dose-Response Relationship, Drug. Lymph Nodes / pathology. Male. Paraneoplastic Syndromes / pathology. Paraneoplastic Syndromes / veterinary

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  • [Copyright] © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.
  • (PMID = 20500495.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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16. Queirolo P, Laurent S, Boitano M, Carrega P, Saverino D, Alviano F, Caielli A, Camoriano M, Ferlazzo G, Pistillo MP: Targeting ctla-4 directly on melanoma cells: A possible novel perspective in the immunotherapy of cutaneous melanoma. J Clin Oncol; 2009 May 20;27(15_suppl):e22138

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting ctla-4 directly on melanoma cells: A possible novel perspective in the immunotherapy of cutaneous melanoma.
  • : e22138 Background: CTLA-4 (CD152) is an omodimeric membrane glycoprotein which behaves as the major negative regulator of T cell-mediated immune response.
  • CTLA-4 inhibitory function in T cells mainly occurs upon engagement with the B7 ligands expressed on antigen presenting cells, resulting in inhibition of cytokine production and T cell proliferation.
  • CTLA-4 expression has also been documented in established human melanoma cell lines and primary melanoma tumours.
  • METHODS: Seven primary cultures were derived from melanoma samples by mechanical tissue dissociation, enzymatic digestion and filtration of single cell suspensions.
  • Flow cytometry (FACS) with an anti-melanoma (MCSP) mAb was used to assess the growth of melanoma cells.
  • Cytokine secretion and apoptotic cells were evaluated by Elisa and Annexin V/PI staining after treatment with an agonistic anti-CTLA-4 mAb (3D5).
  • The angiogenic property of melanoma culture supernatants was evaluated on mesenchimal stromal cells (msc) isolated from human thoracic aortas.
  • CTLA-4 expressed by these cells is functional as its ligation, with an anti-CTLA-4 agonistic mAb, is able to induce inhibition of cell proliferation, due to apoptosis induction, and of IL-8, TNF-alpha and VEGF cytokine secretion.
  • CONCLUSIONS: Given the physiologic inhibitory function of CTLA-4, our results suggest its possible role in the functional biology of melanoma and open up the possibility of an anti-melanoma immunotherapy based on targeting CTLA-4 directly on tumour cells as this might allow inhibition of tumour cell growth and angiogenesis.

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  • (PMID = 27963585.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Peros G, Sakorafas GH, Konstantoudakis G, Giannopoulos GA, Petropoulou K, Parasi A: Duodeno-pancreatic neuroendocrine tumours. Eur J Cancer Care (Engl); 2010 May;19(3):393-402
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duodeno-pancreatic neuroendocrine tumours.
  • Duodeno-pancreatic neuroendocrine tumours (DP-ETs) are increasingly diagnosed today due to the widespread use of modern imaging methods.
  • Duodeno-pancreatic endocrine tumours should be treated by radical surgical resection, which offers a high chance for cure when the disease is localized.
  • A high index of suspicion is required in these patients for the presence of a multiple endocrine neoplasia type syndrome.
  • Histological/immunohistochemical diagnosis was somatostatin-producing tumour in the first patient, oncocytic endocrine tumour positive for neurone-specific enolase and focally for chromogranin in the second patient, glucagonoma and pancreatic polypeptide-producing endocrine pancreatic tumour in the third patient, and gastrin, somatostatin, calcitonin, insulin and adrenocorticotropic hormone (ACTH)-producing tumour in the fourth.
  • The second patient died 6.5 years following surgery due to disseminated disease.
  • [MeSH-major] Duodenal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biopsy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Proteins / metabolism. Treatment Outcome

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  • (PMID = 19708940.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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18. Kovács RK, Korom I, Dobozy A, Farkas G, Ormos J, Kemény L: Necrolytic migratory erythema. J Cutan Pathol; 2006 Mar;33(3):242-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.
  • Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.
  • OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.
  • Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.
  • After distal resection of the pancreas her skin symptoms resolved in a few days time.
  • Histology was consistent with glucagonoma.
  • CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.
  • Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Glucagonoma / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Humans. Necrosis. Paraneoplastic Syndromes. Treatment Outcome

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  • (PMID = 16466513.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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19. Kindmark H, Sundin A, Granberg D, Dunder K, Skogseid B, Janson ET, Welin S, Oberg K, Eriksson B: Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years. Med Oncol; 2007;24(3):330-7
Hazardous Substances Data Bank. GLUCAGON .

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  • [Title] Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years.
  • BACKGROUND: Glucagon-secreting endocrine pancreatic tumor is a rare disease, hence controlled studies on clinical management are lacking.
  • In an attempt to assess the efficacy of diagnostic and therapeutic measures in patients with glucagonoma, a retrospective study was performed using the archives of a tertiary care center.
  • PATIENTS AND METHODS: Records from 340 patients with endocrine pancreatic tumors were reassessed and 23 patients with malignant endocrine pancreatic tumor and elevated plasma glucagon levels were identified.
  • RESULTS: About 7% of patients with histologically verified tumors fullfilled our criteria for glucagonoma.
  • Only 22% of these patients had developed diabetes prior to the diagnosis of glucagonoma.
  • Seventy eight percent had metastatic disease to the liver at diagnosis.
  • During the study period, 11 patients died at a median of 80 months from diagnosis whereas 11 patients are still alive after a median follow up of 52 months.
  • CONCLUSIONS: Glucagonomas represent 7% of our comprehensive referral material of endocrine pancreatic tumors.
  • Necrolytic migratory erythema was a common finding (52%) and diabetes less frequent at presentation than previously reported.
  • Tumors were positive on somatostatin receptor scintigraphy and objective responses were seen to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Erythema / complications. Glucagonoma / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Glucagon / blood. Humans. Interferons. Liver Neoplasms / secondary. Male. Middle Aged. Receptors, Somatostatin / metabolism. Retrospective Studies. Sex Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 17873310.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9007-92-5 / Glucagon; 9008-11-1 / Interferons
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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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21. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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22. Dennison SR, Whittaker M, Harris F, Phoenix DA: Anticancer alpha-helical peptides and structure/function relationships underpinning their interactions with tumour cell membranes. Curr Protein Pept Sci; 2006 Dec;7(6):487-99

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anticancer alpha-helical peptides and structure/function relationships underpinning their interactions with tumour cell membranes.
  • These molecules are alpha-helical defence peptides, which show potent anticancer activity (alpha-ACPs) in addition to their established roles as antimicrobial factors and modulators of innate immune systems.
  • Generally, alpha-ACPs exhibit selectivity for cancer and microbial cells primarily due to their elevated levels of negative membrane surface charge as compared to non-cancerous eukaryotic cells.
  • The anticancer activity of alpha-ACPs normally occurs at micromolar levels but is not accompanied by significant levels of haemolysis or toxicity to other mammalian cells.
  • Structure/function studies have established that architectural features of alpha-ACPs such as amphiphilicty levels and hydrophobic arc size are of major importance to the ability of these peptides to invade cancer cell membranes.
  • In the vast majority of cases the mechanisms underlying such killing involves disruption of mitochondrial membrane integrity and/or that of the plasma membrane of the target tumour cells.
  • Usually, these membrane interactions lead to loss of membrane integrity and cell death utilising apoptic and necrotic pathways.
  • It is concluded that that alpha-ACPs are major contenders in the search for new anticancer drugs, underlined by the fact that a number of these peptides have been patented in this capacity.
  • [MeSH-major] Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Membrane / drug effects. Peptides / drug effects
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Humans. Molecular Sequence Data. Structure-Activity Relationship

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  • (PMID = 17168782.001).
  • [ISSN] 1389-2037
  • [Journal-full-title] Current protein & peptide science
  • [ISO-abbreviation] Curr. Protein Pept. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides
  • [Number-of-references] 158
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23. Sgambato A, Caredda E, Leocata P, Rossi G, Boninsegna A, Vitale A, Grandi T, Cittadini A, Migaldi M: Expression of alpha-dystroglycan correlates with tumour grade and predicts survival in oral squamous cell carcinoma. Pathology; 2010 Apr;42(3):248-54
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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 alpha-dystroglycan correlates with tumour grade and predicts survival in oral squamous cell carcinoma.
  • Decreased expression of DG has been reported in several human cancers and related to tumour aggressiveness.
  • METHODS: Expression of the alpha-DG subunit was evaluated by immunostaining in a series of oral squamous cell carcinoma (OSCC) and its relation with traditional prognostic indicators and with the clinical outcome of the patients was evaluated.
  • RESULTS: Alpha-DG expression was easily detected in normal epithelium with a mean percentage of positive cells >80% but was undetectable in a significant fraction (59%) of OSCC.
  • Loss of alpha-DG staining correlated with higher tumour grade (p = 0.04) and stage (p = 0.01), with nodal involvement (p = 0.001) and with an increased risk of recurrence (p = 0.002) and death (p = 0.004) in a univariate analysis, but it was not confirmed as an independent predictor of clinical outcome in a multivariate analysis.
  • CONCLUSIONS: Loss of alpha-DG expression, which corresponds to loss of a functional DG complex, is a frequent event in human OSCC.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Dystroglycans / biosynthesis. Mouth Neoplasms / metabolism. Mouth Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Prognosis

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  • (PMID = 20350218.001).
  • [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 / DAG1 protein, human; 146888-27-9 / Dystroglycans
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24. Lui PC, Fan YS, Xu G, Ngai CY, Fung KP, Tse GM, Yu AM, Li JY: Apoptotic and necrotic effects of tumour necrosis factor-alpha potentiated with hyperthermia on L929 and tumour necrosis factor-alpha-resistant L929. Int J Hyperthermia; 2010;26(6):556-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptotic and necrotic effects of tumour necrosis factor-alpha potentiated with hyperthermia on L929 and tumour necrosis factor-alpha-resistant L929.
  • PURPOSE: The cytotoxic effect of the combination treatment of TNF-alpha and hyperthermia on L929 and TNF-alpha-resistant L929 (rL929) cells was investigated.
  • MATERIALS AND METHODS: L929 cells were treated with TNF-alpha (5 ng/mL), heating at 43 degrees C or the combination of TNF-alpha and heating.
  • The cells were harvested at different time within the 24-hour period.
  • The viability and the type of cell death of the harvested cells were examined.
  • RESULTS: When L929 cells were treated with a combination of TNF-alpha and heating the cells died quickly and apoptosis increased to an overwhelming extent, especially in the group pre-treated with TNF-alpha for 1 h prior to heating.
  • Although rL929 cells were resistant to TNF-alpha alone, the cells became sensitive to TNF-alpha treatment when combined with heating.
  • Similar to the L929 cell, the cells also died rapidly and exhibited apoptosis to a higher extent.
  • Agarose gel electrophoresis of DNA extracted from treated cells showed that the DNA fragments were multiples of approximately 200 bp.
  • Furthermore, by studying the kinetics of cell death and apoptosis, we found that the loss of cell membrane integrity preceded the DNA fragmentation in both L929 and rL929 cells.
  • CONCLUSION: The results suggested that hyperthermia may enhance the necrotic and apoptotic effects of TNF-alpha on some tumour cells and overcome the resistance of some tumour cells to TNF-alpha.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance / physiology. Fever / physiopathology. Fibrosarcoma / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Disease Models, Animal. Mice. Necrosis

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  • (PMID = 20707650.001).
  • [ISSN] 1464-5157
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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25. Friedrich RE, Zustin J, Scheuer HA: Adenomatoid odontogenic tumour of the mandible. Anticancer Res; 2010 May;30(5):1787-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenomatoid odontogenic tumour of the mandible.
  • Adenomatoid odontogenic tumour (AOT) is a benign tumour of odontogenic origin.
  • The differential diagnosis of AOT is crucial in terms of surgical management.
  • The 23-year old male patient presented in this case study was referred to the maxillofacial surgery clinic due to the incidental radiological finding of a large osteolytic lesion of the anterior mandible with a retained permanent canine at the base of the bone.
  • Some areas of the tumour were alpha-smooth-muscle-actin positive, indicating a myoepithelial differentiation.
  • Differential diagnosis of AOT to other odontogenic tumours, such as ameloblastoma, is crucial for therapy.
  • Exact morphological diagnosis avoids extensive ablative surgery.
  • [MeSH-major] Mandibular Neoplasms / diagnosis. Odontogenic Tumors / diagnosis
  • [MeSH-minor] Actins / metabolism. Adult. Bone Remodeling. Cell Differentiation. Cell Membrane / metabolism. Epithelium / metabolism. Humans. Immunohistochemistry / methods. Keratins / metabolism. Male. Muscle, Smooth / metabolism

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  • (PMID = 20592380.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Actins; 68238-35-7 / Keratins
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26. Stika J, Vondrácek J, Hofmanová J, Simek V, Kozubík A: MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis. Cancer Lett; 2006 Jun 18;237(2):263-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis.
  • We investigated the role of the 5-lipoxygenase (5-LOX) pathway of arachidonic acid metabolism in tumour necrosis factor-alpha (TNF-alpha)-induced differentiation of human leukemic HL-60 cells using MK-886, an inhibitor of 5-LOX activating protein.
  • MK-886 augmented cell cycle arrest and differentiation induced by TNF-alpha; however, both effects were probably 5-LOX-independent, because a general LOX inhibitor, NDGA, had no effect.
  • Apoptosis was significantly elevated after combined TNF-alpha and MK-886 treatment, which could be partially associated with changes of Mcl-1 protein expression.
  • Thus, in addition to apoptosis, MK-886 can enhance TNF-alpha-induced differentiation.
  • [MeSH-major] Apoptosis. Indoles / pharmacology. Lipoxygenase Inhibitors / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Arachidonate 5-Lipoxygenase / metabolism. Cell Cycle. Cell Differentiation. Cell Line, Tumor. Cell Survival. HL-60 Cells. Humans. Signal Transduction. Time Factors

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  • (PMID = 16039040.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Indoles; 0 / Lipoxygenase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 118414-82-7 / L 663536; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase
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27. Theas MS, Rival C, Jarazo-Dietrich S, Jacobo P, Guazzone VA, Lustig L: Tumour necrosis factor-alpha released by testicular macrophages induces apoptosis of germ cells in autoimmune orchitis. Hum Reprod; 2008 Aug;23(8):1865-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour necrosis factor-alpha released by testicular macrophages induces apoptosis of germ cells in autoimmune orchitis.
  • BACKGROUND: Experimental autoimmune orchitis (EAO) is a model of chronic inflammation and infertility useful for studying testicular immune and germ cell (GC) interactions.
  • Based on the previous results showing that the number of macrophages and apoptotic GC expressing tumour necrosis factor (TNF) receptor 1 increased in EAO, we studied the role of macrophages and TNF-alpha in GC apoptosis.
  • TNF-alpha content (enzyme-linked immunosorbent assay) was significantly higher in the CMTM from EAO versus C rats on Day 80 (P < 0.05).
  • The apoptotic effect of CMTM from Day 80 rats was abrogated by a selective TNF-alpha blocker (Etanercept).
  • Moreover, TNF-alpha in vitro induced GC apoptosis.
  • TNF-alpha expression (by immunofluorescence) was observed in testicular (ED2(+)) and non-resident (ED1(+)) macrophages, the percentage of TNF-alpha(+) macrophages being similar in focal and severe orchitis.
  • CONCLUSIONS: Results demonstrated that soluble factors released from testicular EAO macrophages induce apoptosis of GC, biased by the local inflammatory environment, and that TNF-alpha is a relevant cytokine involved in testicular damage during severe orchitis.
  • [MeSH-major] Apoptosis / drug effects. Autoimmune Diseases / physiopathology. Germ Cells / cytology. Macrophages / secretion. Orchitis / physiopathology. Tumor Necrosis Factor-alpha / secretion
  • [MeSH-minor] Animals. Cell Survival / drug effects. Culture Media, Conditioned / pharmacology. Male. Rats. Rats, Sprague-Dawley. Testis / cytology. Testis / immunology. Testis / pathology

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  • (PMID = 18579514.001).
  • [ISSN] 1460-2350
  • [Journal-full-title] Human reproduction (Oxford, England)
  • [ISO-abbreviation] Hum. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Tumor Necrosis Factor-alpha
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28. An HJ, Seo MJ, Choi IY, Park RK, Jeong S, Lee JY, Kim HM, Um JY, Hong SH: Induction of nitric oxide & tumour necrosis factor-alpha by Psoralea corylifolia. Indian J Med Res; 2008 Dec;128(6):752-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of nitric oxide & tumour necrosis factor-alpha by Psoralea corylifolia.
  • BACKGROUND & OBJECTIVES: Psoralea corylifolia (PC) is an herb widely used in medicine for the treatment of a variety of ailment.
  • In the present study we investigated effect of PC on nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) production in mouse peritoneal macrophages and also examined the mechanism by which PC regulates NO production.
  • METHODS: MTT assay performed for cell viability test and nitrite concentration was measured by using Griess reagent.
  • The amount of TNF-alpha secreted by the cells was measured by a modified enzyme-linked immunosorbent assay (ELISA).
  • The increased production of NO from rIFN-gamma plus PC-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor kappa B (NF-kappaB).
  • Furthermore, treatment of peritoneal macrophages with rIFN-gamma plus PC caused a significant increase in tumour necrosis factor-alpha (TNF-alpha) production.
  • PDTC also decreased the effect of PC on TNF-alpha production significantly.
  • INTERPRETATION & CONCLUSION: As NO and TNF-alpha play an important role in immune function and host defense, PC treatment could modulate several aspects of host defense mechanisms due to stimulation of the inducible nitric oxide synthase.
  • [MeSH-major] Macrophages, Peritoneal / drug effects. Nitric Oxide / biosynthesis. Plant Extracts / pharmacology. Psoralea. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Cell Survival / drug effects. Dose-Response Relationship, Drug. Interferon-gamma / pharmacology. Male. Mice. Mice, Inbred C57BL

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  • (PMID = 19246800.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 82115-62-6 / Interferon-gamma
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29. Aggarwal P, Kehoe S: Serum tumour markers in gynaecological cancers. Maturitas; 2010 Sep;67(1):46-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum tumour markers in gynaecological cancers.
  • Serum tumour markers have had a role in screening, diagnosis and monitoring of some gynaecological cancers.
  • Equally, this CA125, if elevated pre-operatively can be used to predict chemotherapeutic responses, and even disease relapse prior to any symptoms or clinical findings.
  • Other useful markers in ovarian cancer are betaHCG and AFP produced by germ cell tumours. betaHCG is also of extreme importance in both the diagnosis and management of choriocarcinomas.
  • [MeSH-major] Biomarkers, Tumor / blood. CA-125 Antigen / blood. Choriocarcinoma / diagnosis. Chorionic Gonadotropin, beta Subunit, Human / blood. Membrane Proteins / blood. Neoplasms, Germ Cell and Embryonal / diagnosis. Ovarian Neoplasms / diagnosis. alpha-Fetoproteins / metabolism

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20510555.001).
  • [ISSN] 1873-4111
  • [Journal-full-title] Maturitas
  • [ISO-abbreviation] Maturitas
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / MUC16 protein, human; 0 / Membrane Proteins; 0 / alpha-Fetoproteins
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30. Baldwin HM, Ito-Ihara T, Isaacs JD, Hilkens CM: Tumour necrosis factor alpha blockade impairs dendritic cell survival and function in rheumatoid arthritis. Ann Rheum Dis; 2010 Jun;69(6):1200-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour necrosis factor alpha blockade impairs dendritic cell survival and function in rheumatoid arthritis.
  • OBJECTIVES: Tumour necrosis factor alpha (TNFalpha) blockade is an effective therapy for rheumatoid arthritis (RA).
  • This study investigated whether anti-TNFalpha therapeutics exerted their immunoregulatory effects through modulation of dendritic cell (DC) function.
  • DC were analysed for survival, phenotype, cytokine production and T-cell stimulatory capacity.
  • Furthermore, anti-TNFalpha-treated DC were poor stimulators of T-cell proliferation and polarised T-cell development towards a higher IL-10/lower IFNgamma cytokine profile.
  • Similarly, DC derived from RA patients after anti-TNFalpha treatment showed impaired upregulation of CD80 and CD86 upon lipopolysaccharide activation and displayed poor T-cell stimulatory activity.
  • CONCLUSIONS: The data show that TNFalpha blockade has profound effects on DC function with downstream, potentially immunoregulatory, effects on T cells.
  • [MeSH-major] Antirheumatic Agents / pharmacology. Arthritis, Rheumatoid / pathology. Dendritic Cells / drug effects. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Adalimumab. Adult. Aged. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Apoptosis / drug effects. Cell Survival / drug effects. Cells, Cultured. Cytokines / biosynthesis. Etanercept. Female. Humans. Immunoglobulin G / therapeutic use. Immunophenotyping. Infliximab. Lipopolysaccharides / immunology. Lymphocyte Activation / drug effects. Male. Middle Aged. Receptors, Tumor Necrosis Factor / therapeutic use. T-Lymphocyte Subsets / immunology

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  • [CommentIn] Nat Rev Rheumatol. 2010 Jul;6(7):383 [20614506.001]
  • (PMID = 19773288.001).
  • [ISSN] 1468-2060
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Grant] United Kingdom / Arthritis Research UK / / 16361
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antirheumatic Agents; 0 / Cytokines; 0 / Immunoglobulin G; 0 / Lipopolysaccharides; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; FYS6T7F842 / Adalimumab; OP401G7OJC / Etanercept
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31. Lima V, Brito GA, Cunha FQ, Rebouças CG, Falcão BA, Augusto RF, Souza ML, Leitão BT, Ribeiro RA: Effects of the tumour necrosis factor-alpha inhibitors pentoxifylline and thalidomide in short-term experimental oral mucositis in hamsters. Eur J Oral Sci; 2005 Jun;113(3):210-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the tumour necrosis factor-alpha inhibitors pentoxifylline and thalidomide in short-term experimental oral mucositis in hamsters.
  • On days 4, 5, 10, 12, 14 and 16, lesions induced by 5-FU were examined macroscopically and microscopically, and the presence and intensity of hyperemia, erythema, edema, inflammatory cell infiltration, hemorrhagic areas, ulcers and abscesses were recorded.
  • The results indicate a protective effect of PTX and TLD, suggesting an important role for tumour necrosis factor-alpha (TNF-alpha) in the pathophysiology of 5-FU induced-oral mucositis in hamsters.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Pentoxifylline / therapeutic use. Stomatitis / prevention & control. Thalidomide / therapeutic use. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Abscess / pathology. Animals. Antimetabolites, Antineoplastic / adverse effects. Cricetinae. Disease Models, Animal. Edema / pathology. Erythema / pathology. Fluorouracil / adverse effects. Hemorrhage / pathology. Hyperemia / pathology. Leukocyte Count. Male. Mesocricetus. Mouth Mucosa / drug effects. Mouth Mucosa / injuries. Mouth Mucosa / pathology. Neutrophils / drug effects. Neutrophils / pathology. Oral Ulcer / pathology. Peroxidase / analysis. Peroxidase / drug effects. Protective Agents / therapeutic use. Time Factors

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  • [Copyright] (c) Eur J Oral Sci, 2005
  • (PMID = 15953245.001).
  • [ISSN] 0909-8836
  • [Journal-full-title] European journal of oral sciences
  • [ISO-abbreviation] Eur. J. Oral Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Immunosuppressive Agents; 0 / Protective Agents; 0 / Tumor Necrosis Factor-alpha; 4Z8R6ORS6L / Thalidomide; EC 1.11.1.7 / Peroxidase; SD6QCT3TSU / Pentoxifylline; U3P01618RT / Fluorouracil
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32. Kumar S, Guleria R, Mohan A, Singh V, Ali A, Bharti AC, Das BC: Utility of plasma tumour necrosis factor-alpha and transforming growth factor-beta1 as predictors of survival and treatment outcome in advanced non-small cell lung carcinoma. Biomarkers; 2010 Aug;15(5):446-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Utility of plasma tumour necrosis factor-alpha and transforming growth factor-beta1 as predictors of survival and treatment outcome in advanced non-small cell lung carcinoma.
  • We hypothesized that plasma level of tumour necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta1 may be a potential tool for diagnosis, prognosis and prediction of treatment outcome in non-small cell lung carcinoma (NSCLC).
  • Plasma levels of TNF-alpha and TGF-beta1 were quantified in 100 NSCLC patients and 100 controls.
  • Association of TNF-alpha and TGF-beta1 with response to therapy and survival was determined in 42 patients.
  • An increased presence of TNF-alpha and TGF-beta1 was observed in NSCLC compared with controls.
  • TNF-alpha and TGF-beta1 levels did not correlate with survival and response to chemotherapy.
  • TNF-alpha and TGF-beta1 do not appear to be reliable markers for predicting survival and response to therapy in advanced NSCLC.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / blood. Lung Neoplasms / blood. Transforming Growth Factor beta1 / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / blood. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis. Sensitivity and Specificity. Survival Analysis. Treatment Outcome

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  • (PMID = 20486867.001).
  • [ISSN] 1366-5804
  • [Journal-full-title] Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
  • [ISO-abbreviation] Biomarkers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha
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33. Frew IJ, Krek W: Multitasking by pVHL in tumour suppression. Curr Opin Cell Biol; 2007 Dec;19(6):685-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multitasking by pVHL in tumour suppression.
  • Functional inactivation of the von Hippel-Lindau (VHL) tumour suppressor gene product, pVHL, leads to cancer in humans.
  • It is widely accepted that pVHL functions to destabilise hypoxia inducible factor alpha (HIFalpha) subunits, key effectors of the hypoxia signalling pathway.
  • However, growing evidence indicates that tumour suppression by pVHL also involves the control of a wide variety of HIFalpha-independent processes including microtubule dynamics, primary cilium maintenance, cell proliferation, neuronal apoptosis, extracellular matrix deposition and responses to DNA damage.
  • Moreover, it is becoming apparent that tumour initiation requires not only VHL mutation but also the alteration of additional cooperating cancer pathways.
  • These studies are beginning to provide insights into the signalling networks involving pVHL that normally control diverse cellular processes and how disruption of these networks leads to tumour formation.
  • [MeSH-major] Genes, Tumor Suppressor / physiology. Neoplasms / genetics. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Signal Transduction / physiology

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  • (PMID = 18006292.001).
  • [ISSN] 0955-0674
  • [Journal-full-title] Current opinion in cell biology
  • [ISO-abbreviation] Curr. Opin. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Number-of-references] 55
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34. Leisser C, Saleh L, Haider S, Husslein H, Sonderegger S, Knöfler M: Tumour necrosis factor-alpha impairs chorionic gonadotrophin beta-subunit expression and cell fusion of human villous cytotrophoblast. Mol Hum Reprod; 2006 Oct;12(10):601-9
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  • [Title] Tumour necrosis factor-alpha impairs chorionic gonadotrophin beta-subunit expression and cell fusion of human villous cytotrophoblast.
  • Quantitative real-time PCR revealed a 1.8- and 6.9-fold increase of hCG-alpha and hCG-beta mRNA levels, respectively, between 36 and 60 h of term trophoblast syncytialization.
  • Compared with controls, neither interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-10, IL-13 and IL-15 nor tumour necrosis factor (TNF)-alpha significantly altered hCG-alpha mRNA expression.
  • In contrast, TNF-alpha suppressed hCG-beta mRNA 3.8- and 1.8-fold at 36 and 60 h of term trophoblast differentiation.
  • Accordingly, hCG secretion was impaired by TNF-alpha but not by the different ILs.
  • Moreover, TNF-alpha reduced luciferase expression of reporter plasmids harbouring the proximal hCG-beta5 promoter to 35 and 77%, respectively, in primary term trophoblasts and trophoblastic SHGPL-5 cells.
  • In addition, counting of nuclei in syncytialized, desmoplakin-negative areas revealed a 1.9-fold reduction of term trophoblast fusion in the presence of TNF-alpha.
  • Concomitantly, TNF-alpha impaired induction of endogenous and secreted hCG-beta protein levels in these cultures.
  • The data suggest that TNF-alpha decreases hCG-beta mRNA and protein expression by reducing gene transcription and trophoblast cell fusion.
  • Suppression of these processes by TNF-alpha could partly explain the adverse effects of the cytokine on placental function and pregnancy outcome.
  • [MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / metabolism. Chorionic Villi / metabolism. Trophoblasts / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Differentiation. Cell Fusion. Cell Line. Down-Regulation. Female. Glycoprotein Hormones, alpha Subunit / metabolism. Humans. Pregnancy. Promoter Regions, Genetic / drug effects. Promoter Regions, Genetic / genetics. RNA, Messenger / metabolism. Transfection

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  • (PMID = 16896069.001).
  • [ISSN] 1360-9947
  • [Journal-full-title] Molecular human reproduction
  • [ISO-abbreviation] Mol. Hum. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Glycoprotein Hormones, alpha Subunit; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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35. Abreu Velez AM, Howard MS: Diagnosis and treatment of cutaneous paraneoplastic disorders. Dermatol Ther; 2010 Nov-Dec;23(6):662-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and treatment of cutaneous paraneoplastic disorders.
  • Cutaneous signs of these disorders afford clinicians opportunities for early diagnosis and treatment.
  • We aim to succinctly review the recognition, diagnosis, and treatment of selected cutaneous paraneoplastic diseases.
  • Skin disorders that may be associated with paraneoplastic syndromes include: cutaneous metastases, tripe palms, Sweet's syndrome, glucagonoma, Paget's disease and extramammary Paget's disease, acanthosis nigricans, Birt-Hogg-Dube syndrome, basal cell nevus syndrome, Bazex syndrome (acrokeratosis paraneoplastica), carcinoid syndrome, Cowden's disease(multiple hamartoma syndrome), dermatomyositis, erythema gyratum repens, ichthyosis aquisita, von Recklinghausen's disease, pityriasis rotunda, pyoderma gangrenosum, Quincke's edema (angioedema and paraneoplastic uricaria), paraneoplastic pemphigus, Degos' disease, superior vena cava syndrome, Werner's syndrome, diffuse normolipemic plane xanthomas, and yellow nail syndrome.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / therapy. Skin Diseases / diagnosis. Skin Diseases / therapy

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054710.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
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36. Cartwright JE, Balarajah G: Trophoblast interactions with endothelial cells are increased by interleukin-1beta and tumour necrosis factor alpha and involve vascular cell adhesion molecule-1 and alpha4beta1. Exp Cell Res; 2005 Mar 10;304(1):328-36

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trophoblast interactions with endothelial cells are increased by interleukin-1beta and tumour necrosis factor alpha and involve vascular cell adhesion molecule-1 and alpha4beta1.
  • Interactions between fetal extravillous trophoblast cells and maternal uterine cells are of critical importance in successful placentation.
  • In the first trimester, trophoblasts invade the uterine environment and reach the spiral arteries where they interact with vascular cells; however, little is known of the nature of these interactions.
  • We have developed a fluorescent binding assay to investigate the contact between trophoblasts and endothelial cells and to determine its regulation by cytokines and adhesion molecules.
  • Stimulation of an endothelial cell line (SGHEC-7) with interleukin-1beta or tumour necrosis factor-alpha significantly increased adhesion of the first-trimester extravillous trophoblast-derived cell line, SGHPL-4.
  • Using blocking antibodies, vascular cell adhesion molecule-1 (VCAM-1) and integrin alpha4beta1 (VLA-4), but not intercellular adhesion molecule-1 (ICAM-1), were shown to be important in trophoblast binding to activated endothelial cells.
  • SGHPL-4 cells were shown to express HLA-G, alpha4beta1 and ICAM-1 at high levels and LFA-1 and VCAM-1 at lower levels.
  • ICAM-1 and VCAM-1 are expressed on SGHEC-7 cells and their expression was confirmed on primary decidual endothelial cells.
  • [MeSH-major] Decidua / cytology. Endothelial Cells / metabolism. Integrin alpha4beta1 / physiology. Interleukin-1 / pharmacology. Trophoblasts / physiology. Tumor Necrosis Factor-alpha / pharmacology. Vascular Cell Adhesion Molecule-1 / physiology
  • [MeSH-minor] Cell Line. Female. Humans. Intercellular Adhesion Molecule-1 / metabolism. Pregnancy

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  • (PMID = 15707597.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alpha4beta1; 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1
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37. Chew V, Tow C, Teo M, Wong HL, Chan J, Gehring A, Loh M, Bolze A, Quek R, Lee VK, Lee KH, Abastado JP, Toh HC, Nardin A: Inflammatory tumour microenvironment is associated with superior survival in hepatocellular carcinoma patients. J Hepatol; 2010 Mar;52(3):370-9
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  • [Title] Inflammatory tumour microenvironment is associated with superior survival in hepatocellular carcinoma patients.
  • As the status of the tumour immune microenvironment can affect progression of established tumours, we evaluated potential immune mechanisms associated with survival in HCC.
  • METHODS: Immune gene expression profiles were analyzed in tumour and non-tumour liver tissues from resected HCC patients using quantitative PCR and immunohistochemistry.
  • Tumour-infiltrating leukocytes (TILs) were isolated to verify the expression of immune genes and to identify proliferating TILs.
  • These parameters were analyzed statistically in relation with patient survival and tumour phenotype (apoptosis and proliferation).
  • RESULTS: The immune microenvironment within tumours was found to be heterogeneous, although globally more inert compared to the adjacent non-tumour liver tissue.
  • Importantly, proliferating immune cells, predominantly NK and T cells, are present in tumours of patients with longer survival, and exclusively in areas devoid of proliferating tumour cells.
  • NK and CD8(+) T cell densities are correlated positively with tumour apoptosis, and negatively with tumour proliferation.
  • CONCLUSIONS: Hence, an inflammatory immune microenvironment within HCC tumours could be an important means to control tumour progression via TIL activation and proliferation.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. CD8-Positive T-Lymphocytes / pathology. Cell Line, Tumor. Cell Proliferation. Chemokine CCL2 / genetics. Chemokine CCL2 / metabolism. Female. Humans. Interleukin-6 / genetics. Interleukin-6 / metabolism. Killer Cells, Natural / pathology. Lymphocytes, Tumor-Infiltrating / pathology. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Rate. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright (c) 2009 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
  • (PMID = 19720422.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chemokine CCL2; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
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38. Ding M, Yuan YJ: Study on the mechanisms of an extract of Salvia miltiorrhiza on the regulation of permeability of endothelial cells exposed to tumour necrosis factor-alpha. J Pharm Pharmacol; 2007 Jul;59(7):1027-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Study on the mechanisms of an extract of Salvia miltiorrhiza on the regulation of permeability of endothelial cells exposed to tumour necrosis factor-alpha.
  • Exposure of endothelial cells to tumour necrosis factor-alpha (TNF-alpha) results in increased endothelial permeability, accompanied by a loss of cell-cell adherence junctions.
  • The importance of tyrosine phosphatase and kinase activity in oxidant-mediated loss of cell junction structures has been demonstrated.
  • The purpose of this study was to determine whether tyrosine phosphorylation contributes to TNF-alpha-mediated disorganization of endothelial cell junctions and how an extract of Salvia miltiorrhiza (ESM) and its active ingredients, Danshensu (DSS) and salvianolic acid B (Sal B), exert their protective effect in maintaining cell integrity.
  • Immunoblotting results indicated that TNF-alpha exposure resulted in tyrosine phosphorylation of junctional proteins such as vascular endothelial cadherin and beta-catenin, which was attenuated by ESM and its active ingredients DSS and Sal B.
  • In addition, immunoprecipitation showed ESM and its active ingredients prevented beta-catenin disassociation from the cytoskeleton in TNF-alpha-treated human umbilical vein endothelial cells.
  • The results suggest that TNF-alpha produced biological effects at least partly by junctional protein phosphotyrosine modifications by increasing the total cellular phosphorylation level.
  • [MeSH-major] Cell Membrane Permeability / drug effects. Endothelial Cells / drug effects. Salvia miltiorrhiza / chemistry. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Adherens Junctions / metabolism. Analysis of Variance. Benzaldehydes / metabolism. Benzofurans / pharmacology. Cadherins / metabolism. Catechols / metabolism. Cells, Cultured. Chromatography, High Pressure Liquid. Enzyme Activation. Fluorescent Antibody Technique. Humans. Lactates / pharmacology. Phosphorylation. Phosphotyrosine / metabolism. Plant Extracts / chemistry. Plant Extracts / pharmacology. Umbilical Veins / cytology. Vascular Endothelial Growth Factor A / biosynthesis. beta Catenin / metabolism

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  • (PMID = 17637199.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzaldehydes; 0 / Benzofurans; 0 / Cadherins; 0 / Catechols; 0 / Lactates; 0 / Plant Extracts; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; 115939-25-8 / salvianolic acid B; 21820-51-9 / Phosphotyrosine; 23028-17-3 / 3,4-dihydroxyphenyllactic acid; 4PVP2HCH4T / protocatechualdehyde
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39. Wang Y, Thorlacius H: Mast cell-derived tumour necrosis factor-alpha mediates macrophage inflammatory protein-2-induced recruitment of neutrophils in mice. Br J Pharmacol; 2005 Aug;145(8):1062-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mast cell-derived tumour necrosis factor-alpha mediates macrophage inflammatory protein-2-induced recruitment of neutrophils in mice.
  • Recent studies have indicated that mast cells play an intermediate role in chemokine-induced neutrophil recruitment in vivo.
  • The aim of the present investigation was to determine the role of tumour necrosis factor-alpha (TNF-alpha) in neutrophil recruitment provoked by the CXC chemokine macrophage inflammatory protein-2 (MIP-2).
  • For this purpose, we used mast cell- and TNF-alpha-deficient mice and studied neutrophil adhesion to endothelial cells in vitro and neutrophil recruitment in the mouse cremaster muscle in vivo.
  • This MIP-2-regulated neutrophil recruitment was abolished in mast cell-deficient mice.
  • TNF-alpha increased E-selectin mRNA expression in both wild-type (WT) and mast cell-deficient mice.
  • In contrast, MIP-2 challenge increased gene expression of E-selectin in WT but not in mast cell-deficient animals.
  • Moreover, MIP-2-provoked extravascular accumulation of neutrophils was reduced by 78% in mice lacking TNF-alpha.
  • In order to better define the role of mast cell-derived TNF-alpha in neutrophil responses to MIP-2, we used an in vitro endothelial cell adhesion assay with and without mast cells.
  • Interestingly, MIP-2-induced neutrophil adhesion to endothelial cells was decreased by 58% using TNF-alpha-deficient compared to WT mast cells.
  • Moreover, mast cell secretion of TNF-alpha increased by more than 71% in response to challenge with MIP-2.
  • Taken together, our results suggest that MIP-2-induced neutrophil recruitment is mediated by TNF-alpha released from local mast cells.
  • These findings help to explain the complex molecular interactions between chemokines, mast cell activation and neutrophil infiltration in vivo.
  • [MeSH-major] Chemokines / pharmacology. Mast Cells / drug effects. Neutrophil Infiltration / drug effects. Neutrophils / cytology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Chemokine CXCL2. Dose-Response Relationship, Drug. E-Selectin / biosynthesis. Endothelial Cells / cytology. Endothelial Cells / drug effects. Enzyme-Linked Immunosorbent Assay. Male. Mice. Mice, Inbred Strains. RNA, Messenger / biosynthesis. Receptors, Interleukin-8B / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15937521.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CXCL2; 0 / Chemokines; 0 / Cxcl2 protein, mouse; 0 / E-Selectin; 0 / RNA, Messenger; 0 / Receptors, Interleukin-8B; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1576224
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40. Marko PB, Miljković J, Zemljic TG: Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors. Acta Dermatovenerol Alp Pannonica Adriat; 2005 Dec;14(4):161-4, 166
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  • [Title] Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.
  • The computed tomographic scan of the abdomen revealed multiple hepatic tumors.
  • Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrine tumor.
  • Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.
  • The serum glucagon level was markedly increased.
  • The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.
  • Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.
  • As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.
  • The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.
  • [MeSH-major] Dermatitis / etiology. Erythema / etiology. Liver Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Male. Middle Aged. Octreotide / therapeutic use

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  • (PMID = 16435046.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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41. Lisi S, Sisto M: Effects of biological drug adalimumab on tumour necrosis factor-alpha-converting enzyme activation. Immunol Cell Biol; 2010 Mar-Apr;88(3):297-304
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  • [Title] Effects of biological drug adalimumab on tumour necrosis factor-alpha-converting enzyme activation.
  • Tumour necrosis factor-alpha (TNF-alpha)-converting enzyme (TACE) is a membrane-bound metalloprotease and disintegrin.
  • It is produced by a number of host cells and is known to shed and release cell-bound cytokines, particularly members of the TNF family.
  • In this study, we tested the hypothesis that anti-Ro/SSA autoantibodies, purified from IgG fractions of patients with primary Sjögren's syndrome, are capable to regulate TACE expression and activation in human salivary gland epithelial cells (SGEC).
  • We also evaluated the potential physiological and therapeutic consequences of TNF-alpha blocking by the biological agent adalimumab, the first fully human (100% human peptide sequences) therapeutic anti-TNF-alpha antibody, on post-translational regulation of TACE.
  • [MeSH-major] ADAM Proteins / biosynthesis. Anti-Inflammatory Agents / pharmacology. Antibodies, Monoclonal / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Salivary Glands / enzymology. Sjogren's Syndrome / enzymology
  • [MeSH-minor] Adalimumab. Antibodies, Monoclonal, Humanized. Autoantibodies / immunology. Autoantibodies / metabolism. Cells, Cultured. Enzyme Activation / drug effects. Enzyme Activation / immunology. Epithelium / enzymology. Epithelium / immunology. Humans. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19949420.001).
  • [ISSN] 1440-1711
  • [Journal-full-title] Immunology and cell biology
  • [ISO-abbreviation] Immunol. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Autoantibodies; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase; FYS6T7F842 / Adalimumab
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42. Foka P, Singh NN, Salter RC, Ramji DP: The tumour necrosis factor-alpha-mediated suppression of the CCAAT/enhancer binding protein-alpha gene transcription in hepatocytes involves inhibition of autoregulation. Int J Biochem Cell Biol; 2009 May;41(5):1189-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The tumour necrosis factor-alpha-mediated suppression of the CCAAT/enhancer binding protein-alpha gene transcription in hepatocytes involves inhibition of autoregulation.
  • Tumour necrosis factor-alpha (TNF-alpha) is a key regulator of the immune and inflammatory responses along with numerous other cellular changes during physiological and pathophysiological conditions.
  • The cellular actions of TNF-alpha are associated with both the activation and the inhibition of gene transcription.
  • In contrast to gene activation, the mechanisms underlying the TNF-alpha-mediated transcriptional inhibition remain largely unclear.
  • We have investigated this aspect using the transcription factor CCAAT/enhancer binding protein-alpha (C/EBPalpha) as a model gene.
  • TNF-alpha decreased the expression of C/EBPalpha mRNA and protein in the human hepatoma Hep3B cell line.
  • The activity of the proximal promoter of both the human and the Xenopus C/EBPalpha genes in transfected Hep3B cells was inhibited by TNF-alpha.
  • Transient transfection assays using various Xenopus C/EBPalpha promoter-luciferase DNA constructs showed that a C/EBP recognition sequence was essential for the TNF-alpha response.
  • Electrophoretic mobility shift assays showed that C/EBPalpha bound to this site and co-transfection assays revealed that it was a major activator of the promoter and its transactivation potential was reduced by TNF-alpha.
  • The potential role of nuclear factor kappaB (NF-kappaB) in the response was also investigated in the light of its pivotal role in TNF-alpha signalling.
  • Inhibition of NF-kappaB using pharmacological agents or by transfection of a plasmid specifying for a superrepressor attenuated the TNF-alpha-inhibited C/EBPalpha promoter activity.
  • In addition, an involvement of NF-kappaB in DNA-protein interactions at the C/EBP recognition sequence was identified.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Hepatocytes / physiology. NF-kappa B / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Electrophoretic Mobility Shift Assay. Humans. Promoter Regions, Genetic. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transfection. Up-Regulation. Xenopus laevis

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  • (PMID = 19027873.001).
  • [ISSN] 1878-5875
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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43. Luo X, Li HX, Liu RX, Wu ZS, Yang YJ, Yang GS: Beta-catenin protein utilized by Tumour necrosis factor-alpha in porcine preadipocytes to suppress differentiation. BMB Rep; 2009 Jun 30;42(6):338-43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beta-catenin protein utilized by Tumour necrosis factor-alpha in porcine preadipocytes to suppress differentiation.
  • In this study, we revealed that tumour necrosis factor-alpha (TNF-alpha), a potential negative regulator of adipocyte differentiation, inhibits porcine adipogenesis through activation of the Wnt/beta-catenin signaling pathway.
  • Under the optimal concentration of TNF-alpha, the intracellular beta-catenin protein was stabilized.
  • Thus, the intracellular lipid accumulation of porcine preadipocyte was suppressed and the expression of important adipocyte marker genes, including peroxisome proliferator-activated receptor-gamma (PPARgamma) and CCAAT/enhancer binding protein-alpha (C/EBPalpha), were inhibited.
  • However, a loss of beta-catenin in porcine preadipocytes enhanced the adipogenic differentiation and attenuated TNF-alpha induced anti-adipogenesis.
  • Taken together, this study indicated that TNF-alpha inhibits adipogenesis through stabilization of beta-catenin protein in porcine preadipocytes.
  • [MeSH-major] Adipocytes / drug effects. Cell Differentiation / drug effects. Tumor Necrosis Factor-alpha / pharmacology. beta Catenin / metabolism
  • [MeSH-minor] Adipogenesis / drug effects. Adipogenesis / genetics. Animals. Cells, Cultured. Down-Regulation / physiology. Gene Expression Regulation / drug effects. Male. Protein Stability / drug effects. RNA, Small Interfering / pharmacology. Signal Transduction / drug effects. Swine

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  • (PMID = 19558791.001).
  • [ISSN] 1976-6696
  • [Journal-full-title] BMB reports
  • [ISO-abbreviation] BMB Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Tumor Necrosis Factor-alpha; 0 / beta Catenin
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44. 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.
  • To test this hypothesis, we used an in vitro model in which 31EG4-2A4 mouse mammary epithelial cells grown in a collagen gel form compact spheroidal colonies.
  • 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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45. Kim EY, Chi HH, Rajaiah R, Moudgil KD: Exogenous tumour necrosis factor alpha induces suppression of autoimmune arthritis. Arthritis Res Ther; 2008;10(1):R38
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  • [Title] Exogenous tumour necrosis factor alpha induces suppression of autoimmune arthritis.
  • INTRODUCTION: Our previous studies showed that arthritic Lewis (LEW) rats produced the highest levels of tumour necrosis factor (TNF)alpha in the recovery phase of adjuvant arthritis (AA), suggesting a correlation between high TNFalpha levels and reduced severity of arthritis.
  • To further explore this correlation, we compared the TNFalpha secretion profile of the AA-resistant Wistar Kyoto (WKY) rats with that of LEW rats, determined the effect of exogenous TNFalpha on the course of AA in LEW rats, and examined various mechanisms involved in TNFalpha-induced disease modulation.
  • At different time points thereafter, subgroups of rats were killed and their draining lymph node cells were tested for cytokine production.
  • In parallel, TNFalpha-treated rats were examined for changes in other cytokines, in CD4+CD25+ T cell frequency, and in indoleamine 2,3-dioxygenase (IDO) mRNA expression levels.
  • Furthermore, TNFalpha treatment significantly down modulated the severity of AA in LEW rats, and decreased the interferon (IFN)-gamma secretion in response to the pathogenic determinant of the disease-related antigen.
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Arthritis, Experimental / prevention & control. Lymph Nodes / metabolism. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 18380898.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI007540
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC3386491
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46. Rydén M, Arner P: Tumour necrosis factor-alpha in human adipose tissue -- from signalling mechanisms to clinical implications. J Intern Med; 2007 Oct;262(4):431-8
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  • [Title] Tumour necrosis factor-alpha in human adipose tissue -- from signalling mechanisms to clinical implications.
  • From its initial implication in the development of cachexia in the early 1980s, it is now almost 15 years ago that tumour necrosis factor-alpha (TNF-alpha) was first shown to be involved in the development of insulin resistance in obesity.
  • This intensive research has demonstrated both similarities and differences between rodents and humans regarding the molecular mechanisms and metabolic consequences of TNF-alpha overexpression.
  • This review will focus on the role of TNF-alpha in human white adipose tissue with particular emphasis on its regulation of lipolysis - an important pathway in adipocytes which is linked to insulin-resistant phenotypes in obesity and the metabolic syndrome.
  • [MeSH-major] Adipose Tissue / metabolism. Obesity / metabolism. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Blood Glucose / metabolism. Cachexia / metabolism. Cell Communication / physiology. Gene Expression / physiology. Gene Expression Regulation / physiology. Humans. Insulin Resistance

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  • (PMID = 17875179.001).
  • [ISSN] 0954-6820
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 78
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47. Thejass P, Kuttan G: Allyl isothiocyanate (AITC) and phenyl isothiocyanate (PITC) inhibit tumour-specific angiogenesis by downregulating nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) production. Nitric Oxide; 2007 Mar;16(2):247-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allyl isothiocyanate (AITC) and phenyl isothiocyanate (PITC) inhibit tumour-specific angiogenesis by downregulating nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) production.
  • The pro-inflammatory cytokine, tumour necrosis factor-alpha (TNF-alpha), is a mediator of nitric oxide synthesis.
  • We analyzed the effect of allyl isothiocyanate (AITC) and phenyl isothiocyanate (PITC) on serum NO as well as TNF-alpha level during angiogenesis.
  • In vivo antiangiogenic activity was studied using B16F-10 melanoma cell-induced capillary formation in C57BL/6 mice.
  • Intraperitoneal administration of AITC and PITC at a concentration of 25 microg/dose/animal significantly inhibited tumour-directed capillary formation.
  • Treatment of AITC and PITC significantly downregulated serum NO as well as TNF-alpha level in angiogenesis-induced animals compared to untreated control animals.
  • The in vitro antiangiogenic study, using rat aortic ring assay, showed that both AITC and PITC at non-toxic concentrations inhibited the production of proangiogenic factors from B16F-10 melanoma cells which was evident with the inhibition of microvessel outgrowth from aortic rings.
  • Both AITC and PITC significantly inhibited sodium nitroprusside as well as TNF-alpha-induced microvessel outgrowth from rat aortic ring.
  • Administration of AITC and PITC also significantly reduced NO and TNF-alpha production by LPS-stimulated macrophages both in vivo as well as in vitro.
  • Bio-assay using serum of angiogenesis-induced animals and supernatant from LPS-stimulated macrophages clearly confirmed the downregulatory action of AITC and PITC on TNF-alpha production.
  • These results clearly demonstrated that AITC and PITC inhibited tumour-specific angiogenesis by downregulating NO and TNF-alpha production.

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  • (PMID = 17097904.001).
  • [ISSN] 1089-8603
  • [Journal-full-title] Nitric oxide : biology and chemistry
  • [ISO-abbreviation] Nitric Oxide
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isothiocyanates; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide
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48. Docherty HM, Hay CW, Ferguson LA, Barrow J, Durward E, Docherty K: Relative contribution of PDX-1, MafA and E47/beta2 to the regulation of the human insulin promoter. Biochem J; 2005 Aug 1;389(Pt 3):813-20
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  • Of these, the homoeodomain protein PDX-1 (pancreatic duodenal homeobox factor-1), the basic leucine zipper protein MafA and the basic helix-loop-helix heterodimer E47/BETA2 (beta-cell E box transactivator 2; referred to here as beta2) bind to important regulatory sites.
  • Mutagenesis of the PDX-1, MafA and E47/beta2 binding sites reduced promoter activity by 60, 74 and 94% respectively, in INS-1 beta-cells.
  • In the islet glucagonoma cell line alphaTC1.6, overexpression of PDX-1 and MafA separately increased promoter activity approx.
  • In HeLa cells, PDX-1 stimulated the basal promoter by approx.
  • PDX-1 was shown further to activate the endogenous insulin 1 gene in alphaTC1.6 cells, whereas MafA activated the insulin 2 gene.

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  • (PMID = 15862113.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / MAFA protein, human; 0 / Maf Transcription Factors, Large; 0 / NEUROD1 protein, human; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Tcf7l1 protein, rat; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein
  • [Other-IDs] NLM/ PMC1180732
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49. Iftakhar-E-Khuda I, Koide N, Hassan F, Noman AS, Dagvadorj J, Tumurkhuu G, Naiki Y, Komatsu T, Yoshida T, Yokochi T: Novel mechanism of U18666A-induced tumour necrosis factor-alpha production in RAW 264.7 macrophage cells. Clin Exp Immunol; 2009 Mar;155(3):552-8
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  • [Title] Novel mechanism of U18666A-induced tumour necrosis factor-alpha production in RAW 264.7 macrophage cells.
  • U18666A is a cholesterol transport-inhibiting agent that is used widely to mimic Niemann-Pick type C disease.
  • The effect of U18666A on tumour necrosis factor (TNF)-alpha production in mouse macrophage cell line, RAW 264.7 cells and peritoneal macrophages was examined.
  • U18666A induced TNF-alpha mRNA expression 48 h after the treatment, and TNF-alpha production 48 and 72 h after stimulation in RAW 264.7 cells.
  • Anti-oxidant N-acetyl-L-cysteine (NAC) abolished U18666A-induced TNF-alpha production.
  • A p38 inhibitor reduced U18666A-induced TNF-alpha production.
  • Taken together, U18666A was suggested to induce TNF-alpha production in RAW 264.7 cells via free cholesterol accumulation-mediated ROS generation.
  • [MeSH-major] Androstenes / pharmacology. Anticholesteremic Agents / pharmacology. Macrophages / metabolism. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Cell Line. Cholesterol / metabolism. Enzyme Activation. Mice. Niemann-Pick Diseases / immunology. Reactive Oxygen Species / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19220841.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androstenes; 0 / Anticholesteremic Agents; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 3039-71-2 / 3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one; 97C5T2UQ7J / Cholesterol; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2669532
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50. Gómez-Laguna J, Millán Y, Reymundo C, Domingo V, Martín de Las Mulas J: Bilateral retiform Sertoli-Leydig cell tumour in a bitch. Alpha-inhibin and epithelial membrane antigen as useful tools for differential diagnosis. J Comp Pathol; 2008 Aug-Oct;139(2-3):137-40
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  • [Title] Bilateral retiform Sertoli-Leydig cell tumour in a bitch. Alpha-inhibin and epithelial membrane antigen as useful tools for differential diagnosis.
  • Sertoli-Leydig cell tumours with a retiform pattern similar to the pattern of the rete testis are a subtype of sex cord-stromal tumours recognized in the human WHO histological classification of ovarian tumours but not in the equivalent classification for domestic animals.
  • The morphology of the tumour may be confused with that of the more common ovarian epithelial tumours.
  • The gross, microscopical and immunohistochemical features of a canine retiform Sertoli-Leydig cell tumour and its comparison with the human counterpart are presented in this report.
  • Microscopically, the tumour was cystic with tubulopapillary growth characterized by narrow, elongated branching tubules.
  • Immunohistochemically, the tumour cells expressed alpha-inhibin, while epithelial membrane antigen was not detected, indicating a sex cord-stromal origin of the tumour.
  • Additionally, the tumour cells expressed cytokeratin and vimentin in addition to oestrogen receptor alpha and progesterone receptor.
  • [MeSH-major] Dog Diseases / metabolism. Dog Diseases / pathology. Inhibins / biosynthesis. Mucin-1 / biosynthesis. Ovarian Neoplasms / veterinary. Sertoli-Leydig Cell Tumor / veterinary
  • [MeSH-minor] Animals. Diagnosis, Differential. Dogs. Female. Immunohistochemistry. Neoplasms, Glandular and Epithelial / pathology

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  • (PMID = 18620701.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mucin-1; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
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51. Sánchez Andrés A, Valdés Diéguez E, Marco Macián A, Carrasco Moreno JI: [Immature ovarian tumour and dilated myocardiopathy]. An Pediatr (Barc); 2010 Dec;73(6):347-51
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  • [Title] [Immature ovarian tumour and dilated myocardiopathy].
  • [Transliterated title] Teratoma inmaduro de ovario y miocardiopatía dilatada.
  • Asymptomatic 2 month-old infant referred for evaluation of a hard abdominal mass on the left side.
  • The ultrasound examination showed a solid-cystic tumour above the left kidney.
  • The alpha-fetoprotein level was 2000ng/ml.
  • The meta-iodobenzylguanidine (123-I-MIBG) showed no tumour uptake.
  • The highly vascularised retroperitoneal tumour was resected without incident and confirmed the diagnosis of an immature Norris grade 2 teratoma grade.
  • Dilated cardiomyopathy (DCM) secondary to, chromaffin cell tumours (phaeochromocytoma, neuroblastoma, ganglioneuroblastoma), leukaemia infiltrates, and treatment with anthracyclines have been described, but there is no case reported in the literature regarding a teratoma with dilated cardiomyopathy.
  • Various cytokines, such as INF-α, IL-1, IL-6 may be secreted by tumour, promoting fibroblast activity in the heart and inducing apoptosis and myocardial fibrosis.
  • Thus, in the case presented resection of the tumour mass responsible for this production, enables the heart to return to normal.

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  • [Copyright] Copyright © 2010 Asociación Española de Pediatría. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20863775.001).
  • [ISSN] 1695-9531
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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52. Maltesen HR, Nielsen CH, Dalbøge CS, Baslund B: Methylprednisolone prevents tumour necrosis factor-alpha-dependent multinucleated giant cell formation. Rheumatology (Oxford); 2010 Nov;49(11):2037-42
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  • [Title] Methylprednisolone prevents tumour necrosis factor-alpha-dependent multinucleated giant cell formation.
  • OBJECTIVES: Granulomas contain multinucleated giant cells (MGCs), the function of which remains largely unknown.
  • In patients with autoimmune granulomatous disease, the granulomas can be resolved during treatment with glucocorticosteroid (GCS).
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antibodies, Monoclonal / drug effects. Giant Cells / drug effects. Methylprednisolone / pharmacology. Monocytes / drug effects. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adalimumab. Antibodies, Monoclonal, Humanized. Blood Buffy Coat. Cells, Cultured. Humans

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  • (PMID = 20634232.001).
  • [ISSN] 1462-0332
  • [Journal-full-title] Rheumatology (Oxford, England)
  • [ISO-abbreviation] Rheumatology (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Tumor Necrosis Factor-alpha; FYS6T7F842 / Adalimumab; X4W7ZR7023 / Methylprednisolone
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53. Bannwart CF, Peraçoli JC, Nakaira-Takahagi E, Peraçoli MT: Inhibitory effect of silibinin on tumour necrosis factor-alpha and hydrogen peroxide production by human monocytes. Nat Prod Res; 2010 Nov;24(18):1747-57
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  • [Title] Inhibitory effect of silibinin on tumour necrosis factor-alpha and hydrogen peroxide production by human monocytes.
  • Monocytes obtained from healthy individuals were incubated with silibinin to evaluate cell viability, hydrogen peroxide (H(2)O(2)) release and tumour necrosis factor-alpha (TNF-α) production by these cells.
  • The duration of treatment and different silibinin concentrations had no significant effect on cell viability.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antioxidants / pharmacology. Hydrogen Peroxide / metabolism. Milk Thistle / chemistry. Plant Extracts / pharmacology. Seeds / chemistry. Silymarin / pharmacology. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 20981616.001).
  • [ISSN] 1478-6427
  • [Journal-full-title] Natural product research
  • [ISO-abbreviation] Nat. Prod. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antioxidants; 0 / Plant Extracts; 0 / Silymarin; 0 / Tumor Necrosis Factor-alpha; 4RKY41TBTF / silybin; BBX060AN9V / Hydrogen Peroxide
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54. Fernández R, González S, Rey S, Cortés PP, Maisey KR, Reyes EP, Larraín C, Zapata P: Lipopolysaccharide-induced carotid body inflammation in cats: functional manifestations, histopathology and involvement of tumour necrosis factor-alpha. Exp Physiol; 2008 Jul;93(7):892-907
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  • [Title] Lipopolysaccharide-induced carotid body inflammation in cats: functional manifestations, histopathology and involvement of tumour necrosis factor-alpha.
  • The latter caused: (i) disorganization of CB glomoids, increased connective tissue, and rapid recruitment of polymorphonuclear cells into the vascular bed and parenchyma within 4 h;.
  • Searching for pro-inflammatory mediators, tumour necrosis factor-alpha (TNF-alpha) was localized by immunohistochemistry in glomus and endothelial cells; reverse transcriptase-polymerase chain reaction revealed that the CB expresses the mRNAs for both type-1 (TNF-R1) and type-2 TNF-alpha receptors (TNF-R2); Western blot confirmed a band of the size expected for TNF-R1; and histochemistry showed the presence of TNF-R1 in glomus cells and of TNF-R2 in endothelial cells.
  • Experiments in vitro showed that the frequency of carotid nerve discharges recorded from CBs perfused and superfused under normoxic conditions was not significantly modified by TNF-alpha, but that the enhanced frequency of chemosensory discharges recorded along responses to hypoxic stimulation was transiently diminished in a dose-dependent manner by TNF-alpha injections.
  • The results suggest that the CB may operate as a sensor for immune signals, that the CB exhibits histological features of acute inflammation induced by LPS, that TNF-alpha may participate in LPS-induced changes in chemosensory activity and that some pathophysiological reactions to high levels of LPS in the bloodstream may originate from changes in CB function.
  • [MeSH-major] Carotid Body / metabolism. Carotid Body / pathology. Neuritis / metabolism. Neuritis / pathology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cats. Cell Movement / physiology. Disease Models, Animal. Electrophysiology. Inflammation / metabolism. Inflammation / physiopathology. Lipopolysaccharides. Male. Neutrophils / pathology. Pulmonary Ventilation / physiology. RNA, Messenger / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism

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  • [ErratumIn] Exp Physiol. 2012 May;97(5):687
  • (PMID = 18562477.001).
  • [ISSN] 0958-0670
  • [Journal-full-title] Experimental physiology
  • [ISO-abbreviation] Exp. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
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55. 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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56. Bevaart L, Goldstein J, Vitale L, Russoniello C, Treml J, Zhang J, Graziano RF, Leusen JH, van de Winkel JG, Keler T: Direct targeting of genetically modified tumour cells to Fc gammaRI triggers potent tumour cytotoxicity. Br J Haematol; 2006 Feb;132(3):317-25
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  • [Title] Direct targeting of genetically modified tumour cells to Fc gammaRI triggers potent tumour cytotoxicity.
  • Expression of the type I receptor for Fc domain of immunoglobulin (Ig)G (Fc gammaRI or CD64) is restricted to myeloid effector cells, such as monocytes, macrophages and a subset of dendritic cells.
  • Previous work has indicated a role for Fc gammaRI in antibody-dependent phagocytosis and lysis of tumour cells.
  • We hypothesised that tagging of tumour cells with an anti-Fc gammaRI single chain Fv (sFv) may facilitate targeting to this receptor on effector cells, thereby initiating tumour cytotoxicity.
  • Transfected tumour cells expressed high surface levels of functional H22-sFv, which greatly enhanced susceptibility for phagocytosis and lysis by monocytes and macrophages.
  • The expression of H22-sFv evoked the ability of tumour cells to directly activate monocytes, as evidenced by phosphorylation of mitogen-activated protein kinase and secretion of the inflammatory cytokines interleukin (IL)-1beta, tumour necrosis factor-alpha and IL-6.
  • Moreover, growth of tumour cells in mice expressing H22-sFv was profoundly delayed (or absent) in transgenic mice expressing human Fc gammaRI.
  • These results demonstrated that tumour cells can be readily modified to activate cell effector mechanisms, a strategy that may be useful for in vivo targeting in patients.
  • [MeSH-minor] Animals. Antibodies, Neoplasm / immunology. Cell Line, Tumor. Cytotoxicity, Immunologic / genetics. Cytotoxicity, Immunologic / immunology. Gene Expression Regulation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic / immunology. Genetic Vectors / genetics. Humans. Interleukin-1 / immunology. Interleukin-6 / immunology. Macrophages / immunology. Mice. Mice, Inbred C57BL. Monocytes / immunology. Phagocytosis / genetics. Phagocytosis / immunology. Phosphorylation. Protein Kinases / metabolism. Protein-Serine-Threonine Kinases / metabolism. Transfection. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 16409296.001).
  • [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 / Antibodies, Neoplasm; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Receptors, IgG; 0 / Tumor Necrosis Factor-alpha; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / MAK protein, human; EC 2.7.11.22 / Mak protein, mouse
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57. Hendriksen EM, Span PN, Schuuring J, Peters JP, Sweep FC, van der Kogel AJ, Bussink J: Angiogenesis, hypoxia and VEGF expression during tumour growth in a human xenograft tumour model. Microvasc Res; 2009 Mar;77(2):96-103
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  • [Title] Angiogenesis, hypoxia and VEGF expression during tumour growth in a human xenograft tumour model.
  • Tumour growth and spread of tumour cells requires angiogenesis.
  • Incipient angiogenesis is not induced by tumour cell hypoxia but probably by proangiogenic factors.
  • If the oxygen supply is insufficient, the resulting hypoxia stimulates angiogenesis through upregulation of HIF-1 alpha and VEGF.
  • The aim of the study was to analyze the interrelationship between hypoxia and angiogenesis during tumour growth.
  • Therefore the tumour vasculature architecture and functional properties of the vessels were studied during subsequent phases of tumour growth in relation to hypoxia and VEGF-expression.
  • Tumours from the human glioblastoma multiforme tumour line E106 were transplanted in athymic mice.
  • VEGF was present early in the onset of angiogenesis independent of HIF-1 alpha.
  • During tumour growth VEGF increased from 0.94 to 7.27 ng/mg assessed by ELISA.
  • The observation that tumour vasculature develops in early phases under normoxic and at later phases under hypoxic conditions with the presence of both conditions in the larger tumours, suggested that anti-angiogenic therapy should be directed towards HIF-1 alpha dependent and HIF 1-alpha independent pathways.
  • [MeSH-minor] Animals. Anoxia / metabolism. Anoxia / pathology. Blood Vessels / pathology. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / metabolism. Transplantation, Heterologous

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  • (PMID = 19118564.001).
  • [ISSN] 1095-9319
  • [Journal-full-title] Microvascular research
  • [ISO-abbreviation] Microvasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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58. Bruzzone A, Piñero CP, Castillo LF, Sarappa MG, Rojas P, Lanari C, Lüthy IA: Alpha2-adrenoceptor action on cell proliferation and mammary tumour growth in mice. Br J Pharmacol; 2008 Oct;155(4):494-504
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  • [Title] Alpha2-adrenoceptor action on cell proliferation and mammary tumour growth in mice.
  • BACKGROUND AND PURPOSE: Breast cancer, the most common cancer in women in most countries, is a highly stressful disease.
  • Catecholamines released during stress bind to adrenoceptors and we have recently described alpha(2)-adrenoceptors in human breast cell lines, linked to enhanced cell proliferation.
  • The purpose was to assess the in vivo effects of compounds acting on alpha(2)-adrenoceptors in a reliable model of breast cancer.
  • EXPERIMENTAL APPROACH: The expression of alpha(2)-adrenoceptors was confirmed by immunocytochemistry, immunofluorescence and reverse transcription-PCR in the mouse mammary tumour cell line MC4-L5.
  • KEY RESULTS: Incubation for 2 days with alpha(2)-adrenoceptor agonists (clonidine and dexmedetomidine) significantly enhanced proliferation of the mouse mammary tumour cell line MC4-L5.
  • These agonists also significantly stimulated tumour growth of the progestin-dependent tumour C4-HD even in the presence of medroxyprogesterone acetate (MPA).
  • In every tumour tested (C4-HD, CC4-2-HD and CC4-3-HI), regardless of MPA sensitivity, clonidine significantly enhanced tumour growth in the absence of MPA.
  • The alpha(2)-adrenoceptor antagonists, yohimbine and rauwolscine, completely reversed the effects of clonidine.
  • However, the group receiving yohimbine alone showed a nonsignificant but constant increase in tumour growth, whereas rauwolscine alone diminished tumour growth significantly, behaving as a reverse agonist.
  • CONCLUSIONS AND IMPLICATIONS: Alpha(2)-adrenoceptor agonists enhanced tumour growth and rauwolscine behaved in vivo as a reverse agonist, suggesting that it may be tested for adjuvant treatment.
  • [MeSH-major] Adrenergic alpha-2 Receptor Agonists. Adrenergic alpha-Agonists / pharmacology. Cell Proliferation / drug effects. Mammary Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Adrenergic alpha-2 Receptor Antagonists. Adrenergic alpha-Antagonists / pharmacology. Animals. Cell Line, Tumor. Clonidine / pharmacology. Dexmedetomidine / pharmacology. Drug Inverse Agonism. Female. Medroxyprogesterone Acetate / pharmacology. Mice. Mice, Inbred BALB C. Receptors, Adrenergic, alpha-2 / metabolism. Yohimbine / pharmacology

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  • (PMID = 18604234.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic alpha-2 Receptor Agonists; 0 / Adrenergic alpha-2 Receptor Antagonists; 0 / Adrenergic alpha-Agonists; 0 / Adrenergic alpha-Antagonists; 0 / Receptors, Adrenergic, alpha-2; 2Y49VWD90Q / Yohimbine; 67VB76HONO / Dexmedetomidine; C2QI4IOI2G / Medroxyprogesterone Acetate; MN3L5RMN02 / Clonidine
  • [Other-IDs] NLM/ PMC2579667
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59. Roeske JC, Stinchcomb TG: The average number of alpha-particle hits to the cell nucleus required to eradicate a tumour cell population. Phys Med Biol; 2006 May 7;51(9):N179-86
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  • [Title] The average number of alpha-particle hits to the cell nucleus required to eradicate a tumour cell population.
  • Alpha-particle emitters are currently being considered for the treatment of micrometastatic disease.
  • Based on in vitro studies, it has been speculated that only a few alpha-particle hits to the cell nucleus are considered lethal.
  • However, such estimates do not consider the stochastic variations in the number of alpha-particle hits, energy deposited, or in the cell survival process itself.
  • Using a tumour control probability (TCP) model for alpha-particle emitters, we derive an estimate of the average number of hits to the cell nucleus required to provide a high probability of eradicating a tumour cell population.
  • In simulation studies, our results demonstrate that the average number of hits required to achieve a 90% TCP for 10(4) clonogenic cells ranges from 18 to 108.
  • Those cells that have large cell nuclei, high radiosensitivities and alpha-particle emissions occurring primarily in the nuclei tended to require more hits.
  • As the clinical implementation of alpha-particle emitters is considered, this type of analysis may be useful in interpreting clinical results and in designing treatment strategies to achieve a favourable therapeutic outcome.
  • [MeSH-major] Alpha Particles / therapeutic use. Cell Nucleus / radiation effects. Cell Survival / radiation effects. Models, Biological. Neoplasms / physiopathology. Neoplasms / radiotherapy
  • [MeSH-minor] Animals. Computer Simulation. Dose-Response Relationship, Radiation. Humans. Radiotherapy Dosage. Tumor Cells, Cultured

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  • (PMID = 16625028.001).
  • [ISSN] 0031-9155
  • [Journal-full-title] Physics in medicine and biology
  • [ISO-abbreviation] Phys Med Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
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60. Sivaprasad U, Basu A: Inhibition of ERK attenuates autophagy and potentiates tumour necrosis factor-alpha-induced cell death in MCF-7 cells. J Cell Mol Med; 2008 Aug;12(4):1265-71
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  • [Title] Inhibition of ERK attenuates autophagy and potentiates tumour necrosis factor-alpha-induced cell death in MCF-7 cells.
  • The role of autophagy in cell death is under considerable debate.
  • The process of autophagy has been shown to lead to either cell survival or cell death depending on cell type and stimulus.
  • In the present study, we determined the contribution of ERK1/2 signalling to autophagy and cell death induced by tumour necrosis factor-alpha (TNF) in MCF-7 breast cancer cells.
  • Treatment of MCF-7 cells with TNF caused a time-dependent increase in ERK1/2 activity.
  • Pharmacological inhibition of ERK1/2 phosphorylation with U0126 or PD98059 resulted in a decrease in TNF-induced autophagy that was accompanied by an increase in cleavage of caspase-7, -8, -9 and PARP Furthermore, inhibition of ERK1/2 signalling resulted in decreased clonogenic capacity of MCF-7 cells.

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  • (PMID = 18266953.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA071727; United States / NCI NIH HHS / CA / CA71727
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Microtubule-Associated Proteins; 0 / Protein Kinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 0 / enhanced green fluorescent protein; 0 / light chain 3, human; 147336-22-9 / Green Fluorescent Proteins; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC3865671
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61. Morel S, Burnier L, Roatti A, Chassot A, Roth I, Sutter E, Galan K, Pfenniger A, Chanson M, Kwak BR: Unexpected role for the human Cx37 C1019T polymorphism in tumour cell proliferation. Carcinogenesis; 2010 Nov;31(11):1922-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unexpected role for the human Cx37 C1019T polymorphism in tumour cell proliferation.
  • Connexins are a large family of proteins that form gap junction channels allowing exchange of ions and small metabolites between neighboring cells.
  • They have been implicated in pathological processes such as tumourigenesis in which they may act as tumour suppressors.
  • In this study, we have used communication-deficient HeLa and SK-HEP-1 cells transfected with Cx37-319S, Cx37-319P or empty vector.
  • We showed that the expression of Cx37-319P limited proliferation of HeLa and SK-HEP-1 cells, whereas Cx37-319S expression was without effect.
  • Using an in vitro kinase assay, we demonstrated phosphorylation of Cx37 CT by glycogen synthase kinase-3 (GSK-3), a kinase known to be implicated in cell proliferation and cancer.
  • This latter effect on GJIC involved the beta and not the alpha isoform of GSK-3.
  • In contrast, GSK-3 inhibitors were without effect on HeLa cells expressing Cx37-319S.
  • In conclusion, our data indicate functional effects of the Cx37 C1019T polymorphism on GJIC that might contribute to tumour cell growth.
  • [MeSH-major] Cell Proliferation. Connexins / genetics. Neoplasms / genetics. Neoplasms / pathology. Polymorphism, Genetic / physiology
  • [MeSH-minor] Blotting, Western. Cell Communication. Cell Cycle. Fluorescent Antibody Technique. Gap Junctions. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Glycogen Synthase Kinase 3 / metabolism. HeLa Cells. Humans. Phosphorylation. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20705954.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Connexins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / connexin 37; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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62. Lankveld DP, Bull S, Van Dijk P, Fink-Gremmels J, Hellebrekers LJ: Ketamine inhibits LPS-induced tumour necrosis factor-alpha and interleukin-6 in an equine macrophage cell line. Vet Res; 2005 Mar-Apr;36(2):257-62
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  • [Title] Ketamine inhibits LPS-induced tumour necrosis factor-alpha and interleukin-6 in an equine macrophage cell line.
  • In horses, cytokines such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) play a pivotal role in the pathogenesis of equine endotoxaemia following gastrointestinal disorders.
  • Hence, the objective of this study was to assess the influence of ketamine on LPS-induced TNF-alpha and IL-6 formation in an equine macrophage cell line (eCAS cells).
  • The results demonstrate a cytokine-modulating activity of ketamine in an equine cell line, suggesting a beneficial role for ketamine in the treatment of equine endotoxaemia.
  • [MeSH-major] Anesthetics, Dissociative / pharmacology. Horses / immunology. Interleukin-6 / metabolism. Ketamine / pharmacology. Lipopolysaccharides / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Humans. Macrophages / drug effects. Macrophages / immunology

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  • (PMID = 15720977.001).
  • [ISSN] 0928-4249
  • [Journal-full-title] Veterinary research
  • [ISO-abbreviation] Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anesthetics, Dissociative; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 690G0D6V8H / Ketamine
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63. 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.
  • Normal tissue cultures from breast, prostate, renal and bronchial epithelia, small muscle cells, endothelial cells, hepatocytes and fibroblasts were tested accordingly.
  • 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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64. Murayama H, Takahashi M, Takamoto M, Shiba Y, Ise H, Koyama J, Tagawa Y, Iwakura Y, Ikeda U: Deficiency of tumour necrosis factor-alpha and interferon-gamma in bone marrow cells synergistically inhibits neointimal formation following vascular injury. Cardiovasc Res; 2008 Nov 1;80(2):175-80
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  • [Title] Deficiency of tumour necrosis factor-alpha and interferon-gamma in bone marrow cells synergistically inhibits neointimal formation following vascular injury.
  • Since it is now known that vascular injury involves an inflammatory response, we examined the role of tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the neointimal formation after injury.
  • METHODS AND RESULTS: Control (BALB/c), TNF-alpha-deficient (Tnf(-/-)), IFN-gamma-deficient (Ifng(-/-)), or double-deficient (Tnf(-/-)Ifng(-/-)) mice were subjected to wire-mediated vascular injury of the right femoral artery.
  • Immunohistochemical analysis showed that TNF-alpha and IFN-gamma were expressed in neointimal lesions in the control mice, but not in mice with deficiency of the corresponding cytokine.
  • The number of proliferating cell nuclear antigen in the neointimal lesions was significantly decreased in the Tnf(-/-)Ifng(-/-) mice.
  • Bone marrow transplantation experiments revealed that deficiency of TNF-alpha and IFN-gamma specifically in bone marrow cells significantly inhibited neointimal formation after vascular injury.
  • CONCLUSION: The absence of TNF-alpha and IFN-gamma in bone marrow cells synergistically inhibits neointimal formation following vascular injury, and thus, may provide new insights into the mechanisms underlying restenosis after PCI.
  • [MeSH-major] Arterial Occlusive Diseases / prevention & control. Bone Marrow Cells / immunology. Bone Marrow Transplantation. Cell Proliferation. Femoral Artery / pathology. Interferon-gamma / deficiency. Tumor Necrosis Factor-alpha / deficiency. Tunica Intima / pathology
  • [MeSH-minor] Animals. Constriction, Pathologic. Disease Models, Animal. Endothelial Cells / pathology. Macrophages / pathology. Male. Mice. Mice, Inbred BALB C. Mice, Knockout. Myocytes, Smooth Muscle / pathology

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  • (PMID = 18791204.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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65. Smith TG, Brooks JT, Balanos GM, Lappin TR, Layton DM, Leedham DL, Liu C, Maxwell PH, McMullin MF, McNamara CJ, Percy MJ, Pugh CW, Ratcliffe PJ, Talbot NP, Treacy M, Robbins PA: Mutation of von Hippel-Lindau tumour suppressor and human cardiopulmonary physiology. PLoS Med; 2006 Jul;3(7):e290
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  • [Title] Mutation of von Hippel-Lindau tumour suppressor and human cardiopulmonary physiology.
  • BACKGROUND: The von Hippel-Lindau tumour suppressor protein-hypoxia-inducible factor (VHL-HIF) pathway has attracted widespread medical interest as a transcriptional system controlling cellular responses to hypoxia, yet insights into its role in systemic human physiology remain limited.
  • Chuvash polycythaemia has recently been defined as a new form of VHL-associated disease, distinct from the classical VHL-associated inherited cancer syndrome, in which germline homozygosity for a hypomorphic VHL allele causes a generalised abnormality in VHL-HIF signalling.
  • [MeSH-major] Adaptation, Physiological / genetics. Altitude. Cardiovascular Physiological Phenomena. Hypoxia / physiopathology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Polycythemia / genetics. Respiratory Physiological Phenomena. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 16768548.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / ; United Kingdom / Medical Research Council / / G116/127
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 142M471B3J / Carbon Dioxide; E1UOL152H7 / Iron; EC 2.3.2.27 / Von Hippel-Lindau Tumor Suppressor Protein; EC 4.1.2.13 / Fructose-Bisphosphate Aldolase; EC 6.3.2.- / VHL protein, human; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC1479389
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66. Hutchison S, Choo-Kang BS, Bundick RV, Leishman AJ, Brewer JM, McInnes IB, Garside P: Tumour necrosis factor-alpha blockade suppresses murine allergic airways inflammation. Clin Exp Immunol; 2008 Jan;151(1):114-22
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  • [Title] Tumour necrosis factor-alpha blockade suppresses murine allergic airways inflammation.
  • Asthma is a heterogeneous disease that has been increasing in incidence throughout western societies and cytokines, including proinflammatory tumour necrosis factor alpha (TNF-alpha), have been implicated in the pathogenesis of asthma.
  • Anti-TNF-alpha therapies have been established successfully in the clinic for diseases such as rheumatoid arthritis and Crohn's disease.
  • TNF-alpha-blocking strategies are now being trialled in asthma; however, their mode of action is poorly understood.
  • Based on the observation that TNF-alpha induces lymph node hypertrophy we have attempted to investigate this as a mechanism of action of TNF-alpha in airway inflammation by employing two models of murine airway inflammation, that we have termed short and long models, representing severe and mild/moderate asthma, respectively.
  • In the short model, characterized by eosinophilic and neutrophilic airway inflammation the effect of TNF-alpha blockade was a reduction in draining lymph node (DLN) hypertrophy, eosinophilia, interleukin (IL)-5 production and immunoglobulin E (IgE) production.
  • In the long model, characterized by eosinophilic inflammation, TNF-alpha blockade produced a reduction in DLN hypertrophy and IL-5 production but had limited effects on eosinophilia and IgE production.
  • These results indicate that anti-TNF-alpha can suppress DLN hypertrophy and decrease airway inflammation.
  • Further investigations showed that anti-TNF-alpha-induced inhibition of DLN hypertrophy cannot be explained by preventing l-selectin-dependent capture of lymphocytes into the DLN.
  • Given that overall TNF blockade was able to suppress the short model (severe) more effectively than the long model (mild/moderate), the results suggest that TNF-alpha blocking therapies may be more effective in the treatment of severe asthma.
  • [MeSH-major] Asthma / immunology. Cytokines / immunology. Immunoglobulin G / therapeutic use. Lung / immunology. Receptors, Tumor Necrosis Factor / therapeutic use. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 17931392.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 9006-59-1 / Ovalbumin; OP401G7OJC / Etanercept
  • [Other-IDs] NLM/ PMC2276921
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67. Ierardi E, Meucci G, Hassan C, Zullo A, Imperiali G, De Francesco V, Panella C, Morini S, Minoli G: Tumour necrosis factor alpha in segmental colitis associated with diverticula. Dig Dis Sci; 2008 Jul;53(7):1865-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour necrosis factor alpha in segmental colitis associated with diverticula.
  • The pathogenesis of segmental colitis associated with diverticula (SCAD) is unclear, but tumour necrosis factor alpha (TNF-alpha) has been shown to play a pivotal role in the pathogenesis of inflammatory bowel diseases.
  • The aim of this study was to assess TNF-alpha levels in patients with SCAD.
  • In a post hoc analysis of a prospective multicenter study, tissue samples from 13 patients diagnosed with SCAD were subjected to histological analyses.
  • The severity of the inflammation was assessed by means of a histological score and histomorphometry (number of inflammatory cells/mm2).
  • Immunohistochemical staining with an antibody against TNF-alpha was performed on all biopsies and the degree of staining expressed as the percentage of positive stromal cells/1000 counted (TNF-alpha score).
  • Matched patients with irritable bowel syndrome (IBS) were used as controls.
  • Over-expression of TNF-alpha was found in all SCAD patients (38.6 +/- 10.4%), and it was associated with a high histological score (2.5 +/- 0.5) and neutrophil cell count (16.3 +/- 3/mm2).
  • Our data suggest that TNF-alpha activity is involved in SCAD pathogenesis, similarly to what occurs in Crohn's disease and ulcerative colitis.
  • [MeSH-major] Colitis / metabolism. Diverticulum / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18049899.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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68. Lan CC, Yu HS, Wu CS, Kuo HY, Chai CY, Chen GS: FK506 inhibits tumour necrosis factor-alpha secretion in human keratinocytes via regulation of nuclear factor-kappaB. Br J Dermatol; 2005 Oct;153(4):725-32

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  • [Title] FK506 inhibits tumour necrosis factor-alpha secretion in human keratinocytes via regulation of nuclear factor-kappaB.
  • The use of monoclonal antibody specific for tumour necrosis factor (TNF)-alpha has shown efficacy in treating both psoriasis and Crohn disease.
  • OBJECTIVES: To explore the effects of FK506 on human KCs in terms of TNF-alpha secretion and to investigate the regulatory pathway involved.
  • At indicated time points after UVB irradiation we determined: (i) the TNF-alpha concentrations present in the culture supernatants;.
  • (ii) the activation and translocation of nuclear factor (NF)-kappaB in the cell nucleus; and (iii) the protein expressions of IkappaB kinase (IKK) and IkappaB in the cell lysates.
  • RESULTS: Our results showed that FK506 dose-dependently downregulated the secretion of TNF-alpha from UVB-irradiated KCs.
  • CONCLUSIONS: Our results indicate that FK506 inhibits TNF-alpha secretion in human KCs via direct regulation of NF-kappaB.
  • [MeSH-major] Immunosuppressive Agents / pharmacology. Keratinocytes / drug effects. NF-kappa B / drug effects. Tacrolimus / pharmacology. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Adult. Animals. Cell Survival / drug effects. Cell Survival / radiation effects. Cells, Cultured. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Humans. I-kappa B Kinase / metabolism. Male. Mice. Mice, Inbred C3H. Skin / drug effects. Skin / pathology. Skin / radiation effects. Ultraviolet Rays

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  • (PMID = 16181452.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human; WM0HAQ4WNM / Tacrolimus
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69. Han X, Benight N, Osuntokun B, Loesch K, Frank SJ, Denson LA: Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Gut; 2007 Jan;56(1):73-81
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  • [Title] Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis.
  • BACKGROUND: Neutralisation of tumour necrosis factor alpha (TNFalpha) restores systemic growth hormone function in patients with Crohn's disease, and induces mucosal healing.
  • METHODS: Interleukin 10-deficient mice and wild-type controls received growth hormone or anti-TNFalpha antibody, and T84 human colon carcinoma cells were treated with TNFalpha or growth hormone.
  • Growth hormone activated STAT5, and directly reduced TNFalpha activation of NFkappaB, in T84 cells.
  • Up regulation of STAT5 and PPARgamma, either through neutralisation of TNFalpha or chronic administration of growth hormone, may exert an anti-inflammatory effect in inflammatory bowel disease.

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  • (PMID = 16777921.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058259; United States / NIDDK NIH HHS / DK / R01 DK068164; United States / NIDDK NIH HHS / DK / DK02700; United States / NIDDK NIH HHS / DK / DK068164; United States / NIDDK NIH HHS / DK / DK63956; United States / NIDDK NIH HHS / DK / R01 DK002700; United States / NIDDK NIH HHS / DK / R24 DK64403; United States / NIDDK NIH HHS / DK / K08 DK002700; United States / NIDDK NIH HHS / DK / R24 DK064403; United States / NIDDK NIH HHS / DK / R03 DK063956
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / PPAR gamma; 0 / Receptors, Somatotropin; 0 / Rela protein, mouse; 0 / STAT5 Transcription Factor; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 12629-01-5 / Human Growth Hormone; 130068-27-8 / Interleukin-10
  • [Other-IDs] NLM/ PMC1856672
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70. Boldrini L, Gisfredi S, Ursino S, Lucchi M, Melfi F, Mussi A, Basolo F, Fontanini G: Tumour necrosis factor-alpha: prognostic role and relationship with interleukin-8 and endothelin-1 in non-small cell lung cancer. Int J Mol Med; 2006 May;17(5):887-92
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  • [Title] Tumour necrosis factor-alpha: prognostic role and relationship with interleukin-8 and endothelin-1 in non-small cell lung cancer.
  • We evaluated the expression of the pleiotropic cytokine, tumour necrosis factor-alpha (TNF-alpha), by competitive PCR technique in 47 non-small cell lung cancer (NSCLC) cases and the impact of TNF-alpha on their clinical behaviour.
  • Using univariate analysis, our study demonstrated a positive correlation between high TNF-alpha expression and favourable prognosis in NSCLC in terms of overall survival and disease free interval (p=0.03 and 0.04, respectively) and TNF-alpha maintained its independent role in multivariate analysis.
  • TNF-alpha can stimulate the expression of many molecules, including interleukin-8 (IL-8) and endothelin-1 (ET-1); in our study, the expression of TNF-alpha was significantly associated with high IL-8 mRNA levels (p=0.008) and ET-1 mRNA positivity (p=0.03).
  • We suggested that TNF-alpha can induce ET-1 mRNA expression in NSCLC, similarly to IL-8 expression.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Endothelin-1 / genetics. Interleukin-8 / genetics. Lung Neoplasms / pathology. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16596276.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / Interleukin-8; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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71. Baran B, Bechyne I, Siedlar M, Szpak K, Mytar B, Sroka J, Laczna E, Madeja Z, Zembala M, Czyz J: Blood monocytes stimulate migration of human pancreatic carcinoma cells in vitro: the role of tumour necrosis factor - alpha. Eur J Cell Biol; 2009 Dec;88(12):743-52
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  • [Title] Blood monocytes stimulate migration of human pancreatic carcinoma cells in vitro: the role of tumour necrosis factor - alpha.
  • In some types of cancers, tumour-infiltrating monocytes/macrophages (TIM) may be responsible for the formation of an invasive microenvironment in a manner dependent on the secretion of soluble mediators such as tumour necrosis factor-alpha (TNF).
  • Human pancreatic carcinoma (HPC-4) cells are able to induce TNF production by monocytes.
  • Here, the effect of human peripheral blood monocytes, precursors of TIM, on the motility of co-cultured HPC-4 cells, was directly analysed in vitro.
  • A phenotypic transition, i.e., the appearance of rear-front polarised HPC-4 cells paralleled by their increased motility, and increased motility of monocytes, were observed.
  • This effect was attenuated when HPC-4 cells and monocytes were co-cultured in the presence of inhibitors of TNF production and anti-TNF monoclonal antibodies, indicating the specific role of this cytokine in determining paracrine loops between monocytes and cancer cells.
  • Moreover, exogenous TNF induced HPC-4 cell motility concomitantly to the appearance of cellular features characteristic for epithelial-mesenchymal transition (EMT) such as rear-front polarisation, rearrangements of the actin cytoskeleton characteristic for motile cells and the induction of Snail-1 expression.
  • Since cell movement is crucial for cancer invasion and the formation of metastases, these findings demonstrate an EMT-dependent mechanism of cancer progression which acts through the phenotypic transition of pancreatic cancer cells dependent on monocyte-derived TNF.
  • [MeSH-major] Cell Communication / physiology. Cell Movement / physiology. Leukocytes, Mononuclear / pathology. Pancreatic Neoplasms / pathology. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Cell Differentiation / physiology. Cell Line, Tumor. Cells, Cultured. Coculture Techniques. Humans

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  • (PMID = 19782426.001).
  • [ISSN] 1618-1298
  • [Journal-full-title] European journal of cell biology
  • [ISO-abbreviation] Eur. J. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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72. Geraldino TH, de Vito E, Custódio LA, Conchon-Costa I, Gaziri LC, Felipe I, Loyola W, Bonifácio KL: Increased tumour necrosis factor-alpha production, higher mannose receptor activity and ability to kill Candida by concanavalin-A-activated macrophages. FEMS Immunol Med Microbiol; 2010 Jun 1;59(1):11-7

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  • [Title] Increased tumour necrosis factor-alpha production, higher mannose receptor activity and ability to kill Candida by concanavalin-A-activated macrophages.
  • In a previous study, our group verified that mice pretreated with concanavalin-A (Con-A) produced more tumour necrosis factor (TNF)-alpha and presented greater Candida clearance from the peritoneal cavity, liver and spleen, which yielded a higher survival rate than control animals.
  • The ability of Con-activated macrophages to produce TNF-alpha, ingest via mannose receptors and kill all the isolates was significantly greater compared with PBS-treated macrophages, and activated macrophages exhibited a lower incidence of apoptosis, verified by binding to annexin V-fluorescein isothiocyanate.
  • The transition of yeast cells to filamentous forms during coincubation for 2 h with control macrophages was about 73-80%, whereas in the presence of Con-A-activated macrophages, it was 35-40%.
  • Our results suggest that a greater clearance of C. albicans infection through treatment with Con-A is probably due to the activation of macrophages, which produce more TNF-alpha, express more mannose receptors and are better endowed to kill ingested C. albicans.
  • [MeSH-major] Candida albicans / immunology. Concanavalin A / pharmacology. Immunologic Factors / pharmacology. Lectins, C-Type / metabolism. Macrophages, Peritoneal / immunology. Mannose-Binding Lectins / metabolism. Phagocytosis. Receptors, Cell Surface / metabolism. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 20236321.001).
  • [ISSN] 1574-695X
  • [Journal-full-title] FEMS immunology and medical microbiology
  • [ISO-abbreviation] FEMS Immunol. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Lectins, C-Type; 0 / Mannose-Binding Lectins; 0 / Receptors, Cell Surface; 0 / Tumor Necrosis Factor-alpha; 0 / mannose receptor; 11028-71-0 / Concanavalin A
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73. Pandey AK, Bhardwaj V, Datta M: Tumour necrosis factor-alpha attenuates insulin action on phosphoenolpyruvate carboxykinase gene expression and gluconeogenesis by altering the cellular localization of Foxa2 in HepG2 cells. FEBS J; 2009 Jul;276(14):3757-69
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  • [Title] Tumour necrosis factor-alpha attenuates insulin action on phosphoenolpyruvate carboxykinase gene expression and gluconeogenesis by altering the cellular localization of Foxa2 in HepG2 cells.
  • Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade.
  • The liver is critical in maintaining circulating glucose levels and, in a preliminary investigation using the human hepatoma (HepG2) cell line in this study, we demonstrated the role of TNFalpha in the regulation of this phenomenon and determined the underlying molecular mechanisms.
  • Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration.
  • Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells.
  • [MeSH-major] Carboxy-Lyases / genetics. Gene Expression Regulation, Enzymologic. Gluconeogenesis. Hepatocyte Nuclear Factor 3-beta / metabolism. Insulin / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Cell Line, Tumor. Enzyme Activation. Glucose / metabolism. Glucose-6-Phosphatase / genetics. Humans. Phosphorylation. Promoter Regions, Genetic. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics

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  • (PMID = 19769745.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXA2 protein, human; 0 / Insulin; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.9 / Glucose-6-Phosphatase; EC 4.1.1.- / Carboxy-Lyases; IY9XDZ35W2 / Glucose
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74. Gerlic M, Horowitz J, Farkash S, Horowitz S: The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane lipoproteins. Cell Microbiol; 2007 Jan;9(1):142-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane lipoproteins.
  • Mycoplasma have been shown to be involved in the alteration of several eukaryotic cell functions, such as cytokine production, gene expression and more.
  • We have previously reported that infection of human myelomonocytic U937 cell line with live Mycoplasma fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-alpha)-induced apoptosis.
  • A significant reduction in TNFalpha-induced apoptosis was demonstrated by stimulation of U937 cells with M. fermentans total proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with M. fermentans hydrophilic protein preparation (AqMf).
  • To investigate the mechanism of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane potential (delta psi m) was measured. M. fermentans total proteins LPMf and MALP-2, but not AqMf, inhibited the reduction of delta psi m.
  • NF-kappaB was transactivated in cells treated with M. fermentans lipoproteins, and was essential for host cell survival, but not for the inhibition of TNFalpha-induced apoptosis by LPMf.
  • Our results suggest that the inhibitory effect exerted by M. fermentans on TNFalpha-induced apoptosis in U937 cells is due to the membrane lipoproteins of these bacteria.
  • [MeSH-major] Apoptosis. Bacterial Proteins / metabolism. Lipoproteins / metabolism. Mycoplasma fermentans / chemistry. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Caspase 8 / metabolism. Humans. Lipopeptides. Membrane Potential, Mitochondrial. Membrane Proteins / metabolism. NF-kappa B / metabolism. Oligopeptides / metabolism. U937 Cells

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  • (PMID = 16889623.001).
  • [ISSN] 1462-5814
  • [Journal-full-title] Cellular microbiology
  • [ISO-abbreviation] Cell. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Lipopeptides; 0 / Lipoproteins; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / Oligopeptides; 0 / Tumor Necrosis Factor-alpha; 0 / macrophage stimulatory lipopeptide 2; EC 3.4.22.- / Caspase 8
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75. Kaim U, Moritz A, Failing K, Baumgärtner W: The regression of a canine Langerhans cell tumour is associated with increased expression of IL-2, TNF-alpha, IFN-gamma and iNOS mRNA. Immunology; 2006 Aug;118(4):472-82
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  • [Title] The regression of a canine Langerhans cell tumour is associated with increased expression of IL-2, TNF-alpha, IFN-gamma and iNOS mRNA.
  • Canine cutaneous histiocytoma is a benign epidermal neoplasm of Langerhans cell origin, which usually displays spontaneous regression.
  • Based on the degree of lymphocytic infiltration, 30 histiocytomas were classified into four groups representing different stages of tumour regression.
  • To elucidate further the mechanisms of the antitumour immune response CD3+, CD21+, CD4+, CD8+ and myeloid/histiocyte antigen+ inflammatory cells were differentiated by immunohistochemistry and quantified.
  • In addition, the number of apoptotic cells was detected using the TdT-mediated biotin-dUTP nick-end labelling (TUNEL) method.
  • Furthermore, the expression of interleukin- (IL-2), IL-12(p40), tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), IL-10 and transforming growth factor-beta (TGF-beta) as well as inducible nitric oxid synthase (iNOS) mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR).
  • Phenotyping of inflammatory cells revealed a significantly increased infiltration of all lymphocyte subsets and myeloid/histiocytic cells with the onset of tumour regression.
  • The latter was significantly correlated to up-regulation of IL-2, TNF-alpha, IFN-gamma and iNOS mRNA expression.
  • Expression of remaining cytokines and percentage of apoptotic cells showed no group-specific changes.
  • The results indicate an initial infiltration of CD4+ T cells followed by increased expression of Th1 cytokines and recruitment of antitumour effector cells as the principal mechanism for tumour regression.
  • Canine cutaneous histiocytoma is a unique example for an effective immune response in a naturally occurring neoplasm derived from epidermal Langerhans cells and might represent a valuable animal model to investigate tumour immunity.
  • [MeSH-minor] Animals. Apoptosis. Biomarkers. Cell Count. Dogs. Female. In Situ Nick-End Labeling. Interferon-gamma / genetics. Interleukin-2 / genetics. Langerhans Cells / immunology. Langerhans Cells / pathology. Macrophages / immunology. Macrophages / pathology. Male. Nitric Oxide Synthase Type II / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16764690.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cytokines; 0 / Interleukin-2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II
  • [Other-IDs] NLM/ PMC1782326
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76. Andersson AK, Rönnbäck L, Hansson E: Lactate induces tumour necrosis factor-alpha, interleukin-6 and interleukin-1beta release in microglial- and astroglial-enriched primary cultures. J Neurochem; 2005 Jun;93(5):1327-33
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  • [Title] Lactate induces tumour necrosis factor-alpha, interleukin-6 and interleukin-1beta release in microglial- and astroglial-enriched primary cultures.
  • This study investigated how treatment with NH4Cl and lactate, which increase in the brain as a consequence of hyperammonaemia, affects cells in primary rat cultures enriched in either astrocytes or microglia.
  • Release of the proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-1beta was measured using ELISA.
  • Lactate treatment altered astrocytic appearance, resulting in increased space between individual cells.
  • Lactate, but not NH4Cl, induced release of TNF-alpha and IL-6 in both astroglial- and microglial-enriched cultures, while IL-1beta was released only in microglial cultures.
  • Additionally, the astroglial-enriched cultures containing approximately 10% microglial cells released more cytokines than cultures containing about 5% microglial cells.
  • Taken together, our data suggest that most TNF-alpha, IL-6 and IL-1beta release comes from microglia.
  • [MeSH-major] Astrocytes / metabolism. Interleukin-1 / metabolism. Interleukin-6 / metabolism. Lactates / pharmacology. Microglia / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Ammonium Chloride / pharmacology. Animals. Cell Survival / drug effects. Cells, Cultured. Rats. Rats, Sprague-Dawley

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  • (PMID = 15934951.001).
  • [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 / Interleukin-1; 0 / Interleukin-6; 0 / Lactates; 0 / Tumor Necrosis Factor-alpha; 01Q9PC255D / Ammonium Chloride
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77. Williams RO: Paradoxical effects of tumour necrosis factor-alpha in adjuvant-induced arthritis. Arthritis Res Ther; 2008;10(3):113
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  • [Title] Paradoxical effects of tumour necrosis factor-alpha in adjuvant-induced arthritis.
  • Anti-tumour necrosis factor (TNF)alpha therapy is highly effective in rheumatoid arthritis and it is surprising, therefore, that a recent study showed that intraperitoneal administration of recombinant TNFalpha reduced the severity of adjuvant-induced arthritis and decreased IFNgamma expression in cultured draining lymph node cells.
  • Furthermore, in untreated arthritic rats, maximal TNFalpha expression in draining lymph node cells coincided with spontaneous disease remission, suggesting a role for endogenous TNFalpha in recovery from arthritis.
  • If confirmed in further studies, these findings suggest that, in addition to its well-established pro-inflammatory properties, TNFalpha may also play a disease-limiting role in this model of rheumatoid arthritis by suppressing effector T cell responses.
  • [MeSH-major] Arthritis, Experimental / therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 18564403.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antirheumatic Agents; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2483450
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78. Oldreive CE, Doherty GH: Effects of tumour necrosis factor-alpha on developing cerebellar granule and Purkinje neurons in vitro. J Mol Neurosci; 2010 Sep;42(1):44-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of tumour necrosis factor-alpha on developing cerebellar granule and Purkinje neurons in vitro.
  • Tumour necrosis factor-alpha (TNF-alpha) has been widely implicated in both neurodevelopment and neurodegeneration, yet its effects on individual populations of cerebellar neurons as they develop have not been fully elucidated.
  • Therefore, we established primary neuronal cultures of developing murine cerebellar Purkinje neurons and postnatal cerebellar granule cells to determine the consequences of TNF-alpha exposure for their survival.
  • We discovered that TNF-alpha did not affect the viability of cerebellar granule neurons at any of the ages studied, even though TNF-alpha and its receptors, TNFR1 and TNFR2, are widely expressed in the postnatal cerebellum.
  • In addition, TNF-alpha was neither able to ameliorate, nor enhance, cell death in cerebellar granule cells elicited by a variety of stimuli including homocysteine and alcohol exposure.
  • In contrast, in cultures established at embryonic day 16, TNF-alpha enhanced the number of cerebellar Purkinje neurons in vitro but this effect was not observed in embryonic day 19 cultures.
  • Thus, TNF-alpha has differential and highly specific effects on different populations of cerebellar neurons as they develop.
  • [MeSH-major] Cerebellum / cytology. Neurons / drug effects. Neurons / physiology. Purkinje Cells / drug effects. Purkinje Cells / physiology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cells, Cultured. Female. Mice. Mice, Inbred C57BL. Pregnancy. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism

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  • (PMID = 20419354.001).
  • [ISSN] 1559-1166
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBS/A/00021; United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tnfrsf1a protein, mouse; 0 / Tumor Necrosis Factor-alpha
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79. Golovko O, Nazarova N, Tuohimaa P: Vitamin D-induced up-regulation of tumour necrosis factor alpha (TNF-alpha) in prostate cancer cells. Life Sci; 2005 Jun 17;77(5):562-77
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  • [Title] Vitamin D-induced up-regulation of tumour necrosis factor alpha (TNF-alpha) in prostate cancer cells.
  • 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3 or calcitriol) is an active hormone that regulates cellular proliferation and induces apoptosis in cancer cells.
  • Here we report on a new calcitriol target gene in prostate cancer cells, tumour necrosis factor alpha (TNF-alpha).
  • Calcitriol and its analogue CB1093 up-regulate TNF-alpha mRNA expression in LNCaP and PC-3 cells.
  • The stimulation is dose-dependent in both of these cell lines, demonstrated by the quantitative real-time polymerase chain reaction.
  • Calcitriol and CB1093 act synergistically with human recombinant TNF-alpha in activation of TNF-alpha mRNA expression in LNCaP but not in PC-3 cells.
  • Transcriptional activation of TNF-alpha gene by calcitriol or CB1093 does not lead to TNF-alpha protein secretion, however calcitriol and CB1093 enhance TPA-stimulated TNF-alpha production in LNCaP cells.
  • Nor does calcitriol affect transcriptional regulation of cytokine (IL-1, IL-6) and cytokine receptor genes in LNCaP and PC-3 prostate cancer cell lines.
  • Calcitriol and its analogue CB1093 at 10 nM concentration induce programmed cell death in LNCaP cells.
  • Combined addition of human recombinant TNF-alpha with calcitriol or CB1093 cause enhanced effect in induction of apoptosis.
  • We conclude that under physiological conditions vitamin D activates only the transcription of TNF-alpha gene, for TNF-alpha protein synthesis additional cofactors are required.
  • Therefore a cooperation of vitamin D and TNF-alpha may play an important role in the control of cell growth in prostate cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Calcitriol / analogs & derivatives. Calcitriol / pharmacology. Calcium Channel Agonists / pharmacology. Prostatic Neoplasms / metabolism. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor / drug effects. Dose-Response Relationship, Drug. Humans. Male. RNA, Messenger / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism

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  • (PMID = 15904673.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CB 1093; 0 / Calcium Channel Agonists; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; FXC9231JVH / Calcitriol
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80. Buranawuti K, Boyle MP, Cheng S, Steiner LL, McDougal K, Fallin MD, Merlo C, Zeitlin PL, Rosenstein BJ, Mogayzel PJ Jr, Wang X, Cutting GR: Variants in mannose-binding lectin and tumour necrosis factor alpha affect survival in cystic fibrosis. J Med Genet; 2007 Mar;44(3):209-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variants in mannose-binding lectin and tumour necrosis factor alpha affect survival in cystic fibrosis.
  • OBJECTIVE: To determine if the genotype distribution of variants in three putative cystic fibrosis modifier genes (tumour necrosis factor alpha (TNFalpha), transforming growth factor beta1 (TGFbeta1) or mannose-binding lectin (MBL2)) differed among patients with cystic fibrosis grouped according to age and survival status.

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  • (PMID = 17158822.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL6618; United States / NHLBI NIH HHS / HL / HL71847; United States / NHLBI NIH HHS / HL / HL68927; United States / NHLBI NIH HHS / HL / K23 HL071847; United States / NHLBI NIH HHS / HL / R01 HL068927; United States / NIDDK NIH HHS / DK / R37 DK044003; United States / NIDDK NIH HHS / DK / DK44003; United States / NIDDK NIH HHS / DK / R01 DK044003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MBL2 protein, human; 0 / Mannose-Binding Lectin; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2598033
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81. Ek T, Mellander L, Abrahamsson J: Interferon gamma and tumour necrosis factor alpha in relation to anaemia and prognosis in childhood cancer. Acta Paediatr; 2005 Apr;94(4):435-7
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  • [Title] Interferon gamma and tumour necrosis factor alpha in relation to anaemia and prognosis in childhood cancer.
  • This study examined whether the initial plasma levels of tumour necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma) in 131 children with newly diagnosed cancer were associated with haematopoietic suppression, and whether plasma levels of TNFalpha or haemoglobin at diagnosis affects long-term prognosis in childhood acute lymphoblastic leukaemia (ALL).
  • [MeSH-major] Anemia / blood. Interferon-gamma / blood. Neoplasms / mortality. Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Child. Hemoglobins / analysis. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Prognosis

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  • (PMID = 16092457.001).
  • [ISSN] 0803-5253
  • [Journal-full-title] Acta paediatrica (Oslo, Norway : 1992)
  • [ISO-abbreviation] Acta Paediatr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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82. Assi K, Pillai R, Gómez-Muñoz A, Owen D, Salh B: The specific JNK inhibitor SP600125 targets tumour necrosis factor-alpha production and epithelial cell apoptosis in acute murine colitis. Immunology; 2006 May;118(1):112-21
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  • [Title] The specific JNK inhibitor SP600125 targets tumour necrosis factor-alpha production and epithelial cell apoptosis in acute murine colitis.
  • Stress-activated protein kinases (SAPKs) are activated in human inflammatory bowel disease (IBD).
  • Recently it has been demonstrated that p38MAPK (mitogen-activated protein kinase) inhibition using SB203580 is effective in reducing disease in both dextran sulphate sodium (DSS)-induced and 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced murine colitides, underscoring the importance of this pathway in gastrointestinal inflammation.
  • However, the contribution of c-Jun N-terminal kinase (JNK) in intestinal inflammation is unknown.
  • Based on the known involvement of JNK in tumour necrosis factor-alpha (TNF-alpha) expression and in mediating the effects of oxidant stress, we hypothesized that JNK inhibition would also affect colitis.
  • Both total colonic and mesenteric lymphocyte CD3/CD28-stimulated TNF-alpha levels were dramatically reduced under the same circumstances.
  • Immunofluorescence of the colon for the active form of JNK revealed a prominent signal arising from the infiltrating inflammatory cells.
  • Strikingly, we also demonstrate reduced epithelial cell apoptosis in response to treatment with SP600125.
  • [MeSH-major] Anthracenes / pharmacology. Apoptosis / drug effects. Colitis, Ulcerative / immunology. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Blotting, Western. Colon / immunology. Cytokines / metabolism. Dextran Sulfate. Disease Models, Animal. Epithelial Cells / pathology. Intestinal Mucosa / pathology. Macrophages / drug effects. Mice. Mice, Inbred C57BL. Signal Transduction / drug effects. Signal Transduction / immunology. Weight Loss / drug effects

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  • (PMID = 16630028.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracenes; 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; 9042-14-2 / Dextran Sulfate; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1782268
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83. Baj-Krzyworzeka M, Baran J, Weglarczyk K, Szatanek R, Szaflarska A, Siedlar M, Zembala M: Tumour-derived microvesicles (TMV) mimic the effect of tumour cells on monocyte subpopulations. Anticancer Res; 2010 Sep;30(9):3515-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour-derived microvesicles (TMV) mimic the effect of tumour cells on monocyte subpopulations.
  • BACKGROUND: Monocytes/macrophages may be affected by tumour cells via cell-to-cell contact, soluble factors and by tumour-derived microvesicles (TMV).
  • Moreover cytokine release and production of reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) by CD14(++)CD16(-) and CD14(+)CD16(++) cells after TMV stimulation was determined.
  • RESULTS: It was found that TMV are engulfed more efficiently by CD14(++)CD16(-) than CD14(+)CD16(++) cells.
  • TMV-activated CD14(++)CD16(-) cells produce more ROI and interleukin -10 (IL-10) than CD14(++)CD16(+).
  • CD14(+)CD16(++) cells following TMV stimulation showed an increased release of tumour necrosis factor alpha, IL-12p40 and RNI.
  • CONCLUSION: TMV significantly modulate biological activity of monocyte subsets with a pattern similar to tumour cells.
  • Therefore, TMV mimic the activating effect of tumour cells on monocytes as assessed by release of cytokines, ROI and RNI.
  • [MeSH-major] Cell Membrane / immunology. Monocytes / immunology. Neoplasms / immunology
  • [MeSH-minor] Cell Line, Tumor. Cell Separation. Cytokines / biosynthesis. Flow Cytometry. Humans. Macrophages / immunology. Microvessels / immunology

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  • (PMID = 20944131.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines
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84. Li G, Dong S, Qu J, Sun Z, Huang Z, Ye L, Liang H, Ai X, Zhang W, Chen X: Synergism of hydroxyapatite nanoparticles and recombinant mutant human tumour necrosis factor-alpha in chemotherapy of multidrug-resistant hepatocellular carcinoma. Liver Int; 2010 Apr;30(4):585-92
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  • [Title] Synergism of hydroxyapatite nanoparticles and recombinant mutant human tumour necrosis factor-alpha in chemotherapy of multidrug-resistant hepatocellular carcinoma.
  • Former studies have identified the multidrug-resistant nature and possible mechanisms of hepatoma cells both in vitro and in vivo.
  • METHODS: The treatment was exploited to inhibit the MDR cells by co-administration of the recombinant mutant human tumour necrosis factor-alpha (rmhTNF-alpha), a sublethal dose of chemicals [adriamycin (ADM), mitomycin and 5-FU] and hydroxyapatite nanoparticles (nHAPs).
  • RESULTS: The chemicals acted synergistically with rmhTNF-alpha and nHAP in suppressing the growth of hepatoma cells and inducing apoptosis of the cells, with the MDR phenotype reversed, as measured by intracellular ADM retention.
  • Analysis of mRNA and protein revealed that rmhTNF-alpha inhibited the gene expression of XIAP, survivin, Ki67, PCNA, MDR1 and BCRP to some extent.
  • CONCLUSIONS: rmhTNF-alpha was not only able to restore the chemotherapeutic sensitivity to HepG2/ADM, its xenograft model and clinical samples but also further inhibited the growth of these tumours by a combination of nHAP.
  • These results strongly suggested that chemicals in combination with rmhTNF-alpha and nHAP may be beneficial for the local treatment of advanced HCC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Hepatocellular / drug therapy. Drug Resistance, Multiple. Durapatite / pharmacology. Liver Neoplasms / drug therapy. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance, Neoplasm. Drug Synergism. Female. Genes, MDR / drug effects. Humans. Mice. Mice, Inbred BALB C. Multidrug Resistance-Associated Proteins / drug effects. Multidrug Resistance-Associated Proteins / genetics. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / genetics. Neoplasms, Experimental / pathology. Probability. RNA, Messenger / metabolism. Random Allocation. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Liver Int. 2010 Apr;30(4):496-8 [20456038.001]
  • (PMID = 19780956.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 91D9GV0Z28 / Durapatite
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85. Singh V, Singh SM: A tumour stage-dependent evolution of drug resistant T cell lymphoma: role of soluble mediators of tumour and host origin. Leuk Res; 2009 May;33(5):700-9
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  • [Title] A tumour stage-dependent evolution of drug resistant T cell lymphoma: role of soluble mediators of tumour and host origin.
  • The present investigation was carried out to investigate if soluble mediators present in tumour microenvironment and systemic circulation of a tumour-bearing host can regulate growth properties and response of the cells of a T cell lymphoma to chemotherapeutic drug: cisplatin, depending on the stage of tumour progression.
  • In order to investigate this, tumour cells of a murine T cell lymphoma, designated as Dalton's lymphoma (DL), were incubated in vitro for 48 h in the presence of ascitic fluid and serum obtained from cisplatin treated or untreated tumour hosts at early or late tumour-bearing stages and cell survival was estimated.
  • It was observed that tumour serum and ascitic fluid showed a tumour stage-dependent differential ability to regulate tumour cell survival and susceptibility of the tumour cells to the cytotoxic action of cisplatin.
  • A tumour stage-dependent qualitative and quantitative difference in the profile of cell survival regulating cytokines: IL-1, IL-2, IFN-gamma, TNF-alpha, VEGF and TGF-beta in the ascitic fluid and serum of the tumour-bearing host was observed to be associated with a tumour stage-dependent differential regulation of survival of tumour cells by modulation in the expression of growth regulating proteins: IL-2R, p53, CAD, Hsp70 and Bcl-2.
  • Further the result also showed that production of IL-1, TNF-alpha, and NO by macrophages could be implicated in the differential action of tumour sera on the altered survival responses of tumour cells depending on the stage of tumour growth.
  • Possible mechanisms involved in the tumour stage-dependent differential survival response of tumour cells and evolution of drug resistance are discussed.
  • The finding of this investigation will have clinical implications in designing of therapeutic strategies for T cell lymphoma based on manipulation of tumour growth regulatory mediators present in the tumour microenvironment.
  • [MeSH-major] Lymphoma, T-Cell / pathology
  • [MeSH-minor] Animals. Blood. Blotting, Western. Cell Survival. Cytokines / metabolism. Drug Resistance, Neoplasm. Electrophoresis, Polyacrylamide Gel. Enzyme-Linked Immunosorbent Assay. Mice. Mice, Inbred BALB C. Tumor Cells, Cultured

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  • (PMID = 18930317.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
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86. Kubo T, Sugita T, Shimose S, Matsuo T, Arihiro K, Ochi M: Expression of hypoxia-inducible factor-1alpha and its relationship to tumour angiogenesis and cell proliferation in cartilage tumours. J Bone Joint Surg Br; 2008 Mar;90(3):364-70
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  • [Title] Expression of hypoxia-inducible factor-1alpha and its relationship to tumour angiogenesis and cell proliferation in cartilage tumours.
  • The expression of HIF-1alpha, HIF-2alpha, proliferating cell nuclear antigen (PCNA) and microvessel density (MVD) were measured immunohistochemically in 29 specimens of cartilage tumour.
  • The tumour size (> or = 8 cm), histological grade (grade 2 and grade 3) surgical margin (marginal and intralesional) and HIF-1alpha expression (positive) correlated significantly with a shorter disease-free survival.
  • Our findings suggest that HIF-1alpha protein may be a useful objective marker in the assessment of the prognosis in chondrosarcoma, since it plays an important role in tumour angiogenesis and cell proliferation.
  • [MeSH-major] Biomarkers, Tumor / analysis. Chondrosarcoma / metabolism. Chondrosarcoma / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / analysis. Neoplasms, Connective Tissue / metabolism. Neoplasms, Connective Tissue / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Basic Helix-Loop-Helix Transcription Factors / analysis. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Proliferation. Disease-Free Survival. Female. Humans. Immunohistochemistry. Male. Microcirculation. Middle Aged. Neovascularization, Pathologic. Proliferating Cell Nuclear Antigen / analysis. Survival Analysis

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  • (PMID = 18310762.001).
  • [ISSN] 0301-620X
  • [Journal-full-title] The Journal of bone and joint surgery. British volume
  • [ISO-abbreviation] J Bone Joint Surg Br
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proliferating Cell Nuclear Antigen; 0 / endothelial PAS domain-containing protein 1
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87. Crocker IP, Wareing M, Ferris GR, Jones CJ, Cartwright JE, Baker PN, Aplin JD: The effect of vascular origin, oxygen, and tumour necrosis factor alpha on trophoblast invasion of maternal arteries in vitro. J Pathol; 2005 Aug;206(4):476-85
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  • [Title] The effect of vascular origin, oxygen, and tumour necrosis factor alpha on trophoblast invasion of maternal arteries in vitro.
  • Regulatory factors may include inherent vessel susceptibility, local oxygen levels and tumour necrosis factor alpha (TNFalpha).
  • [MeSH-major] Myometrium / blood supply. Omentum / blood supply. Oxygen / physiology. Trophoblasts / physiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Arteries. Cell Aggregation / physiology. Cell Differentiation / physiology. Cell Movement / physiology. Cells, Cultured. Coculture Techniques / methods. Endothelium, Vascular / physiology. Female. Humans. Microscopy, Electron / methods. Microscopy, Fluorescence / methods. Models, Biological. Muscle, Smooth, Vascular / physiology. Muscle, Smooth, Vascular / ultrastructure. Placenta / cytology. Placental Circulation / physiology. Placentation / physiology. Pregnancy. Pregnancy Trimester, First

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  • [Copyright] Copyright 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15940663.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; S88TT14065 / Oxygen
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88. Bekeredjian-Ding I, Schäfer M, Hartmann E, Pries R, Parcina M, Schneider P, Giese T, Endres S, Wollenberg B, Hartmann G: Tumour-derived prostaglandin E and transforming growth factor-beta synergize to inhibit plasmacytoid dendritic cell-derived interferon-alpha. Immunology; 2009 Nov;128(3):439-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour-derived prostaglandin E and transforming growth factor-beta synergize to inhibit plasmacytoid dendritic cell-derived interferon-alpha.
  • In previous studies we reported that plasmacytoid dendritic cells (PDC) infiltrating head and neck cancer tissue are functionally impaired, but the molecular basis for the functional deficiency remained unclear.
  • Here we demonstrate that tumour-derived prostaglandin E2 (PGE(2)) and transforming growth factor-beta (TGF-beta) increase interleukin-8 (IL-8) but synergistically inhibit interferon-alpha (IFN-alpha) and tumour necrosis factor (TNF) production of Toll-like receptor 7 (TLR7)- and Toll-like receptor 9 (TLR9)-stimulated PDC.
  • The contribution of tumour-derived TGF-beta was confirmed by the TGF-beta antagonist SB-431542.
  • Suppression of tumour-derived PGE(2) and TGF-beta restored TLR-induced IFN-alpha production of PDC.
  • Additionally, PGE(2)- and TGF-beta-treated PDC display a 'tolerogenic' phenotype because of a downregulation of CD40 accompanied by an upregulation of CD86.
  • Finally, in TLR-stimulated PDC, PGE(2) and TGF-beta reduce the CCR7:CXCR4 ratio, suggesting that PDC are impaired in their ability to migrate to tumour-draining lymph nodes but are retained in stromal cell-derived factor 1 (SDF-1)-expressing tissues.
  • Based on these data, cyclooxygenase inhibitors and TGF-beta antagonists may improve TLR7- and TLR9-based tumour immunotherapy.
  • [MeSH-major] Dendritic Cells / drug effects. Dinoprostone / pharmacology. Head and Neck Neoplasms / immunology. Receptors, CCR7 / biosynthesis. Transforming Growth Factor beta / pharmacology
  • [MeSH-minor] Antigens, CD40 / biosynthesis. Antigens, CD40 / genetics. Antigens, CD86 / biosynthesis. Antigens, CD86 / genetics. Benzamides / pharmacology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / immunology. Cyclooxygenase Inhibitors / pharmacology. Dioxoles / pharmacology. Humans. Interferon-alpha / secretion. Receptors, CXCR4 / biosynthesis. Receptors, CXCR4 / genetics. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 20067543.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Antigens, CD40; 0 / Antigens, CD86; 0 / Benzamides; 0 / CCR7 protein, human; 0 / CXCR4 protein, human; 0 / Cyclooxygenase Inhibitors; 0 / Dioxoles; 0 / Interferon-alpha; 0 / Receptors, CCR7; 0 / Receptors, CXCR4; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2770691
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89. Jarai R, Kaun C, Weiss TW, Speidl WS, Rychli K, Maurer G, Huber K, Wojta J: Human cardiac fibroblasts express B-type natriuretic peptide: fluvastatin ameliorates its up-regulation by interleukin-1alpha, tumour necrosis factor-alpha and transforming growth factor-beta. J Cell Mol Med; 2009 Nov-Dec;13(11-12):4415-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human cardiac fibroblasts express B-type natriuretic peptide: fluvastatin ameliorates its up-regulation by interleukin-1alpha, tumour necrosis factor-alpha and transforming growth factor-beta.
  • We treated cultured human adult cardiac fibroblasts (HACF) with 2000 U/ml tumour necrosis factor-alpha (TNF-alpha), 200 U/ml interleukin-1alpha (IL-1alpha) or 50 ng/ml transforming growth factor-beta (TGF-beta) in the presence or absence of 500 nM fluvastatin.
  • Treatment of HACF with TNF-alpha, IL-1alpha or TGF-beta significantly increased Nt-proBNP levels compared with untreated cells.
  • [MeSH-major] Fatty Acids, Monounsaturated / pharmacology. Fibroblasts / metabolism. Indoles / pharmacology. Interleukin-1alpha / pharmacology. Myocardium / cytology. Transforming Growth Factor beta / pharmacology. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects

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  • (PMID = 19228263.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fatty Acids, Monounsaturated; 0 / Indoles; 0 / Interleukin-11; 0 / Interleukin-1alpha; 0 / Interleukin-6; 0 / Leukemia Inhibitory Factor; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / pro-brain natriuretic peptide (1-76); 106956-32-5 / Oncostatin M; 114471-18-0 / Natriuretic Peptide, Brain; 4L066368AS / fluvastatin
  • [Other-IDs] NLM/ PMC4515057
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90. Campos Alberto EJ, Shimojo N, Aoyagi M, Kohno Y: Differential effects of tumour necrosis factor-alpha and interleukin-12 on isopentenyl pyrophosphate-stimulated interferon-gamma production by cord blood Vgamma9 T cells. Immunology; 2009 Jun;127(2):171-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential effects of tumour necrosis factor-alpha and interleukin-12 on isopentenyl pyrophosphate-stimulated interferon-gamma production by cord blood Vgamma9 T cells.
  • Lower numbers of Vgamma9Vdelta2 T cells in cord blood (CB) than in adult peripheral blood (PB), as well as their impaired ability to produce interferon-gamma (IFN-gamma) in response to stimulation, are associated with functional deficiency in the immune system in newborns.
  • In this study, we stimulated CB Vgamma9 T cells with their T-cell receptor-specific ligand, isopentenyl pyrophosphate (IPP), plus exogenous costimulatory cytokines such as interleukin-2 (IL-2), IL-12 and tumour necrosis factor-alpha (TNF-alpha), which are known to play important roles in the activation of PB gammadelta T cells.
  • Our data show that CB Vgamma9 T cells are able to produce IFN-gamma at levels comparable to PB Vgamma9 T cells by the addition of TNF-alpha in the presence of IPP and IL-2; however, under the same culture conditions, IL-12 does not efficiently activate CB Vgamma9 T cells to produce IFN-gamma.
  • The frequency of TNF-alpha receptor II-positive Vgamma9T cells and the expression levels of TNF-alpha receptor II are similar in CB and PB; in contrast, the frequency of IL-12 receptor betaI (IL-12RbetaI) -positive Vgamma9T cells and expression levels of IL-12RbetaI are significantly lower in CB than PB.
  • TNF-alpha but not IL-12 increases the expression of IL-2Rbeta on CB Vgamma9 T cells.
  • These results provide new insights into the role of TNF-alpha in the activation of CB Vgamma9 T cells.
  • [MeSH-major] Fetal Blood / immunology. Interferon-gamma / biosynthesis. Interleukin-12 / immunology. T-Lymphocyte Subsets / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Adult. Cells, Cultured. Hemiterpenes / immunology. Humans. Infant, Newborn. Lymphocyte Activation / immunology. Middle Aged. Organophosphorus Compounds / immunology. Receptors, Antigen, T-Cell, gamma-delta / blood

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  • (PMID = 19019091.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemiterpenes; 0 / Organophosphorus Compounds; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 358-71-4 / isopentenyl pyrophosphate; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2691782
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91. Giatromanolaki A, Koukourakis MI, Sivridis E, Chlouverakis G, Vourvouhaki E, Turley H, Harris AL, Gatter KC: Activated VEGFR2/KDR pathway in tumour cells and tumour associated vessels of colorectal cancer. Eur J Clin Invest; 2007 Nov;37(11):878-86
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  • [Title] Activated VEGFR2/KDR pathway in tumour cells and tumour associated vessels of colorectal cancer.
  • BACKGROUND: Vascular endothelial cell growth factor (VEGF) acts by phosphorylating specific tyrosine kinase receptors on endothelial cell membrane promoting angiogenesis.
  • RESULTS: pVEGFR2/KDR was weakly expressed in the normal colon, but it was expressed strongly in the cytoplasm and nuclei of cancer cells and in the tumour associated vasculature, mainly at the invading tumour edge. pVEGFR2/KDR expression in cancer cells was significantly associated with a tumour diameter > 6 cm (P = 0.04), poor histological differentiation (P = 0.004) and with high CEF1alpha expression (P = 0.05).
  • High pVEGFR2/KDR expressing vascular density was significantly related with a high VEGF and HIF1alpha expression in cancer cells (P = 0.02 and 0.03, respectively).
  • This was also related significantly to high pVEGFR2/KDR expression in cancer cells.
  • CONCLUSIONS: pVEGFR2 receptors are largely expressed in colon cancer cells and intratumoural vasculature.
  • [MeSH-major] Adenocarcinoma / metabolism. Cell Differentiation / physiology. Colorectal Neoplasms / diagnosis. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Survival Rate

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  • (PMID = 17883421.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [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; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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92. Davis JR, McNeilly JR, Norris AJ, Pope C, Wilding M, McDowell G, Holland JP, McNeilly AS: Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis. Clin Endocrinol (Oxf); 2006 Nov;65(5):648-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis.
  • OBJECTIVE: The pathogenesis of human pituitary adenomas remains unclear, but we report a case of FSH-secreting pituitary adenoma whose monohormonal phenotype suggests it was of fetal origin.
  • MEASUREMENTS: Endocrine studies were performed before and after curative surgery, with assessment of tumour hormone secretion in vitro, and immunostaining of tumour tissue for a series of gonadotrope proteins.
  • RESULTS: Immunocytochemistry showed that tumour cells were monohormonal for FSH.
  • Normal components of gonadotrope signalling pathways were expressed, including oestrogen receptor-alpha, activin receptors, secretogranin-II and chromogranin-A. beta-glycan, the putative inhibin coreceptor, was absent.
  • Tumour culture in vitro confirmed secretion of FSH with minimal LH, that was unsuppressed by oestradiol or inhibin-A.
  • Human fetal pituitary tissue contained FSH-only cells at 18 weeks gestation, whereas normal adult pituitary tissue contained only bihormonal gonadotropes.
  • CONCLUSIONS: We propose that this pituitary adenoma represents an indolent tumour of monohormonal fetal gonadotrope cells that originated early in gestation.
  • Pituitary tumours may therefore arise from abnormal persistence of fetal cell types, with extremely slow growth over many years until reaching a size threshold to generate an endocrine syndrome.
  • Understanding fetal pituitary architecture and function may be more informative for new insights into pituitary tumour pathogenesis than classical theories of cancer biology that invoke unrestrained cell proliferation.
  • [MeSH-major] Adenoma / embryology. Gonadotrophs / secretion. Pituitary Neoplasms / embryology
  • [MeSH-minor] Adult. Estradiol / blood. Female. Follicle Stimulating Hormone / analysis. Follicle Stimulating Hormone / blood. Follicle Stimulating Hormone / secretion. Humans. Immunohistochemistry / methods. Immunoradiometric Assay / methods. Luteinizing Hormone / blood. Pituitary Gland, Anterior / embryology. Pituitary Gland, Anterior / secretion. Polycystic Ovary Syndrome / blood. Polycystic Ovary Syndrome / embryology. Polycystic Ovary Syndrome / etiology. Tissue Culture Techniques

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  • (PMID = 17054468.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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93. Song S, Zhang K, You H, Wang J, Wang Z, Yan C, Liu F: Significant anti-tumour activity of adoptively transferred T cells elicited by intratumoral dendritic cell vaccine injection through enhancing the ratio of CD8(+) T cell/regulatory T cells in tumour. Clin Exp Immunol; 2010 Oct;162(1):75-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significant anti-tumour activity of adoptively transferred T cells elicited by intratumoral dendritic cell vaccine injection through enhancing the ratio of CD8(+) T cell/regulatory T cells in tumour.
  • We have shown that immunization with dendritic cells (DCs) pulsed with hepatitis B virus core antigen virus-like particles (HBc-VLP) packaging with cytosine-guanine dinucleotide (CpG) (HBc-VLP/CpG) alone were able to delay melanoma growth but not able to eradicate the established tumour in mice.
  • We tested whether, by modulating the vaccination approaches and injection times, the anti-tumour activity could be enhanced.
  • We used a B16-HBc melanoma murine model not only to compare the efficacy of DC vaccine immunized via footpads, intravenously or via intratumoral injections in treating melanoma and priming tumour-specific immune responses, but also to observe how DC vaccination could improve the efficacy of adoptively transferred T cells to induce an enhanced anti-tumour immune response.
  • Our results indicate that, although all vaccination approaches were able to protect mice from developing melanoma, only three intratumoral injections of DCs could induce a significant anti-tumour response.
  • Furthermore, the combination of intratumoral DC vaccination and adoptive T cell transfer led to a more robust anti-tumour response than the use of each treatment individually by increasing CD8(+) T cells or the ratio of CD8(+) T cell/regulatory T cells in the tumour site.
  • Moreover, the combination vaccination induced tumour-specific immune responses that led to tumour regression and protected surviving mice from tumour rechallenge, which is attributed to an increase in CD127-expressing and interferon-γ-producing CD8(+) T cells.
  • Taken together, these results indicate that repeated intratumoral DC vaccination not only induces expansion of antigen-specific T cells against tumour-associated antigens in tumour sites, but also leads to elimination of pre-established tumours, supporting this combined approach as a potent strategy for DC-based cancer immunotherapy.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Dendritic Cells / immunology. Immunotherapy, Adoptive / methods. Melanoma, Experimental / therapy. T-Lymphocytes / transplantation. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Animals. CD4-CD8 Ratio. Cancer Vaccines / administration & dosage. Cancer Vaccines / immunology. Cell Line, Tumor. Combined Modality Therapy. Dinucleoside Phosphates / immunology. Hepatitis B Core Antigens / immunology. Interferon-gamma / immunology. Interferon-gamma / metabolism. Interleukin-7 Receptor alpha Subunit / immunology. Interleukin-7 Receptor alpha Subunit / metabolism. Mice. Mice, Inbred C57BL. Time Factors. Vaccination / methods

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  • [Copyright] © 2010 The Authors. Clinical and Experimental Immunology © 2010 British Society for Immunology.
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  • (PMID = 20735440.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Dinucleoside Phosphates; 0 / Hepatitis B Core Antigens; 0 / Interleukin-7 Receptor alpha Subunit; 2382-65-2 / cytidylyl-3'-5'-guanosine; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2990932
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94. Carli CB, de Matos DC, Lopes FC, Maia DC, Dias MB, Sannomiya M, Rodrigues CM, Andreo MA, Vilegas W, Colombo LL, Carlos IZ: Isolated flavonoids against mammary tumour cells LM2. Z Naturforsch C; 2009 Jan-Feb;64(1-2):32-6
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  • [Title] Isolated flavonoids against mammary tumour cells LM2.
  • The antitumour activity was measured by the MTT assay in murine mammary tumour cells (LM2) and the IC50 values of the flavonoids tested ranged from (31.5 +/- 2.97) to (203.1 +/- 5.9) microg/ml.
  • The flavonoids 1 (myricetin-3-O-alpha-L-rhamnopyranoside) and 3 (quercetin-3-O-galactopyranoside) from D. elliptica were the most active ones against the tumour cells.
  • The same samples were tested to determine the inhibition of the release of nitric oxide (NO) and of the tumour necrosis factor-alpha (TNF-alpha) in murine macrophages by the Griess and ELISA sandwich assay, respectively.
  • Almost all the samples showed inhibitory activity to the release of NO but not of TNF-alpha.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Cisplatin / pharmacology. Female. Malpighiaceae. Mice. Mice, Inbred BALB C. Myrtaceae

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  • (PMID = 19323263.001).
  • [ISSN] 0939-5075
  • [Journal-full-title] Zeitschrift für Naturforschung. C, Journal of biosciences
  • [ISO-abbreviation] Z. Naturforsch., C, J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavonoids; Q20Q21Q62J / Cisplatin
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95. Gu Y, Hu X, Liu C, Qv X, Xu C: Interleukin (IL)-17 promotes macrophages to produce IL-8, IL-6 and tumour necrosis factor-alpha in aplastic anaemia. Br J Haematol; 2008 Jul;142(1):109-14
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  • [Title] Interleukin (IL)-17 promotes macrophages to produce IL-8, IL-6 and tumour necrosis factor-alpha in aplastic anaemia.
  • Aplastic anaemia (AA) is thought to be an autoimmune-mediated disease with active destruction of haematopoietic cells through a T helper type 1 (Th1) cell response.
  • Interleukin (IL)-17 is a potent proinflammatory cytokine produced by activated memory T cells.
  • Recent studies indicate that IL-17 might be an essential effector cytokine in the T-cell mediated autoimmune process.
  • It can drive the production of tumour necrosis factor-alpha (TNF-alpha), IL-1 beta, IL-6 and IL-8 by a variety of cells.
  • AA patients showed an elevated expression of IL17A mRNA in bone marrow mononuclear cells and peripheral blood mononuclear cells.
  • IL-17 stimulation also resulted in the production of TNF-alpha.
  • These results suggested that elevated expression of IL-17 and IL-17-induced IL-6, IL-8 and TNF-alpha may be involved in the mechanisms of AA.
  • [MeSH-major] Anemia, Aplastic / metabolism. Interleukin-17 / pharmacology. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis. Macrophages / metabolism. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Cells, Cultured. Female. Humans. Male. Middle Aged. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation. Young Adult

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  • (PMID = 18477039.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-17; 0 / Interleukin-6; 0 / Interleukin-8; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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96. Houghton-Triviño N, Salgado DM, Rodríguez JA, Bosch I, Castellanos JE: Levels of soluble ST2 in serum associated with severity of dengue due to tumour necrosis factor alpha stimulation. J Gen Virol; 2010 Mar;91(Pt 3):697-706
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  • [Title] Levels of soluble ST2 in serum associated with severity of dengue due to tumour necrosis factor alpha stimulation.
  • The interleukin-1 receptor-like-1 protein (IL1RL1), also known as ST2, has been shown previously to regulate T-cell function and is produced by T cells and endothelial cells.
  • It was reported recently to be elevated in mild dengue patients during acute disease.
  • The RNA expression of ST2 was evaluated by real-time quantitative RT-PCR using patients' peripheral blood mononuclear cells (PBMCs) and in vitro using human umbilical vein endothelial cells (HUVECs) exposed to sera from dengue patients.
  • DHF patients had higher levels of serum sST2, tumour necrosis factor alpha (TNF-alpha), interleukin (IL)-8 and IL-10 compared with DF patients and normal healthy control individuals.
  • Neutralization of TNF-alpha in patient sera by pre-treatment with a TNF-alpha antibody inhibited the upregulation of sST2 expression in HUVECs.
  • These results implicate serum TNF-alpha in the modulation of expression of sST2 in an in vitro system, and indicate that sST2 could be associated with the severity of disease.
  • Further studies to determine whether sST2 levels are predictive of the severe form of the disease and the role of sST2 in immune regulation are warranted.
  • [MeSH-major] Dengue / immunology. Dengue / pathology. Receptors, Cell Surface / blood. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Adolescent. Adult. Biomarkers. Cell Line. Cells, Cultured. Child. Child, Preschool. Endothelial Cells / immunology. Enzyme-Linked Immunosorbent Assay / methods. Female. Gene Expression Profiling. Humans. Leukocytes, Mononuclear / immunology. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction / methods. Serum / chemistry. Young Adult

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  • (PMID = 19889931.001).
  • [ISSN] 1465-2099
  • [Journal-full-title] The Journal of general virology
  • [ISO-abbreviation] J. Gen. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / IL1RL1 protein, human; 0 / Receptors, Cell Surface; 0 / Tumor Necrosis Factor-alpha
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97. Guruvayoorappan C, Kuttan G: (+)-Catechin inhibits tumour angiogenesis and regulates the production of nitric oxide and TNF-alpha in LPS-stimulated macrophages. Innate Immun; 2008 Jun;14(3):160-74
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  • [Title] (+)-Catechin inhibits tumour angiogenesis and regulates the production of nitric oxide and TNF-alpha in LPS-stimulated macrophages.
  • In vivo angiogenic activity was studied using B16F-10 melanoma cell-induced capillary formation in C57BL/6 mice.
  • Administration of (+)-catechin significantly inhibited (36.09%) the number of tumour-directed capillaries induced by injecting B16F-10 melanoma cells on the ventral side of C57BL/6 mice.
  • The cytokine profile in the serum of these animals showed a drastically increased level of proinflammatory cytokines such as IL-1 beta, IL-6, TNF-alpha, GM-CSF and the direct endothelial cell proliferating agent, VEGF.
  • In vitro L929 bioassay revealed the inhibition of TNF-alpha production by (+)-catechin treatment.
  • In the rat aortic ring assay, (+)-catechin inhibited the microvessel outgrowth at non-toxic concentrations. (+)-Catechin at non-toxic concentrations (5-25 microg/ml) showed significant inhibition in the proliferation, migration and tube formation of endothelial cells, which are the key events in the process of angiogenesis. (+)-Catechin also showed inhibitory effect on VEGF mRNA levels in B16F-10 melanoma cells. (+)-Catechin inhibited the production of NO and TNF-alpha in LPS-stimulated primary macrophages.
  • Taken together, these results demonstrate that (+)-catechin inhibits tumour-specific angiogenesis by regulating the production of pro- and anti-angiogenic factors such as pro-inflammatory cytokines, nitric oxide, VEGF, IL-2 and TIMP-1.
  • These results also suggest that (+)-catechin could significantly inhibit nitrite and TNF-alpha production in LPS-stimulated macrophages.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Catechin / pharmacology. Lipopolysaccharides / pharmacology. Macrophages / drug effects. Macrophages / metabolism. Nitric Oxide / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Aorta / cytology. Aorta / drug effects. Cell Movement / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Endothelial Cells / cytology. Endothelial Cells / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Interleukin-2 / metabolism. Male. Mice. Neoplasm Transplantation. Neoplasms / blood supply. Neoplasms / genetics. Neoplasms / metabolism. Neoplasms / pathology. Nitrites / blood. RNA, Messenger / genetics. Rats. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 18562575.001).
  • [ISSN] 1753-4259
  • [Journal-full-title] Innate immunity
  • [ISO-abbreviation] Innate Immun
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Interleukin-2; 0 / Lipopolysaccharides; 0 / Nitrites; 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 31C4KY9ESH / Nitric Oxide; 8R1V1STN48 / Catechin
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98. Zhou P, Li E, Shea-Donohue T, Singer SM: Tumour necrosis factor alpha contributes to protection against Giardia lamblia infection in mice. Parasite Immunol; 2007 Jul;29(7):367-74
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  • [Title] Tumour necrosis factor alpha contributes to protection against Giardia lamblia infection in mice.
  • Effective control of Giardia infections in mice has been shown to involve IgA, T cells, mast cells and IL-6.
  • We now show that Tumour necrosis factor alpha (TNFalpha) also plays an important role in the early control of giardiasis.
  • However, anti-parasite IgA levels, mast cell responses, and IL-4 and IL-6 mRNA levels do not appear significantly altered in the absence of TNFalpha.

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  • (PMID = 17576366.001).
  • [ISSN] 0141-9838
  • [Journal-full-title] Parasite immunology
  • [ISO-abbreviation] Parasite Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI-049565; United States / NIAID NIH HHS / AI / AI/DK-049316; United States / NIAID NIH HHS / AI / R01 AI049565-05; United States / NIAID NIH HHS / AI / R01 AI049316; United States / NIDDK NIH HHS / DK / R01 DK049316; United States / NIAID NIH HHS / AI / R01 AI049565
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS53599; NLM/ PMC2443547
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99. Poiana C, Virtej I, Carsote M, Banceanu G, Sajin M, Stanescu B, Ioachim D, Hortopan D, Coculescu M: Virilising Sertoli-Leydig cell tumour associated with thyroid papillary carcinoma: case report and general considerations. Gynecol Endocrinol; 2010 Aug;26(8):617-22
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  • [Title] Virilising Sertoli-Leydig cell tumour associated with thyroid papillary carcinoma: case report and general considerations.
  • We present a case of a Sertoli-Leydig cell tumour manifested with progressive hirsutism, frontal alopecia and secondary amenorrhea in a 46-years-old female, evolving for 6 years until presentation.
  • The histopathological report mentioned a Sertoli-Leydig cell tumor with intermediate grade of differentiation.
  • Immunohistochemical stains showed positive reaction for alpha-inhibin, calretin and for progesterone receptor.
  • At 6 months follow-up the diagnosis of a left lobe thyroid nodule leaded to fine needle aspiration biopsy with suspicion of papillary carcinoma.
  • Total thyroidectomy established the diagnosis of thyroid papillary carcinoma (2.17/2.18 cm) T2N0M0, stage II, followed by radioiodine administration.
  • This is to our knowledge the first presented case of ovarian Sertoli-Leydig cell tumour associated with papillary thyroid carcinoma.
  • [MeSH-major] Carcinoma, Papillary / complications. Hirsutism / etiology. Ovarian Neoplasms / complications. Sertoli-Leydig Cell Tumor / complications. Thyroid Neoplasms / complications

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  • (PMID = 20632913.001).
  • [ISSN] 1473-0766
  • [Journal-full-title] Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
  • [ISO-abbreviation] Gynecol. Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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100. Hosokawa I, Hosokawa Y, Ozaki K, Nakae H, Matsuo T: Adrenomedullin suppresses tumour necrosis factor alpha-induced CXC chemokine ligand 10 production by human gingival fibroblasts. Clin Exp Immunol; 2008 Jun;152(3):568-75

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenomedullin suppresses tumour necrosis factor alpha-induced CXC chemokine ligand 10 production by human gingival fibroblasts.
  • Periodontal disease is an inflammatory disorder characterized by the involvement of chemokines that are important for the recruitment of leucocytes.
  • Several cytokines, including tumour necrosis factor alpha (TNF-alpha), are involved in regulating levels of chemokines in periodontal disease.
  • CXC chemokine ligand 10 (CXCL10) is a chemokine related to the migration of T helper 1 cells.
  • We revealed that TNF-alpha stimulation induced CXCL10 production by HGFs.
  • AM treatment supressed CXCL10 production by TNF-alpha-stimulated HGFs.
  • TNF-alpha treatment enhanced CRLR and RAMP2 mRNA expression in HGFs.
  • These results suggest that the CXCL10 produced by HGFs may be involved in the migration of leucocytes into inflamed tissues and related to exacerbation of periodontal disease.
  • AM might be a therapeutic target of periodontal disease, because AM can inhibit CXCL10 production by HGFs.
  • [MeSH-major] Adrenomedullin / pharmacology. Chemokine CXCL10 / biosynthesis. Gingiva / drug effects. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Calcitonin Receptor-Like Protein. Cells, Cultured. Chronic Disease. Female. Fibroblasts / drug effects. Fibroblasts / immunology. Humans. Intracellular Signaling Peptides and Proteins / genetics. Male. Membrane Proteins / biosynthesis. Membrane Proteins / genetics. Middle Aged. Periodontitis / metabolism. Periodontium / metabolism. RNA, Messenger / genetics. Receptor Activity-Modifying Protein 2. Receptor Activity-Modifying Proteins. Receptors, Adrenomedullin. Receptors, Calcitonin / biosynthesis. Receptors, Calcitonin / genetics. Receptors, Peptide / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18435806.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CALCRL protein, human; 0 / CXCL10 protein, human; 0 / Calcitonin Receptor-Like Protein; 0 / Chemokine CXCL10; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / RAMP2 protein, human; 0 / RNA, Messenger; 0 / Receptor Activity-Modifying Protein 2; 0 / Receptor Activity-Modifying Proteins; 0 / Receptors, Adrenomedullin; 0 / Receptors, Calcitonin; 0 / Receptors, Peptide; 0 / Tumor Necrosis Factor-alpha; 148498-78-6 / Adrenomedullin
  • [Other-IDs] NLM/ PMC2453202
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