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1. Yip WK, Abdullah MA, Yusoff SM, Seow HF: Increase in tumour-infiltrating lymphocytes with regulatory T cell immunophenotypes and reduced zeta-chain expression in nasopharyngeal carcinoma patients. Clin Exp Immunol; 2009 Mar;155(3):412-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increase in tumour-infiltrating lymphocytes with regulatory T cell immunophenotypes and reduced zeta-chain expression in nasopharyngeal carcinoma patients.
  • The pathological significance of the mechanisms of tumour immune-evasion and/or immunosuppression, such as loss of T cell signalling and increase in regulatory T cells (T(regs)), has not been well established in the nasopharyngeal carcinoma (NPC) microenvironment.
  • To evaluate the T(reg) immunophenotypes in tumour-infiltrating lymphocytes (TILs), we performed a double-enzymatic immunostaining for detection of forkhead box P3 (FoxP3) and other markers including CD4, CD8, and CD25 on 64 NPC and 36 non-malignant nasopharyngeal (NP) paraffin-embedded tissues.
  • Increased CD4(+)FoxP3(+)/CD4(+) proportion and FoxP3(+)/CD8(+) ratio were associated with keratinizing squamous cell carcinoma.
  • These data provide evidence for the imbalances of T(reg) and effector T cell phenotypes and down-regulation of signal-transducing molecules in TILs, supporting their role in suppression of immune response and immune evasion of NPC.
  • [MeSH-major] Carcinoma / immunology. Lymphocytes, Tumor-Infiltrating / immunology. Nasopharyngeal Neoplasms / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Antigens, CD3 / analysis. Biomarkers / analysis. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Carcinoma, Squamous Cell / immunology. Female. Forkhead Transcription Factors / analysis. Humans. Immunohistochemistry. Interleukin-2 Receptor alpha Subunit / analysis. Lymphocyte Count. Male. Middle Aged. Nasopharynx / immunology. Statistics, Nonparametric

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  • [Cites] J Immunol. 2001 Aug 1;167(3):1137-40 [11466326.001]
  • [Cites] Oral Oncol. 2008 May;44(5):464-70 [17826303.001]
  • [Cites] J Pathol. 2002 Dec;198(4):468-75 [12434416.001]
  • [Cites] Cancer Immunol Immunother. 2003 Jan;52(1):28-32 [12536237.001]
  • [Cites] Nat Immunol. 2003 Apr;4(4):330-6 [12612578.001]
  • [Cites] J Clin Invest. 2003 Nov;112(9):1437-43 [14597769.001]
  • [Cites] Cancer Immunol Immunother. 2004 Oct;53(10):865-78 [15118842.001]
  • [Cites] Nat Rev Immunol. 2004 Sep;4(9):675-87 [15343367.001]
  • [Cites] Cancer. 1979 Sep;44(3):1029-44 [225002.001]
  • [Cites] Mol Carcinog. 1993;7(4):238-48 [8352883.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):4102-6 [8358739.001]
  • [Cites] Am J Otolaryngol. 1995 Mar-Apr;16(2):103-8 [7540805.001]
  • [Cites] Am J Pathol. 1995 Oct;147(4):1152-60 [7573360.001]
  • [Cites] Int J Cancer. 1995 Oct 9;63(2):205-12 [7591205.001]
  • [Cites] Eur J Immunol. 1996 Jun;26(6):1308-13 [8647210.001]
  • [Cites] Springer Semin Immunopathol. 1996;18(2):227-42 [8908702.001]
  • [Cites] J Clin Invest. 1998 Jun 1;101(11):2579-88 [9616229.001]
  • [Cites] J Immunother. 1998 Jul;21(4):295-306 [9672851.001]
  • [Cites] Clin Cancer Res. 1995 Nov;1(11):1327-35 [9815928.001]
  • [Cites] Clin Cancer Res. 1996 Jan;2(1):161-73 [9816103.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1422-7 [10197606.001]
  • [Cites] Oral Oncol. 1999 Jul;35(4):421-4 [10645409.001]
  • [Cites] J Immunol Methods. 2000 Jan 13;233(1-2):179-83 [10798913.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):74-80 [11205921.001]
  • [Cites] Hum Pathol. 2001 Jan;32(1):42-9 [11172294.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3 Suppl):947s-957s [11300496.001]
  • [Cites] Br J Cancer. 2001 Jun 15;84(12):1624-9 [11401315.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1599-605 [10197635.001]
  • [Cites] Cancer Lett. 1999 Jun 1;140(1-2):93-8 [10403546.001]
  • [Cites] Br J Cancer. 2005 Mar 14;92(5):799-806 [15756250.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4091-6 [15753306.001]
  • [Cites] Immunity. 2005 Mar;22(3):329-41 [15780990.001]
  • [Cites] Eur J Immunol. 2005 Jun;35(6):1681-91 [15902688.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8326-31 [16322292.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18538-43 [16344461.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):465-72 [16428488.001]
  • [Cites] Nan Fang Yi Ke Da Xue Xue Bao. 2006 Jan;26(1):94-7 [16495186.001]
  • [Cites] Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3355-60 [16740757.001]
  • [Cites] J Exp Med. 2006 Jul 10;203(7):1701-11 [16818678.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5423-34 [17000676.001]
  • [Cites] Eur J Immunol. 2007 Jan;37(1):129-38 [17154262.001]
  • [Cites] Ann Oncol. 2007 Jan;18(1):29-35 [17060483.001]
  • [Cites] Br J Cancer. 2007 Feb 26;96(4):617-22 [17262084.001]
  • [Cites] Clin Immunol. 2007 Apr;123(1):18-29 [17185041.001]
  • [Cites] Int Immunol. 2007 Apr;19(4):345-54 [17329235.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2075-81 [17404089.001]
  • [Cites] Exp Oncol. 2007 Mar;29(1):2-12 [17431381.001]
  • [Cites] Gastroenterology. 2007 Jun;132(7):2328-39 [17570208.001]
  • [Cites] J Clin Oncol. 2007 Jun 20;25(18):2586-93 [17577038.001]
  • [Cites] Br J Dermatol. 2007 Sep;157(3):531-9 [17596146.001]
  • [Cites] Cancer Treat Rev. 2007 Oct;33(6):499-505 [17544585.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2983-90 [17644734.001]
  • [Cites] Leukemia. 2007 Dec;21(12):2512-8 [17713545.001]
  • [Cites] Eur J Surg Oncol. 2008 Feb;34(2):173-9 [17928188.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3137-45 [12374681.001]
  • (PMID = 19220831.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Biomarkers; 0 / CD3 antigen, zeta chain; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
  • [Other-IDs] NLM/ PMC2669517
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2. Willenbrock K, Renné C, Gaulard P, Hansmann ML: In angioimmunoblastic T-cell lymphoma, neoplastic T cells may be a minor cell population. A molecular single-cell and immunohistochemical study. Virchows Arch; 2005 Jan;446(1):15-20
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  • [Title] In angioimmunoblastic T-cell lymphoma, neoplastic T cells may be a minor cell population. A molecular single-cell and immunohistochemical study.
  • The significance of T-cell proliferations in angioimmunoblastic lymphoma (AILD) is still enigmatic.
  • Although classified as a malignant T-cell lymphoma in the World Health Organisation lymphoma classification, some cases of AILD lack dominant T-cell clones.
  • In a previous study, based on single-cell polymerase chain reaction (PCR), we obtained similar results as studies of AILD using Southern blot or conventional PCR: some cases of AILD contained large T-cell clones, and, in other cases, T-cell clones were undetectable.
  • As in single-cell studies, only a limited number of cells could be investigated; thus, we wanted to gain more insight into the amount and distribution of tumour cells.
  • By applying triple immunofluorescent staining with antibodies directed against T-cell receptor Vbeta-family-specific epitopes, we investigated T-cell populations in AILD and their localisation in the tissue in relation to B cells (CD20) and follicular dendritic cells (CD21).
  • In two of five cases investigated, only a minority of the T-cells compartment belonged to the tumour clone.
  • [MeSH-major] Immunoblastic Lymphadenopathy / immunology. Lymphoma, T-Cell / immunology. T-Lymphocytes / pathology
  • [MeSH-minor] Antigens, CD20 / analysis. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Polymerase Chain Reaction. Receptors, Antigen, T-Cell, alpha-beta / analysis. Receptors, Complement 3d / analysis

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  • [Cites] Virchows Arch. 1994;424(6):593-600 [8055152.001]
  • [Cites] Leuk Lymphoma. 2000 Aug;38(5-6):541-5 [10953975.001]
  • [Cites] N Engl J Med. 1975 Jan 2;292(1):1-8 [1078547.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):661-9 [10666395.001]
  • [Cites] Am J Pathol. 2000 Mar;156(3):1067-71 [10702422.001]
  • [Cites] Blood. 1995 May 15;85(10):2862-9 [7742548.001]
  • [Cites] Am J Pathol. 2001 May;158(5):1851-7 [11337383.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):10962-6 [7971992.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1985;406(1):105-24 [3922106.001]
  • [Cites] EMBO J. 1993 Dec 15;12(13):4955-67 [8262038.001]
  • [Cites] J Exp Med. 1996 Oct 1;184(4):1495-505 [8879220.001]
  • [Cites] Eur J Immunol. 1998 Aug;28(8):2424-31 [9710220.001]
  • [Cites] Blood. 1994 Jul 15;84(2):574-81 [8025283.001]
  • [Cites] Leukemia. 1997 Jul;11(7):1055-62 [9204991.001]
  • [Cites] Lancet. 1974 Jun 1;1(7866):1070-3 [4135245.001]
  • [Cites] Am J Pathol. 1988 Dec;133(3):549-56 [2849301.001]
  • [Cites] Am J Pathol. 1986 Mar;122(3):392-7 [3082212.001]
  • [Cites] Dtsch Med Wochenschr. 1975 May 23;100(21):1157-63 [1132324.001]
  • (PMID = 15480765.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Complement 3d
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3. Appetecchia M, Ferretti E, Carducci M, Izzo F, Carpanese L, Marandino F, Terzoli E: Malignant glucagonoma. New options of treatment. J Exp Clin Cancer Res; 2006 Mar;25(1):135-9
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  • [Title] Malignant glucagonoma. New options of treatment.
  • Few cases of malignant glucagonomas have been described in the literature.
  • In this paper we present a case of a 77-year-old woman with necrolytic migratory erythema and high plasma glucagon and chromogranin A levels caused by a neuroendocrine tumour.
  • An abdominal CT scan suggested a pancreatic lesion and two liver metastases.
  • The patient underwent pancreatic debulking and liver metastasectomy.
  • Histological and immunohistochemical investigations revealed a well differentiated neuroendocrine tumour with vascular invasion and scattered immunopositivity for somatostatin receptors.
  • The patient was treated with octreotide (30 mg i.m. every 28 days) and interferon-alpha (6 MU s.cc 3 times per week) plus three cycles of hepatic chemoembolisation.
  • The patient is now asymptomatic with persistent hepatic disease and normal serum glucagon levels forty months after primary treatment.
  • So far, only few immunohistochemical studies are reported on malignant glucagonoma and combined treatment schedules.
  • We demonstrated, for the first time, a scattered immunopositivity for somatostatin receptors in a malignant glucagonoma.
  • A combined antiproliferative medical treatment and the hepatic chemoembolization have been able to control tumor growth and disease symptoms for a long time after surgery.
  • [MeSH-major] Glucagonoma / therapy
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Female. Glucagon / blood. Humans. Immunohistochemistry. Interferon-alpha / metabolism. Neuroendocrine Tumors / blood. Octreotide / pharmacology. Proglucagon / metabolism. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16761630.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Interferon-alpha; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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4. Mathsson L, Tejde A, Carlson K, Höglund M, Nilsson B, Nilsson-Ekdahl K, Rönnelid J: Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones. Br J Haematol; 2005 Jun;129(6):830-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones.
  • Complement blockade resulted in increased IgG CG-induced interleukin (IL)-10 production that was inversely correlated with decreased production of tumour necrosis factor-alpha.
  • CG-induced IL-10 might be a growth factor for malignant B-lymphocytes in CG-associated lymphoproliferative diseases with constant complement consumption.
  • [MeSH-minor] Aged. Cells, Cultured. Complement Inactivator Proteins / immunology. Complement Pathway, Classical / immunology. Female. Humans. Hydrogen-Ion Concentration. Immunoglobulin G / immunology. Immunoglobulin M / immunology. Interleukin-10 / biosynthesis. Male. Middle Aged. Monocytes / immunology. Neoplastic Stem Cells / pathology. Temperature. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 15953012.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Complement Inactivator Proteins; 0 / Cryoglobulins; 0 / Cytokines; 0 / Fc gamma receptor IIA; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Receptors, IgG; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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5. Paredes J, Correia AL, Ribeiro AS, Milanezi F, Cameselle-Teijeiro J, Schmitt FC: Breast carcinomas that co-express E- and P-cadherin are associated with p120-catenin cytoplasmic localisation and poor patient survival. J Clin Pathol; 2008 Jul;61(7):856-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Changes in junctional catenin expression may compromise cadherin-mediated adhesion, increasing cell malignant properties such as invasive and metastatic abilities.
  • Altered expression of alpha-, beta-, gamma- and p120-catenin has been reported to be associated with E-cadherin loss or decreased expression, in both breast carcinomas and breast cancer cell lines.
  • These alterations were significantly correlated with lack of both E-cadherin and oestrogen receptor-alpha expression.
  • It was possible to associate the expression of beta-catenin with histological grade, tumour size and nodal status, suggesting a relevant role for this catenin as a prognostic factor.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Breast Neoplasms / metabolism. Cadherins / metabolism. Catenins / metabolism

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  • (PMID = 18381381.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Catenins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / delta catenin
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6. Calzada MJ, del Peso L: Hypoxia-inducible factors and cancer. Clin Transl Oncol; 2007 May;9(5):278-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Decreased oxygen availability is a common feature during embryonic development as well of malignant tumours.
  • As a consequence of HIF stabilisation, the cell constitutively upregulates the hypoxic programme resulting in the expression of genes responsible for global changes in cell proliferation, angiogenesis, metastasis, invasion, de-differentiation and energy metabolism.
  • Of the three known alpha subunits of HIF transcription factors, HIF-1alpha and HIF-2alpha have been the most studied.
  • In this review we provide an overview of the current knowledge on some of the most important aspects of HIFalpha regulation, its role in tumour angiogenesis and energetic metabolism.
  • [MeSH-minor] Genes, Tumor Suppressor / physiology. Humans. von Hippel-Lindau Disease / etiology

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  • [Cites] Biochem Biophys Res Commun. 2004 Jul 30;320(3):945-50 [15240140.001]
  • [Cites] J Biol Chem. 2006 Nov 3;281(44):33095-106 [16954218.001]
  • [Cites] FEBS Lett. 2001 Feb 23;491(1-2):85-90 [11226425.001]
  • [Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]
  • [Cites] Science. 1956 Feb 24;123(3191):309-14 [13298683.001]
  • [Cites] J Lab Clin Med. 1998 Dec;132(6):519-29 [9851743.001]
  • [Cites] Circ Res. 2004 Jul 23;95(2):146-53 [15192019.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14767-72 [17003112.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18154-9 [17114296.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):147-58 [12957289.001]
  • [Cites] Science. 2001 Apr 20;292(5516):468-72 [11292861.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3567-75 [16585181.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):673-82 [12209156.001]
  • [Cites] Biochem J. 2004 May 15;380(Pt 1):289-95 [14992692.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3014-9 [12036906.001]
  • [Cites] Cancer Res. 2002 May 15;62(10 ):2929-36 [12019174.001]
  • [Cites] J Biol Chem. 2003 Mar 28;278(13):11032-40 [12538644.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2277-86 [15781641.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):131-41 [16098466.001]
  • [Cites] Biol Pharm Bull. 2006 Dec;29(12):2335-42 [17142959.001]
  • [Cites] Nature. 2006 Apr 27;440(7088):1222-6 [16642001.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):43611-7 [11574546.001]
  • [Cites] Eur J Biochem. 2003 Mar;270(5):781-90 [12603311.001]
  • [Cites] Nat Rev Cancer. 2004 Jun;4(6):437-47 [15170446.001]
  • [Cites] J Am Soc Nephrol. 2006 Jul;17 (7):1801-6 [16775032.001]
  • [Cites] Biochem J. 2004 Aug 1;381(Pt 3):761-7 [15104534.001]
  • [Cites] Br J Cancer. 2001 Sep 14;85(6):881-90 [11556841.001]
  • [Cites] Blood. 2006 Jan 15;107(2):584-90 [16189264.001]
  • [Cites] Genes Dev. 2004 Dec 1;18(23 ):2893-904 [15545625.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23 ):8595-603 [15574766.001]
  • [Cites] J Biol Chem. 2003 Dec 5;278(49):48690-5 [14506252.001]
  • [Cites] Curr Opin Cell Biol. 2006 Dec;18(6):598-608 [17046224.001]
  • [Cites] Cell Metab. 2006 Mar;3(3):177-85 [16517405.001]
  • [Cites] Cancer Gene Ther. 2006 Feb;13(2):131-40 [16096651.001]
  • [Cites] J Pathol. 2002 Feb;196 (2):204-12 [11793372.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Aug 19;94(17 ):9102-7 [9256442.001]
  • [Cites] EMBO J. 2005 Oct 5;24(19):3446-58 [16096638.001]
  • [Cites] Science. 2001 Nov 9;294(5545):1337-40 [11598268.001]
  • [Cites] J Biol Chem. 2006 Apr 28;281(17 ):12069-80 [16505488.001]
  • [Cites] Mol Cancer Ther. 2004 May;3(5):647-54 [15141023.001]
  • [Cites] Mol Cell Biol. 2001 Feb;21(3):865-74 [11154273.001]
  • [Cites] J Biol Chem. 2003 Oct 3;278(40):38183-7 [12876291.001]
  • [Cites] Science. 2006 May 26;312(5777):1158-9 [16728625.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(22):8336-46 [16966370.001]
  • [Cites] Nature. 2006 May 25;441(7092):437-43 [16724055.001]
  • [Cites] Science. 2001 Apr 20;292(5516):464-8 [11292862.001]
  • [Cites] Mol Cell Biol. 2007 May;27(9):3253-65 [17325032.001]
  • [Cites] Cancer Res. 2001 May 15;61(10 ):4184-9 [11358843.001]
  • [Cites] Biochem J. 2006 Jul 1;397(1):109-20 [16669786.001]
  • [Cites] J Biol Chem. 2005 Jun 10;280(23 ):22473-81 [15802268.001]
  • [Cites] Mol Cell. 2006 May 5;22(3):395-405 [16678111.001]
  • [Cites] Gene Ther. 2002 Feb;9(4):291-6 [11896468.001]
  • [Cites] J Biol Chem. 1997 Sep 19;272(38):23659-67 [9295307.001]
  • [Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8554-60 [15623639.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8386-91 [10880563.001]
  • [Cites] Blood. 2005 Jan 15;105(2):659-69 [15374877.001]
  • [Cites] Cell Metab. 2005 Jun;1(6):357-8 [16054083.001]
  • [Cites] PLoS Biol. 2004 Oct;2(10 ):e289 [15361934.001]
  • [Cites] Cell Metab. 2006 Mar;3(3):187-97 [16517406.001]
  • [Cites] Blood. 1999 Jun 15;93(12):4284-92 [10361126.001]
  • [Cites] J Biol Chem. 2002 Sep 6;277(36):32405-8 [12119283.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1541-5 [10749120.001]
  • [Cites] Mol Cancer Res. 2006 Jul;4(7):471-9 [16849522.001]
  • [Cites] Genes Dev. 2000 Feb 15;14 (4):391-6 [10691731.001]
  • [Cites] J Biol Chem. 2004 Sep 10;279(37):38458-65 [15247232.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1561-9 [16452213.001]
  • [Cites] Mol Cell Biol. 2007 Jan;27(1):157-69 [17060462.001]
  • [Cites] Nature. 1997 Mar 27;386(6623):403-7 [9121557.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 15;351(2):313-20 [17069766.001]
  • [Cites] J Biol Chem. 2007 Apr 27;282(17 ):12707-16 [17324924.001]
  • [Cites] Science. 1988 Dec 9;242(4884):1412-5 [2849206.001]
  • [Cites] Cancer Gene Ther. 2006 Apr;13(4):428-35 [16211089.001]
  • [Cites] Cell. 2001 Oct 5;107(1):43-54 [11595184.001]
  • [Cites] Cell Cycle. 2005 Jul;4(7):881-2 [15970707.001]
  • [Cites] Medicine (Baltimore). 1997 Nov;76(6):381-91 [9413424.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):10548-55 [11136721.001]
  • [Cites] Eur J Biochem. 1995 Dec 1;234(2):632-40 [8536713.001]
  • [Cites] J Biol Chem. 2006 Apr 7;281(14):9030-7 [16452478.001]
  • [Cites] Mol Cell Biol. 2006 May;26(9):3514-26 [16611993.001]
  • [Cites] Mol Cell Biol. 1996 Sep;16(9):4604-13 [8756616.001]
  • [Cites] Nat Med. 2002 Jul;8(7):702-10 [12053176.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26351-5 [12042299.001]
  • [Cites] Cell. 2006 Jul 14;126(1):107-20 [16839880.001]
  • [Cites] Hum Gene Ther. 2002 Sep 20;13(14):1737-50 [12396626.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(8):3163-72 [15798202.001]
  • [Cites] PLoS Biol. 2003 Dec;1(3):E83 [14691554.001]
  • [Cites] Circulation. 2005 May 3;111(17 ):2227-32 [15851592.001]
  • [Cites] Mol Cell Biol. 1994 Sep;14 (9):5997-6003 [8065332.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3299-306 [15833863.001]
  • [Cites] J Biol Chem. 2006 Sep 29;281(39):28712-20 [16885164.001]
  • [Cites] Genes Dev. 2000 Dec 15;14(24):3191-203 [11124810.001]
  • [Cites] Genes Dev. 2006 Mar 1;20(5):557-70 [16510872.001]
  • [Cites] J Biol Chem. 2006 Aug 11;281(32):22575-85 [16760477.001]
  • [Cites] EMBO J. 1998 Jun 1;17(11):3005-15 [9606183.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):425-34 [16766262.001]
  • [Cites] Cancer Cell. 2007 Apr;11(4):335-47 [17418410.001]
  • [Cites] FEBS Lett. 2004 Jan 2;556(1-3):137-42 [14706840.001]
  • [Cites] Hum Mol Genet. 2001 May 1;10 (10 ):1019-27 [11331612.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1553-60 [16452212.001]
  • [Cites] Biochem J. 2005 Aug 15;390(Pt 1):189-97 [15823097.001]
  • [Cites] Trends Cell Biol. 2006 Dec;16(12):616-21 [17070052.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):13508-17 [11815624.001]
  • [Cites] Nat Cell Biol. 2003 Jan;5(1):64-70 [12510195.001]
  • [Cites] Curr Biol. 2003 Apr 15;13(8):R323-5 [12699646.001]
  • [Cites] Mol Cell. 1998 Jun;1(7):959-68 [9651579.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2576-83 [16510575.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):33-43 [15261140.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 29;94(9):4273-8 [9113979.001]
  • [Cites] FASEB J. 2003 Nov;17 (14 ):2115-7 [12958148.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2725-31 [16510593.001]
  • [Cites] Hum Genet. 2000 Aug;107(2):97-114 [11030407.001]
  • [Cites] Nat Genet. 2003 Dec;35(4):331-40 [14608355.001]
  • [Cites] Mol Cell Biol. 1999 Sep;19(9):5902-12 [10454537.001]
  • [Cites] EMBO J. 2003 Aug 15;22(16):4082-90 [12912907.001]
  • [Cites] Cancer Cell. 2006 Nov;10 (5):413-23 [17097563.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(13):5675-86 [15964822.001]
  • [Cites] J Biol Chem. 1997 Oct 31;272(44):27509-12 [9346879.001]
  • [Cites] Nature. 2001 Nov 29;414(6863):550-4 [11734856.001]
  • [Cites] FASEB J. 2003 Feb;17 (2):271-3 [12490539.001]
  • [Cites] Biochem J. 2005 May 1;387(Pt 3):711-7 [15563275.001]
  • [Cites] J Biol Chem. 2002 Apr 26;277(17):15162-70 [11859074.001]
  • [Cites] J Mol Cell Cardiol. 2006 Jul;41(1):68-77 [16765982.001]
  • [Cites] Genomics. 1998 Sep 1;52(2):159-65 [9782081.001]
  • [Cites] Mol Cell Biol. 2006 Apr;26(7):2519-30 [16537898.001]
  • [Cites] Sci STKE. 2005 Oct 18;2005(306):re12 [16234508.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12 ):6264-70 [16778202.001]
  • [Cites] Hum Mol Genet. 2001 May 1;10 (10 ):1029-38 [11331613.001]
  • [Cites] Oncogene. 2003 Apr 10;22(14):2065-72 [12687009.001]
  • [Cites] Oncogene. 2003 Jun 26;22(26):3992-7 [12821933.001]
  • [Cites] Nat Med. 2003 Jun;9(6):653-60 [12778163.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):779-85 [16915281.001]
  • [Cites] J Biol Chem. 2005 May 27;280(21):20580-8 [15781453.001]
  • [Cites] Genes Dev. 1997 Jan 1;11(1):72-82 [9000051.001]
  • [Cites] Mol Cell. 2005 Jan 7;17 (1):11-21 [15629713.001]
  • [Cites] Genes Dev. 2002 Jun 15;16(12 ):1466-71 [12080085.001]
  • [Cites] Blood. 2006 Apr 1;107(7):2705-12 [16304044.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6877-84 [14583486.001]
  • [Cites] Nat Med. 2003 Jun;9(6):677-84 [12778166.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1313-9 [16452184.001]
  • [Cites] Mol Cell Biol. 2001 Jun;21(12):3995-4004 [11359907.001]
  • [Cites] Gene. 2001 Sep 5;275(1):125-32 [11574160.001]
  • [Cites] Science. 2002 Feb 1;295(5556):858-61 [11823643.001]
  • [Cites] Cancer. 2002 Sep 1;95(5):1055-63 [12209691.001]
  • [Cites] Hum Mol Genet. 2005 Aug 1;14(15):2231-9 [15987702.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):22368-74 [11294857.001]
  • [Cites] Biochem J. 2007 Jan 1;401(1):227-34 [16952279.001]
  • [Cites] Cancer Cell. 2004 Nov;6(5):485-95 [15542432.001]
  • [Cites] Nature. 1998 Jul 30;394(6692):485-90 [9697772.001]
  • [Cites] J Biol Chem. 2003 Feb 28;278(9):7520-30 [12464608.001]
  • (PMID = 17525038.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Hypoxia-Inducible Factor 1; 0 / endothelial PAS domain-containing protein 1
  • [Number-of-references] 150
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7. Altadill A, Rodríguez M, González LO, Junquera S, Corte MD, González-Dieguez ML, Linares A, Barbón E, Fresno-Forcelledo M, Rodrigo L, Vizoso FJ: Liver expression of matrix metalloproteases and their inhibitors in hepatocellular carcinoma. Dig Liver Dis; 2009 Oct;41(10):740-8
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  • [Title] Liver expression of matrix metalloproteases and their inhibitors in hepatocellular carcinoma.
  • BACKGROUND: Several studies have suggested the significance of some metalloproteases in the malignant behaviour of hepatocellular carcinoma.
  • Increased TIMP-2 expression was associated with higher preoperative serum levels of alpha-fetoprotein (p<0.01).
  • Unsupervised hierarchical clustering for total score values designated two groups, one of them characterised by high MMPs and TIMPs expressions, including 21 cases (70%) for tumour cell clustering, 5 cases for fibroblasts (16.6%) and 6 cases for inflammatory cells (20%).
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / metabolism. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 13 / metabolism. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Tissue Inhibitor of Metalloproteinase-2 / metabolism

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  • [CommentIn] Dig Liver Dis. 2009 Oct;41(10):707-8 [19699696.001]
  • (PMID = 19372066.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tissue Inhibitor of Metalloproteinase-1; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.24.- / Matrix Metalloproteinase 13; EC 3.4.24.7 / Matrix Metalloproteinase 1
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8. Nishioka C, Ikezoe T, Jing Y, Umezawa K, Yokoyama A: DHMEQ, a novel nuclear factor-kappaB inhibitor, induces selective depletion of alloreactive or phytohaemagglutinin-stimulated peripheral blood mononuclear cells, decreases production of T helper type 1 cytokines, and blocks maturation of dendritic cells. Immunology; 2008 Jun;124(2):198-205
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  • Dehydroxymethylepoxyquinomicin (DHMEQ), a novel nuclear factor kappaB (NF-kappaB) inhibitor, has been shown to be active against variety types of solid tumours as well as haematological malignant cells.
  • In addition, real-time polymerase chain reaction showed that DHMEQ decreased PHA-stimulated expression of T helper type 1 (Th1) cytokines, including interleukin-2, interferon-gamma, and tumour necrosis factor alpha, in PBMC as well as Jurkat T-lymphoblastic leukaemia cells, and also decreased levels of p65 isoforms of NF-kappaB in the nucleus.
  • Furthermore, we found that DHMEQ inhibited the endocytic capacity of dendritic cells (DCs) and down-regulated the expression of cell surface antigen CD40, suggesting that DHMEQ blocked the maturation as well as the function of DCs.
  • Taken together, the results suggest that DHMEQ may be useful for treatment of inflammatory diseases, including graft-versus-host disease after allogenic haematopoietic stem cell transplantation.
  • [MeSH-minor] Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Endocytosis / drug effects. Humans. Jurkat Cells. Lymphocyte Culture Test, Mixed. Phytohemagglutinins / immunology. Th1 Cells / drug effects. Th1 Cells / immunology

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  • [Cites] Biol Blood Marrow Transplant. 1999;5(6):347-56 [10595812.001]
  • [Cites] Transplant Proc. 1993 Feb;25(1 Pt 2):1216-7 [8442093.001]
  • [Cites] Annu Rev Immunol. 2000;18:621-63 [10837071.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1993 Feb;15(1):18-27 [8447559.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2360-7 [8161803.001]
  • [Cites] Nature. 1998 Mar 19;392(6673):245-52 [9521319.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1287-93 [15709200.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2462-71 [15956280.001]
  • [Cites] Arthritis Res Ther. 2005;7(6):R1348-59 [16277688.001]
  • [Cites] Blood. 2006 Jan 15;107(2):827-34 [16174760.001]
  • [Cites] Annu Rev Med. 2006;57:33-47 [16409135.001]
  • [Cites] Blood. 2006 May 1;107(9):3575-83 [16282346.001]
  • [Cites] Leukemia. 2006 May;20(5):800-6 [16525497.001]
  • [Cites] Blood. 2006 Jul 15;108(2):551-8 [16537813.001]
  • [Cites] Cancer Sci. 2006 Oct;97(10):990-5 [16925581.001]
  • [Cites] Biomed Pharmacother. 2006 Nov;60(9):578-86 [16978829.001]
  • [Cites] Transplantation. 2006 Dec 27;82(12):1720-7 [17198266.001]
  • [Cites] Annu Rev Immunol. 2000;18:767-811 [10837075.001]
  • [Cites] J Exp Med. 2001 Nov 19;194(10):1433-40 [11714750.001]
  • [Cites] Immunol Cell Biol. 2002 Feb;80(1):52-64 [11869363.001]
  • [Cites] Nat Med. 2002 Jun;8(6):575-81 [12042807.001]
  • [Cites] J Biol Chem. 2002 Jul 5;277(27):24625-30 [11983688.001]
  • [Cites] J Immunol. 2002 Jul 15;169(2):1058-67 [12097414.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):107-10 [12517785.001]
  • [Cites] Mol Pharmacol. 2003 Dec;64(6):1521-9 [14645683.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 25;101(21):8120-5 [15148407.001]
  • [Cites] J Immunol. 1986 Apr 1;136(7):2348-57 [2419430.001]
  • [Cites] Blood. 1992 Dec 15;80(12):2964-8 [1467511.001]
  • [Cites] J Immunol. 2000 Jan 15;164(2):656-63 [10623807.001]
  • (PMID = 18217958.001).
  • [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 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Benzamides; 0 / Cyclohexanones; 0 / Cytokines; 0 / Phytohemagglutinins; 0 / dehydroxymethylepoxyquinomicin
  • [Other-IDs] NLM/ PMC2566624
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9. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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10. Catassi A, Paleari L, Servent D, Sessa F, Dominioni L, Ognio E, Cilli M, Vacca P, Mingari M, Gaudino G, Bertino P, Paolucci M, Calcaterra A, Cesario A, Granone P, Costa R, Ciarlo M, Alama A, Russo P: Targeting alpha7-nicotinic receptor for the treatment of pleural mesothelioma. Eur J Cancer; 2008 Oct;44(15):2296-311
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  • Human malignant pleural mesothelioma (MPM) is a dreadful disease and there is still no standard therapy available for a consistent therapeutic approach.
  • This research is aimed at the evaluation of the potential therapeutic effect of a specific nicotinic receptor (nAChR) antagonist, namely alpha-Cobratoxin (alpha-CbT).
  • Its effectiveness was tested in mesothelioma cell lines and in primary mesothelioma cells in vitro, as well as in vivo, in orthotopically xenotransplanted NOD/SCID mice.
  • Cells showed alpha7-nAChR expression and their growth was significantly inhibited by alpha-CbT.
  • Severe induction of apoptosis was observed after exposure to alpha-CbT [IC(80-90)].
  • In vivo, the alpha-CbT acute LD(50) was 0.15 mg/kg.
  • Phase II experiments with 0.12 ng/kg alpha-CbT (1/1000 of LD(10)) were done in 53 xenotransplanted mice, inhibiting tumour development as confirmed by chest X-ray examinations, autopsy and microscopical findings.
  • The growth of human proliferating T lymphocytes and of mesothelial cells in primary culture was not affected by alpha-CbT.
  • Non-immunogenic derivatives of the alpha-CbT molecule need to be developed for possible human use.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction / methods. Transplantation, Heterologous. Tumor Cells, Cultured. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 18722110.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Cobra Neurotoxin Proteins; 0 / Neoplasm Proteins; 0 / Nicotinic Antagonists; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 69344-74-7 / alpha-cobratoxin
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11. Yamamoto E, Ino K, Miyoshi E, Shibata K, Takahashi N, Kajiyama H, Nawa A, Nomura S, Nagasaka T, Kikkawa F: Expression of N-acetylglucosaminyltransferase V in endometrial cancer correlates with poor prognosis. Br J Cancer; 2007 Dec 3;97(11):1538-44
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  • N-acetylglucosaminyltransferase V (GnT-V) is an enzyme that catalyses beta1-6 branching of N-acetylglucosamine on asparagine-linked oligosaccharides of cell proteins.
  • High GnT-V expression in tumour cells was found in 43 (58.1%) of the 74 cases, and was positively correlated with advanced patient age, histological grade, and lymph vascular space involvement.
  • These results suggested that high GnT-V expression was correlated with an unfavourable clinical outcome, and that GnT-V is involved in the malignant potential of endometrial cancer by increasing the synthesis of beta1-6 branching of asparagine-linked oligosaccharides.

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  • [Cites] Glycoconj J. 1997 Aug;14(5):623-30 [9298695.001]
  • [Cites] Int J Gynecol Pathol. 1996 Jul;15(3):191-201 [8811379.001]
  • [Cites] Biochem Biophys Res Commun. 2005 May 13;330(3):999-1004 [15809094.001]
  • [Cites] Lancet. 2005 Aug 6-12;366(9484):491-505 [16084259.001]
  • [Cites] Oncology. 2005;69(4):301-10 [16282710.001]
  • [Cites] Clin Cancer Res. 2006 Apr 15;12(8):2506-11 [16638859.001]
  • [Cites] FASEB J. 2006 Dec;20(14):2451-9 [17142794.001]
  • [Cites] Pathol Int. 1999 Oct;49(10):874-80 [10571820.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1772-7 [10815896.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):36720-5 [10962009.001]
  • [Cites] Int J Cancer. 2001 Mar 1;91(5):631-7 [11267972.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):16960-7 [11864986.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):17002-8 [11872751.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):6837-45 [12460896.001]
  • [Cites] Mol Cancer Ther. 2003 Nov;2(11):1207-14 [14617794.001]
  • [Cites] Clin Cancer Res. 2004 Mar 1;10(5):1773-9 [15014031.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1234-41 [15051771.001]
  • [Cites] Science. 1987 May 1;236(4801):582-5 [2953071.001]
  • [Cites] Adv Cancer Res. 1989;52:257-331 [2662714.001]
  • [Cites] Cancer Res. 1991 Jan 15;51(2):718-23 [1985789.001]
  • [Cites] Gynecol Oncol. 1991 Jan;40(1):55-65 [1989916.001]
  • [Cites] J Biol Chem. 1991 Nov 15;266(32):21327-30 [1939168.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;22(5):905-11 [1555983.001]
  • [Cites] Glycobiology. 1993 Apr;3(2):97-130 [8490246.001]
  • [Cites] J Biol Chem. 1999 Oct 22;274(43):31039-46 [10521503.001]
  • (PMID = 17971775.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.4.1.- / N-Acetylglucosaminyltransferases; EC 2.4.1.155 / alpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferase
  • [Other-IDs] NLM/ PMC2360248
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12. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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13. Sánchez Carazo JL, Mahiques Santos L, Oliver Martinez V: Safety of etanercept in psoriasis: a critical review. Drug Saf; 2006;29(8):675-85
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  • The drug is a competitive inhibitor of tumour necrosis factor-alpha (TNFalpha) that prevents interaction between this cytokine and its cell surface receptors.
  • Etanercept also modulates the activity of other inflammatory cytokines and does not induce complement-mediated cell lysis in vitro.
  • The most common adverse effect during drug administration is mild injection site reactions.
  • There are no data showing that treatment with etanercept results in an increase in the occurrence of malignant neoplasms.
  • Etanercept must be used with extreme caution in patients with heart failure because of several reports indicating a worsening or de novo occurrence of congestive heart failure while receiving the drug.
  • In patients with hepatitis C viral infection, etanercept does not increase transaminase levels or viral load and in some instances has allowed the concomitant use of interferon which had previously been discontinued because of a worsening of psoriasis.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Immunoglobulin G / adverse effects. Psoriasis / drug therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Child. Etanercept. Female. Humans. Practice Guidelines as Topic. Pregnancy. Randomized Controlled Trials as Topic. Receptors, Tumor Necrosis Factor

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  • [Cites] Lancet. 2001 Jun 9;357(9271):1842-7 [11410193.001]
  • [Cites] Arthritis Rheum. 2001 Dec;44(12):2862-9 [11762947.001]
  • [Cites] Expert Opin Investig Drugs. 2000 Jul;9(7):1511-22 [11060756.001]
  • [Cites] Acta Derm Venereol Suppl (Stockh). 1989;146:69-71 [2609889.001]
  • [Cites] Arthritis Rheum. 2001 Sep;44(9):1977-83 [11592357.001]
  • [Cites] J Am Coll Cardiol. 1996 Apr;27(5):1201-6 [8609343.001]
  • [Cites] Semin Cutan Med Surg. 2005 Mar;24(1):37-45 [15900797.001]
  • [Cites] J Am Acad Dermatol. 2006 Jan;54(1):160-4 [16384777.001]
  • [Cites] J Am Acad Dermatol. 2002 Dec;47(6):821-33 [12451365.001]
  • [Cites] J Natl Cancer Inst. 1998 Sep 2;90(17):1278-84 [9731734.001]
  • [Cites] J Am Acad Dermatol. 2006 Mar;54(3 Suppl 2):S92-100 [16488335.001]
  • [Cites] Clin Infect Dis. 2004 May 1;38(9):1261-5 [15127338.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2005 Sep;19(5):556-63 [16164708.001]
  • [Cites] Ann Rheum Dis. 2005 Oct;64(10):1414-20 [15843454.001]
  • [Cites] Dermatol Clin. 1996 Jul;14(3):485-96 [8818558.001]
  • [Cites] Drug Saf. 2002;25(3):173-97 [11945114.001]
  • [Cites] N Engl J Med. 1990 Jul 26;323(4):236-41 [2195340.001]
  • [Cites] J Am Acad Dermatol. 2003 Aug;49(2 Suppl):S112-7 [12894134.001]
  • [Cites] Clin Exp Rheumatol. 2000 Jul-Aug;18(4):533-4 [10949736.001]
  • [Cites] Ann Rheum Dis. 2003 Nov;62(11):1078-82 [14583571.001]
  • [Cites] N Engl J Med. 2000 Mar 16;342(11):763-9 [10717011.001]
  • [Cites] J Invest Dermatol. 2001 Dec;117(6):1531-7 [11886519.001]
  • [Cites] JAMA. 2003 Dec 17;290(23 ):3073-80 [14679270.001]
  • [Cites] J Dermatol Sci. 1997 Feb;14(2):145-53 [9039978.001]
  • [Cites] N Engl J Med. 1997 Apr 10;336(15):1041-5 [9091799.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2004-13 [14627785.001]
  • [Cites] Lancet. 2002 Feb 16;359(9306):579-80 [11867114.001]
  • [Cites] J Rheumatol. 2005 Nov;32(11):2183-5 [16265699.001]
  • [Cites] Rheumatology (Oxford). 2001 Nov;40(11):1317-9 [11709621.001]
  • [Cites] Immunol Today. 1999 Jan;20(1):40-6 [10081229.001]
  • [Cites] Arch Dermatol. 2003 Jun;139(6):719-27 [12810502.001]
  • [Cites] J Am Acad Dermatol. 2002 Jan;46(1):1-23; quiz 23-6 [11756941.001]
  • [Cites] Arthritis Rheum. 2002 Feb;47(1):17-21 [11932873.001]
  • [Cites] J Rheumatol. 2000 Aug;27(8):2041-4 [10955351.001]
  • [Cites] Circulation. 2000 Dec 19;102(25):3060-7 [11120695.001]
  • [Cites] Del Med J. 2000 Dec;72(12):517-9 [11200291.001]
  • [Cites] Ann Intern Med. 2003 May 20;138(10):807-11 [12755552.001]
  • [Cites] Arthritis Rheum. 2000 Nov;43(11):2381-2 [11083257.001]
  • [Cites] N Engl J Med. 1996 Jun 27;334(26):1697-702 [8637514.001]
  • [Cites] Int J Cardiol. 2002 Dec;86(2-3):123-30 [12419548.001]
  • [Cites] J Hepatol. 2005 Mar;42(3):315-22 [15791697.001]
  • [Cites] Cytokine. 2002 May 21;18(4):179-83 [12126639.001]
  • [Cites] J Exp Med. 1989 Aug 1;170(2):607-12 [2754393.001]
  • [Cites] Circulation. 2003 Jul 1;107(25):3133-40 [12796126.001]
  • [Cites] Can J Gastroenterol. 2001 Jun;15(6):376-84 [11429667.001]
  • [Cites] J Exp Med. 1991 Dec 1;174(6):1483-9 [1660525.001]
  • [Cites] N Engl J Med. 2001 Oct 11;345(15):1098-104 [11596589.001]
  • [Cites] J Am Acad Dermatol. 2006 Mar;54(3 Suppl 2):S126-8 [16488325.001]
  • [Cites] Arthritis Rheum. 2006 May;54(5):1638-45 [16646026.001]
  • [Cites] Lancet. 2000 Jul 29;356(9227):385-90 [10972371.001]
  • [Cites] Neurology. 1999 Aug 11;53(3):457-65 [10449104.001]
  • [Cites] J Cutan Med Surg. 2003 May-Jun;7(3):198-207 [12717587.001]
  • [Cites] N Engl J Med. 1996 Jun 27;334(26):1717-25 [8637518.001]
  • [Cites] J Am Acad Dermatol. 2003 Jun;48(6):829-35 [12789171.001]
  • [Cites] Intern Med J. 2004 Dec;34(12):687-93 [15610214.001]
  • [Cites] Circulation. 1999 Jun 29;99(25):3224-6 [10385494.001]
  • [Cites] J Clin Invest. 1993 Nov;92(5):2303-12 [8227345.001]
  • [Cites] J Am Acad Dermatol. 2003 Aug;49(2 Suppl):S87-97 [12894131.001]
  • [Cites] N Engl J Med. 1991 Aug 15;325(7):467-72 [1852181.001]
  • [Cites] Ann Intern Med. 1999 Oct 19;131(8):634 [10523238.001]
  • [Cites] J Neuroimmunol. 1991 Apr;32(1):67-74 [2002092.001]
  • [Cites] N Engl J Med. 2001 Jul 26;345(4):248-55 [11474662.001]
  • [Cites] Arthritis Rheum. 2004 Jun;50(6):1740-51 [15188349.001]
  • [Cites] J Am Acad Dermatol. 2003 Aug;49(2 Suppl):S98-104 [12894132.001]
  • [Cites] J Invest Dermatol. 2000 Mar;114(3):587-90 [10692122.001]
  • [Cites] Neurology. 1996 Dec;47(6):1531-4 [8960740.001]
  • [Cites] Circulation. 2001 Feb 27;103(8):1044-7 [11222463.001]
  • [Cites] BioDrugs. 2005;19(1):47-57 [15691217.001]
  • [Cites] Arthritis Rheum. 2003 Feb;48(2):319-24 [12571839.001]
  • [Cites] Rheum Dis Clin North Am. 2004 May;30(2):237-55, v [15172038.001]
  • [Cites] Arch Dermatol. 2001 Jul;137(7):893-9 [11453808.001]
  • [Cites] J Am Acad Dermatol. 2003 Aug;49(2 Suppl):S105-11 [12894133.001]
  • [Cites] Dermatol Ther. 2004;17(5):401-8 [15379775.001]
  • [Cites] Ann Rheum Dis. 2002 Apr;61(4):298-304 [11874829.001]
  • (PMID = 16872241.001).
  • [ISSN] 0114-5916
  • [Journal-full-title] Drug safety
  • [ISO-abbreviation] Drug Saf
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  • [Number-of-references] 86
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14. Nakashima C, Tanioka M, Takahashi K, Miyachi Y: Diffuse large B-cell lymphoma in a patient with rheumatoid arthritis treated with infliximab and methotrexate. Clin Exp Dermatol; 2008 Jul;33(4):437-9
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  • [Title] Diffuse large B-cell lymphoma in a patient with rheumatoid arthritis treated with infliximab and methotrexate.
  • Infliximab is a tumour necrosis factor (TNF)-alpha blocking drug classified as a biological response modifier.
  • It has been suggested that the risk of malignancies, especially lymphomas, is increased in patients with rheumatoid arthritis (RA) treated with anti-TNF-alpha antibody therapy.
  • We present a case of malignant lymphoma during the treatment of RA with infliximab and methotrexate.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antirheumatic Agents / adverse effects. Arthritis, Rheumatoid / drug therapy. Lymphoma, Large B-Cell, Diffuse / chemically induced. Methotrexate / adverse effects. Skin Neoplasms / chemically induced


15. Kenny PA: Three-dimensional extracellular matrix culture models of EGFR signalling and drug response. Biochem Soc Trans; 2007 Aug;35(Pt 4):665-8
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  • Three-dimensional extracellular matrix culture, on substrata such as Matrigel, restores many aspects of the differentiated state to non-malignant cells from a variety of tissues.
  • We have adapted these techniques to study EGFR (epidermal growth factor receptor) signalling and drug response in breast cancer cell lines.
  • EGFR-dependent breast cancer cell lines undergo a striking reversion of the malignant phenotype upon treatment with inhibitors targeting the receptor, or downstream signalling intermediates such as mitogen-activated protein kinase and PI3K (phosphoinositide 3-kinase).
  • Using this approach, we have recently reported that EGFR signalling in breast cancer can be effectively inhibited by blocking the activity of a key protease, TACE [TNFalpha (tumour necrosis factor alpha)-converting enzyme], which regulates the bioavailability of EGFR ligands.
  • [MeSH-minor] Humans. Tumor Cells, Cultured

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  • (PMID = 17635116.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 38
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16. de Mestier L, Hammel P, Hentic O, Dove P, Lévy P, Ruszniewski P: [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency]. Gastroenterol Clin Biol; 2010 Jan;34(1):106-10
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  • [Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].
  • [Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.
  • Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.
  • We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright 2009. Published by Elsevier Masson SAS.
  • (PMID = 19875259.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil
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17. Sheldrake HM, Patterson LH: Function and antagonism of beta3 integrins in the development of cancer therapy. Curr Cancer Drug Targets; 2009 Jun;9(4):519-40
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  • The integrin family of cell surface receptors integrates cell-extracellular matrix interactions with the cell cytoskeleton and signalling across the cell membrane, resulting in an important role in cell adhesion, mobility and migration, proliferation, and survival.
  • Changes in the number and identity of integrin receptors are common in cancer cells resulting in alteration of the ability of malignant cells to interact with the extracellular matrix, and promoting migration as well as facilitating survival outside the tumour normal environment. beta(3) integrins are potentially involved in every step of the metastatic process and expression of both alpha(IIb)beta(3) and alpha(n)beta(3) is correlated with metastatic ability of tumour cells.
  • In this review, we summarize the role of the beta(3)-subfamily of integrins when expressed in normal and tumour tissue, the development of small-molecule antagonists of beta(3) integrins and their potential anti-cancer applications.

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  • (PMID = 19519320.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Disintegrins; 0 / Integrin beta3; 0 / Integrins; 0 / Peptides; 0 / Peptides, Cyclic
  • [Number-of-references] 265
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18. Miao R, Wei J, Zhang Q, Sajja V, Yang J, Wang Q: Redifferentiation of human hepatoma cells (SMMC-7721) induced by two new highly oxygenated bisabolane-type sesquiterpenes. J Biosci; 2008 Dec;33(5):723-30
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  • Bisabolane-type sesquiterpenes are a class of biologically active compounds that has antitumour,antifungal, antibacterial,antioxidant and antivenom properties.We investigated the effect of two new highly oxygenated bisabolane-type sesquiterpenes (HOBS)isolated from Cremanthodium discoideum (C.discoideum) on tumour cells.
  • Our results showed that HOBS induced morphological differentiation and reduced microvilli formation on the cell surface in SMMC-7721 cells.Flow cytometry analysis demonstrated that HOBS could induce cell-cycle arrest in the G1 phase.
  • Moreover,HOBS was able to increase tyrosine-alpha ketoglutarate transaminase activity,decrease alpha- foetoprotein level and gamma-glutamyl transferase activity.
  • In addition,we found that HOBS inhibited the anchorage- independent growth of SMMC-7721 cells in a dose-dependent manner.Taken together,all the above observations indicate that HOBS might be able to normalize malignant SMMC-7721 cells by inhibiting cell proliferation and inducing redifferentiation.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Hepatocellular / metabolism. Sesquiterpenes / pharmacology
  • [MeSH-minor] Asteraceae / chemistry. Cell Cycle / drug effects. Cell Differentiation / drug effects. Hepatocytes / drug effects. Humans. Molecular Structure. Structure-Activity Relationship. alpha-Fetoproteins / metabolism. gamma-Glutamyltransferase / metabolism

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  • [Cites] Gan To Kagaku Ryoho. 1989 Apr;16(4 Pt 2-2):1483-9 [2658830.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1383-9 [15585556.001]
  • [Cites] Pharmacol Res. 2004 Nov;50(5):505-10 [15458771.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2007 Feb;6(1):9-11 [17287158.001]
  • [Cites] Acta Pharmacol Sin. 2000 Apr;21(4):348-52 [11324465.001]
  • [Cites] Nature. 1990 Dec 6;348(6301):555-7 [1701033.001]
  • [Cites] Cancer Lett. 1985 Oct;29(1):1-14 [2866027.001]
  • [Cites] JOP. 2007 May 09;8(3):268-78 [17495355.001]
  • [Cites] J Nat Prod. 1994 May;57(5):658-62 [8064299.001]
  • [Cites] Acta Pharmacol Sin. 2001 Sep;22(9):785-92 [11749857.001]
  • [Cites] Zhongguo Yao Li Xue Bao. 1999 Nov;20(11):1019-24 [11270968.001]
  • [Cites] Chem Pharm Bull (Tokyo). 1985 Aug;33(8):3488-92 [4085078.001]
  • [Cites] Pharmazie. 2002 Nov;57(11):753-7 [12611279.001]
  • [Cites] Science. 1989 Nov 3;246(4930):603-8 [2683075.001]
  • [Cites] Biochem J. 1979 Apr 15;180(1):153-60 [39544.001]
  • [Cites] J Biosci. 2005 Feb;30(1):93-102 [15824445.001]
  • [Cites] J Nat Prod. 1999 Nov;62(11):1479-83 [10579856.001]
  • [Cites] Cell Biol Int. 2004;28(5):329-33 [15193276.001]
  • [Cites] Cell Biol Int. 1998;22(1):41-9 [9828081.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Shi Yan Sheng Wu Xue Bao. 1990 Jun;23(2):167-75 [2165342.001]
  • [Cites] Biomed Environ Sci. 2006 Oct;19(5):385-91 [17190193.001]
  • [Cites] Biochim Biophys Acta. 2005 Sep 10;1745(2):156-65 [16129123.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2776-8 [9096291.001]
  • [Cites] Clin Oncol (R Coll Radiol). 2004 Dec;16(8):569-74 [15630851.001]
  • [Cites] Planta Med. 1979 Feb;35(2):118-24 [419179.001]
  • (PMID = 19179760.001).
  • [ISSN] 0250-5991
  • [Journal-full-title] Journal of biosciences
  • [ISO-abbreviation] J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / 1beta,8-diangeloyloxy-2beta-acetoxy-4alpha-chloro-11-methoxy-3beta, 10-dihydroxybisabola-7(14)-ene; 0 / 1beta,8-diangeloyloxy-2beta-acetoxy-4alpha-chloro-3beta-hydroxy-10, 11-o,o-isopropylidenebis-aboia-7(14)-ene; 0 / Antineoplastic Agents, Phytogenic; 0 / Sesquiterpenes; 0 / alpha-Fetoproteins; EC 2.3.2.2 / gamma-Glutamyltransferase
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19. Ringdén O, Karlsson H, Olsson R, Omazic B, Uhlin M: The allogeneic graft-versus-cancer effect. Br J Haematol; 2009 Dec;147(5):614-33
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  • Allogeneic haematological stem cell transplantation (HSCT) has developed into immunotherapy.
  • Donor CD4+, CD8+ and natural killer (NK) cells have been reported to mediate graft-versus-leukaemia (GVL) effects, using Fas-dependent killing and perforin degranulation to eradicate malignant cells.
  • Cytokines, such as interleukin-2, interferon-gamma and tumour necrosis factor-alpha potentiate the GVL effect.
  • Post-transplant adoptive therapy of cytotoxic T-cells (CTL) against leukaemia-specific antigens, minor histocompatibility antigens, or T-cell receptor genes may constitute successful approaches to induce anti-tumour effects.
  • An anti-tumour effect has also been reported for myeloma, lymphoma and solid tumours.
  • Reduced intensity conditioning enables HSCT in older and disabled patients and relies on the graft-versus-tumour effect.
  • A high CD34+ cell dose of peripheral blood stem cells increases GVL.
  • For instance, T-cell depletion of the graft increases the risk of relapse.
  • [MeSH-major] Graft vs Tumor Effect / immunology. Hematopoietic Stem Cell Transplantation / methods. Neoplasms / therapy

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  • (PMID = 19735262.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 243
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20. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Alterations in dipeptidyl peptidase-IV (DPP-IV) enzymatic activity are characteristic of malignant transformation.
  • Through its well-characterized functionality in regulating the activity of bioactive peptides by removal of the N-terminal dipeptide, DPP-IV activity may have profound effects upon metastatic potential and cell growth.
  • Although DPP-IV/CD26 (EC 3.4.14.5) is the canonical representative of the group, a number of other proteins including DPP-7, 8, 9, and seprase/fibroblast activation protein-alpha (FAP-alpha) have been shown to have similar enzymatic activity.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • In parallel, expression of CXCR4, receptor for glioma cell growth stimulator chemokine SDF-1alpha known to be a DPP-IV substrate, was investigated.
  • This is the first report showing that non-malignant brain tissue contains a DPP-IV-like enzymatic activity attributable mostly to DPP-8/9, while the substantial part of the activity in glioma is due to increased DPP-IV/CD26, localized in both the vascular and parenchymal compartments.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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21. Zisakis A, Piperi C, Themistocleous MS, Korkolopoulou P, Boviatsis EI, Sakas DE, Patsouris E, Lea RW, Kalofoutis A: Comparative analysis of peripheral and localised cytokine secretion in glioblastoma patients. Cytokine; 2007 Aug;39(2):99-105
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  • BACKGROUND: Malignant gliomas are the most common primary brain tumours of both children and adults.
  • The unique aspects of their biology and anatomic site render them refractory to conventional therapeutic strategies such as surgery and chemotherapy.
  • METHODS: To further understand the immunobiology of glioblastomas in clinical settings, we examined the secretion of four main cytokines in the peripheral blood and in primary cell cultures of 33 human glioblastoma patients.
  • An ELISPOT methodology was used for the first time to examine Th1, and Th2 cytokine secretion from both peripheral lymphocytes and glioma tumour cells.
  • RESULTS: Th1 cytokines (tumour necrosis factor (TNF-alpha), interferon (IFN-gamma) were markedly reduced compared to control levels (P=0.01 and P<0.001, respectively), whereas in contrast, Th2 (interleukin (IL)-4 and IL-10) were strongly expressed in both peripheral lymphocytes and glioma cell cultures (P=0.05 and P<0.001, respectively).
  • Furthermore, ELISPOT methodology can be used for monitoring of cytokine secretion from tumour cells, in addition to the well-established peripheral cytokine secretion.
  • [MeSH-minor] Adult. Aged. Cells, Cultured. Female. Humans. Interferon-gamma / metabolism. Interferon-gamma / secretion. Interleukin-10 / metabolism. Interleukin-10 / secretion. Interleukin-1beta / metabolism. Interleukin-1beta / secretion. Interleukin-4 / metabolism. Interleukin-4 / secretion. Male. Middle Aged. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 17697783.001).
  • [ISSN] 1043-4666
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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22. Stirewalt DL, Mhyre AJ, Marcondes M, Pogosova-Agadjanyan E, Abbasi N, Radich JP, Deeg HJ: Tumour necrosis factor-induced gene expression in human marrow stroma: clues to the pathophysiology of MDS? Br J Haematol; 2008 Feb;140(4):444-53
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  • [Title] Tumour necrosis factor-induced gene expression in human marrow stroma: clues to the pathophysiology of MDS?
  • Aberrant regulation of the tumour necrosis factor alpha gene (TNF) and stroma-derived signals are involved in the pathophysiology of myelodysplasia.
  • Therefore, KG1a, a myeloid leukaemia cell line, was exposed to Tnf in the absence or presence of either HS-5 or HS-27a cells, two human stroma cell lines.
  • DNA microarray studies found both discordant and concordant Tnf-induced expression responses in the two stroma cell lines.
  • Overall, the results suggested that Tnf induced a complex set of pro-inflammatory and pro-apoptotic signals in stroma cells that promote apoptosis in malignant myeloid clones.
  • Additional studies will be required to determine which of these signals are critical for the induction of apoptosis in the malignant clones.
  • [MeSH-major] Bone Marrow Cells / drug effects. Gene Expression Regulation / drug effects. Myelodysplastic Syndromes / physiopathology. Stromal Cells / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis Regulatory Proteins / biosynthesis. Apoptosis Regulatory Proteins / genetics. Cell Line. Coculture Techniques. Cytokines / biosynthesis. Cytokines / genetics. Humans. Inflammation Mediators / metabolism. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / drug effects. Tumor Cells, Cultured


23. Sulkowska M, Wincewicz A, Sulkowski S, Koda M, Kanczuga-Koda L: Relations of TGF-beta1 with HIF-1 alpha, GLUT-1 and longer survival of colorectal cancer patients. Pathology; 2009;41(3):254-60
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  • [Title] Relations of TGF-beta1 with HIF-1 alpha, GLUT-1 and longer survival of colorectal cancer patients.
  • AIMS AND METHODS: During colorectal carcinogenesis, transforming growth factor beta 1 (TGF-beta1) undergoes a functional change from suppression of cancer cell proliferation to inhibition of T cell mediated anti-cancer immunity.
  • We aimed to evaluate relations among TGF-beta1 and cancer cell survival factors hypoxia inducible factor-1 alpha (HIF-1 alpha) and glucose transporter 1 (GLUT-1) by immunohistochemistry in 108 colorectal cancers.
  • RESULTS: TGF-beta1 was detected in 87% (94/108), HIF-1 alpha in 85% (92/108), and GLUT-1 in 65% (70/108) of colorectal cancers.
  • GLUT-1 was visualised in a membranous fashion while HIF-1 was expressed in a paranuclear pattern and occasionally in nuclei of malignant cells.
  • Cancer immunoreactivities to TGF-beta1 correlated with HIF-1 alpha (p < 0.001, r = 0.516) and GLUT-1 (p < [corrected] 0.001, r = 0.355) in general and subgroups of different clinicopathological traits.
  • TGF-beta1 expressions of inflammatory infiltrates correlated with longer patient survival (p = 0.05, r = 0.449) and immunoreactivities to HIF-1 alpha of cancer cells (p = 0.008, r = 0.254) particularly in node positive and deeply invading cancers but failed to associate significantly with GLUT-1.
  • CONCLUSIONS: HIF-1 alpha and GLUT-1 could cooperate with TGF-beta1, and TGF-beta1 might mediate cross-talk between the inflammatory environment and tumour with a favourable impact on patient survival.
  • [MeSH-major] Colorectal Neoplasms / metabolism. Colorectal Neoplasms / mortality. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Transforming Growth Factor beta1 / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Receptor Cross-Talk / physiology

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  • [ErratumIn] Pathology. 2009;41(6):612
  • (PMID = 19142800.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transforming Growth Factor beta1
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24. Hadar T, Shvero J, Yaniv E, Shvili I, Leabu M, Koren R: Human topoisomerase II-alpha is highly expressed in sinonasal-inverted papilloma, but not in inflammatory polyp. J Cell Mol Med; 2008 Sep-Oct;12(5A):1551-8
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  • [Title] Human topoisomerase II-alpha is highly expressed in sinonasal-inverted papilloma, but not in inflammatory polyp.
  • Sinonasal-inverted papilloma is a benign tumour with a high rate of recurrence, but possible malignant transformation.
  • Therefore, investigation of predisposition to malignant transformation of sinonasal-inverted papilloma gives clinicians the opportunity for adequate treatment.
  • Topoisomerase II-alpha (topoII-alpha) and Ki67 are markers of cell proliferation in both normal and neoplastic tissues and its level o expression could be used as a predictive parameter.
  • TopoI alpha nuclear immunostaining showed a differential positivity in the investigated cases.
  • The topoII-alpha index was 30.6 +/- 12.8 in inverte papilloma, 10.7 +/- 6.6 in the adjacent epithelium of inverted papilloma, but only 2.3 +/- 2.0 in the normal sinonasal epithelium.
  • The differences in topoII-alpha expression between inverted papilloma and normal sinonasal epithelia were statistically significant.
  • In inflammatory nasal polyp group, topoII-alpha index was 2.4 +/- 2.1, and the difference in the topoII-alpha index between inverted papilloma and inflammatory polyp group was also statistically significant.
  • Significant correlation coefficients were found between topoII-alpha and epithelial thickness (r = 0.70, P > 0.0001), and between Ki67 index and epithelial thickness (r = 0.71, P> 0.0001).
  • Significant correlation coefficient was found between topoII-alpha index and Ki67 index in inverted papilloma (r = 0.42, P > 0.05).
  • These results suggest that the inverte papilloma contains a significantly higher cell population with proliferative activity by comparison with normal sinonasal and inflammatory polyp epithelia, showing a significant correlation between topoII-alpha and Ki67 expression, and indicating that topoII-alpha could be a independent prognostic factor for a putative malignant transformation.

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  • (PMID = 18544048.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC3918071
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25. Buritica C, Serrano M, Zuluaga A, Arrabal M, Regauer S, Nogales FF: Mixed epithelial and stromal tumour of the kidney with luteinised ovarian stroma. J Clin Pathol; 2007 Jan;60(1):98-100
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  • [Title] Mixed epithelial and stromal tumour of the kidney with luteinised ovarian stroma.
  • We report a case of a 9-cm mixed epithelial and stromal tumour of the kidney in an obese 70-year-old woman with diabetes.
  • The ovarian-type stroma had a spindle cell component that was positive for progesterone receptors and had the hitherto unreported presence of abundant foci of luteinised stromal cells with characteristic immunohistochemical positivity to alpha-inhibin, calretinin, aromatase and gonadotropin-releasing hormone (GnRH) receptors.
  • [MeSH-major] Kidney Neoplasms / pathology. Mixed Tumor, Malignant / pathology. Neoplasms, Glandular and Epithelial / pathology

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  • [Cites] Am J Surg Pathol. 2000 Jul;24(7):958-70 [10895818.001]
  • [Cites] Histopathology. 2002 Sep;41(3):277-9 [12207796.001]
  • [Cites] Mod Pathol. 2003 Jun;16(6):584-90 [12808064.001]
  • [Cites] Histopathology. 2003 Jul;43(1):97-8 [12823720.001]
  • [Cites] Virchows Arch. 2004 Oct;445(4):359-67 [15322873.001]
  • [Cites] Arch Pathol Lab Med. 2004 Nov;128(11):1294-6 [15504068.001]
  • [Cites] Mod Pathol. 2005 Apr;18(4):573-6 [15529183.001]
  • [Cites] Am J Surg Pathol. 1994 Nov;18(11):1078-91 [7943529.001]
  • [Cites] Virchows Arch. 1998 May;432(5):451-4 [9645445.001]
  • [Cites] Am J Surg Pathol. 1999 Jan;23(1):1-16 [9888699.001]
  • [Cites] Oncogene. 2004 Dec 2;23(56):9042-51 [15489895.001]
  • [Cites] Arch Pathol Lab Med. 2004 Dec;128(12):1404-11 [15578885.001]
  • [Cites] Urology. 1994 Apr;43(4):549-53 [8154082.001]
  • (PMID = 17213356.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860583
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26. Daniels RA, Turley H, Kimberley FC, Liu XS, Mongkolsapaya J, Ch'En P, Xu XN, Jin BQ, Pezzella F, Screaton GR: Expression of TRAIL and TRAIL receptors in normal and malignant tissues. Cell Res; 2005 Jun;15(6):430-8
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  • [Title] Expression of TRAIL and TRAIL receptors in normal and malignant tissues.
  • TRAIL, tumor necrosis factor-related apoptosis-inducing ligand, is a member of the TNF family of proteins.
  • Tumour cells were initially found to have increased sensitivity to TRAIL compared with normal cells, raising hopes that TRAIL would prove useful as an anti-tumor agent.
  • The production of reliable monoclonal antibodies against TRAIL and its receptors that can stain fixed specimens will allow a thorough analysis of their expression on normal and malignant tissues.
  • Here we report the generation of monoclonal antibodies against TRAIL and its four membrane-bound receptors (TR1-4), which have been used to stain a range of normal and malignant cells, as routinely fixed specimens.
  • TR1 and TR2 expression increases significantly in a number of malignant tissues, but in some common malignancies their expression was low, or patchy, which may limit the therapeutic role of TRAIL.
  • [MeSH-major] Membrane Glycoproteins / biosynthesis. Neoplasms / physiopathology. Receptors, Tumor Necrosis Factor / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Antibodies, Monoclonal / biosynthesis. Apoptosis / drug effects. Apoptosis Regulatory Proteins. Female. GPI-Linked Proteins. Humans. Immunohistochemistry / methods. Jurkat Cells. Male. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor, Member 10c. Staining and Labeling / methods. TNF-Related Apoptosis-Inducing Ligand. Tissue Distribution. Tumor Necrosis Factor Decoy Receptors

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  • (PMID = 15987601.001).
  • [ISSN] 1001-0602
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0400720
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Apoptosis Regulatory Proteins; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 10c; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / Tumor Necrosis Factor-alpha
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27. Nakabayashi H, Yawata T, Shimizu K: Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells. BMC Cancer; 2010;10:339
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  • [Title] Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells.
  • BACKGROUND: The constitutive overexpression of matrix metalloproteinases (MMPs) is frequently observed in malignant tumours.
  • In particular, MMP-2 and MMP-9 have been reported to be closely associated with invasion and angiogenesis in malignant gliomas.
  • Our study aimed to evaluate the antitumour effects of MMI-166 (Nalpha-[4-(2-Phenyl-2H- tetrazole-5-yl) phenyl sulfonyl]-D-tryptophan), a third generation MMP inhibitor, on three human glioma cell lines (T98G, U87MG, and ONS12) in vitro and in vivo.
  • The angiogenesis assay showed that MMI-166 had a suppressive effect on glioma cell-induced angiogenesis.
  • However, MMI-166 did not suppress glioma cell proliferation in the MTT assay.
  • In vivo, MMI-166 suppressed tumour growth in athymic mice implanted orthotropically with T98G cells and showed an inhibitory effect on tumour-induced angiogenesis and tumour growth.
  • This is the first report of the effect of a third generation MMP inhibitor on malignant glioma cells.
  • CONCLUSIONS: These results suggest that MMI-166 may have potentially suppressive effects on the invasion and angiogenesis of malignant gliomas.
  • [MeSH-minor] Animals. Brain Neoplasms / blood supply. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Female. Humans. Matrix Metalloproteinase Inhibitors. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasm Invasiveness. Tumor Cells, Cultured


28. Perluigi M, Giorgi A, Blarzino C, De Marco F, Foppoli C, Di Domenico F, Butterfield DA, Schininà ME, Cini C, Coccia R: Proteomics analysis of protein expression and specific protein oxidation in human papillomavirus transformed keratinocytes upon UVB irradiation. J Cell Mol Med; 2009 Aug;13(8B):1809-22
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  • In order to investigate the involvement of oxidative damage into the mechanisms of tumour progression, we used a parallel proteomic approach to analyse the protein expression profile and to identify oxidatively modified proteins in human papillomavirus (HPV)-transformed keratinocytes (HK-168 cells) upon ultraviolet B (UVB) exposure.
  • The HK-168 cells were obtained from normal human epidermal keratinocytes transfected with the whole genome of the high-risk HPV type 16, unanimously recognized as an etiological agent of cervical carcinoma.
  • Because of its year-long latency, this tumour offers a convenient model to study the role of environmental concurring agents in the multistep malignant progression.
  • Focusing on the oxidative modifications occurring at the protein level, we identified five proteins that showed elevated protein carbonyls levels: alpha-enolase, heat shock protein 75, annexin 2, elongation factor Tu and elongation factor gamma.
  • We suggest that UVB-induced modulation of protein expression combined with oxidative modification lead to protein dysfunction that might contribute to the malignant progression of transformed cells.
  • [MeSH-minor] Blotting, Western. Cell Line, Transformed. Electrophoresis, Gel, Two-Dimensional. Humans. Oxidation-Reduction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 19267883.001).
  • [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 / Proteins
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29. Balkwill F: Tumour necrosis factor and cancer. Nat Rev Cancer; 2009 May;9(5):361-71
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  • [Title] Tumour necrosis factor and cancer.
  • Tumour necrosis factor (TNF) is a major inflammatory cytokine that was first identified for its ability to induce rapid haemorrhagic necrosis of experimental cancers.
  • When efforts to harness this anti-tumour activity in cancer treatments were underway, a paradoxical tumour-promoting role of TNF became apparent.
  • Now that links between inflammation and cancer are appreciated, is TNF a target or a therapeutic in malignant disease -- or both?
  • [MeSH-major] Neoplasms / etiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Clinical Trials as Topic. Cytotoxicity, Immunologic. DNA Damage. Endotoxins / toxicity. Humans. Inflammation / etiology. Receptors, Tumor Necrosis Factor / physiology. Recombinant Proteins / therapeutic use

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  • [Cites] Nature. 2007 Dec 6;450(7171):903-7 [18026089.001]
  • [Cites] Lancet. 2001 Jun 9;357(9271):1842-7 [11410193.001]
  • [Cites] Lancet. 1989 Jul 29;2(8657):244-7 [2569055.001]
  • [Cites] Nat Rev Immunol. 2002 May;2(5):364-71 [12033742.001]
  • [Cites] Eur J Cancer Clin Oncol. 1986 Apr;22(4):419-26 [3089802.001]
  • [Cites] Clin Cancer Res. 2004 Oct 1;10(19):6528-34 [15475440.001]
  • [Cites] Cancer Gene Ther. 2009 Apr;16(4):373-81 [18974777.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5277-81 [2440047.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):445-56 [17996648.001]
  • [Cites] J Immunol. 1999 Nov 15;163(10):5358-66 [10553060.001]
  • [Cites] J Clin Invest. 2008 Feb;118(2):560-70 [18219394.001]
  • [Cites] Cancer Res. 1987 Jun 1;47(11):2986-9 [3567916.001]
  • [Cites] Cancer Res. 2009 Jan 1;69(1):338-48 [19118019.001]
  • [Cites] Mol Cancer Ther. 2006 Feb;5(2):382-90 [16505113.001]
  • [Cites] J Immunol. 2003 Jun 15;170(12):6172-82 [12794148.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5657-62 [10318940.001]
  • [Cites] Cancer Res. 1946 Apr;6:205-16 [21018724.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3814-8 [3889916.001]
  • [Cites] J Clin Invest. 2008 Nov;118(11):3533-6 [18982159.001]
  • [Cites] Nature. 1987 Oct 15-21;329(6140):630-2 [2443857.001]
  • [Cites] Cancer. 2003 Mar 1;97(5):1211-6 [12599227.001]
  • [Cites] J Biol Chem. 1984 Jan 10;259(1):686-91 [6608523.001]
  • [Cites] Curr Opin Pharmacol. 2004 Aug;4(4):314-20 [15251122.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3183-94 [18039949.001]
  • [Cites] Proc R Soc Med. 1910;3(Surg Sect):1-48 [19974799.001]
  • [Cites] J Rheumatol Suppl. 1999 May;57:16-21 [10328138.001]
  • [Cites] Front Biosci. 2008 May 01;13:5094-107 [18508572.001]
  • [Cites] Cancer Metastasis Rev. 2006 Sep;25(3):409-16 [16951987.001]
  • [Cites] J Clin Invest. 2007 Dec;117(12):3833-45 [17992258.001]
  • [Cites] Nat Med. 2007 Sep;13(9):1050-9 [17704786.001]
  • [Cites] Cell. 1990 Apr 20;61(2):361-70 [2158863.001]
  • [Cites] Anticancer Res. 2001 Mar-Apr;21(2B):1355-8 [11396212.001]
  • [Cites] Eur J Immunol. 2005 May;35(5):1592-600 [15832287.001]
  • [Cites] J Immunol. 2006 Apr 15;176(8):5023-32 [16585599.001]
  • [Cites] N Engl J Med. 2006 Feb 16;354(7):697-708 [16481637.001]
  • [Cites] Int J Cancer. 1986 Nov 15;38(5):763-9 [3095251.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9784-8 [1409699.001]
  • [Cites] J Biol Chem. 1990 Apr 5;265(10):5708-17 [2156825.001]
  • [Cites] Hepatology. 2008 Mar;47(3):888-96 [18306229.001]
  • [Cites] Oncogene. 2004 Mar 11;23(10):1902-10 [14661063.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jan 15;105(2):652-6 [18178624.001]
  • [Cites] JAMA. 2006 May 17;295(19):2275-85 [16705109.001]
  • [Cites] Cancer Res. 1993 May 1;53(9):1982-5 [8481899.001]
  • [Cites] Curr Opin Rheumatol. 2008 May;20(3):334-9 [18388527.001]
  • [Cites] J Clin Invest. 2007 Nov;117(11):3283-95 [17960249.001]
  • [Cites] Eur J Immunol. 2000 Jul;30(7):1957-66 [10940885.001]
  • [Cites] Nature. 2009 Jan 1;457(7225):102-6 [19122641.001]
  • [Cites] Cancer Res. 2008 Mar 1;68(5):1443-50 [18316608.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11565-70 [17178846.001]
  • [Cites] Br J Cancer. 2004 Jun 14;90(12):2312-6 [15150588.001]
  • [Cites] J Exp Med. 1996 Oct 1;184(4):1397-411 [8879212.001]
  • [Cites] Nature. 1992 May 7;357(6373):11-2 [1574121.001]
  • [Cites] J Immunol. 2007 Jul 1;179(1):154-61 [17579033.001]
  • [Cites] Nat Rev Immunol. 2003 Sep;3(9):745-56 [12949498.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4273-7 [3108890.001]
  • [Cites] Cancer. 1988 Dec 15;62(12):2467-71 [3191449.001]
  • [Cites] Mol Biol Cell. 2003 May;14(5):1790-800 [12802055.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):5950-9 [16135466.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1038-45 [17283136.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4516-8 [10493498.001]
  • [Cites] Ann Oncol. 2008 Jul;19(7):1340-6 [18325912.001]
  • [Cites] Cell. 2005 Jul 1;121(7):977-90 [15989949.001]
  • [Cites] J Exp Med. 1988 Mar 1;167(3):1067-85 [3351434.001]
  • [Cites] J Immunol. 1987 Jun 1;138(11):4023-32 [3295044.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1776-84 [16541435.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Mar;8(2):124-31 [18336195.001]
  • [Cites] J Immunol. 1984 Feb;132(2):936-44 [6690624.001]
  • [Cites] J Clin Invest. 1993 May;91(5):2194-206 [8387543.001]
  • [Cites] Nat Rev Drug Discov. 2006 Mar;5(3):235-46 [16474316.001]
  • [Cites] Int J Cancer. 2004 Dec 20;112(6):927-33 [15386364.001]
  • [Cites] Cell. 2001 Feb 23;104(4):487-501 [11239407.001]
  • [Cites] Nature. 1985 Aug 8-14;316(6028):552-4 [2993897.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):592-601 [14726502.001]
  • [Cites] Nucleic Acids Res. 1985 Jun 25;13(12):4417-29 [2989794.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):122-9 [17210691.001]
  • [Cites] Nature. 2006 Jul 27;442(7101):461-5 [16688182.001]
  • [Cites] Cell. 2004 Feb 20;116(4):491-7 [14980217.001]
  • [Cites] Nature. 1985 Dec 19-1986 Jan 1;318(6047):665-7 [3001529.001]
  • [Cites] Nature. 1984 Dec 20-1985 Jan 2;312(5996):724-9 [6392892.001]
  • [Cites] Ann Rheum Dis. 1999 Nov;58 Suppl 1:I114-20 [10577987.001]
  • [Cites] Cell. 2004 Aug 6;118(3):285-96 [15294155.001]
  • [Cites] Science. 1990 May 25;248(4958):1019-23 [2160731.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6682-7 [12438267.001]
  • [Cites] J Exp Med. 2008 Jun 9;205(6):1261-8 [18490490.001]
  • [Cites] Immunology. 2005 May;115(1):1-20 [15819693.001]
  • [Cites] Cancer Res. 1988 Feb 1;48(3):650-3 [3335027.001]
  • [Cites] Eur J Cancer. 1990;26(10):1027-30 [2148874.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6319-23 [9177215.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23 (7):2316-28 [12640117.001]
  • [Cites] Cytokine. 2004 Jul 21-Aug 7;27(2-3):58-65 [15242694.001]
  • [Cites] Curr Treat Options Oncol. 2007 Dec;8(6):417-27 [18066703.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9825-34 [17942913.001]
  • [Cites] Cancer Res. 1986 Aug;46(8):3990-3 [2425938.001]
  • [Cites] J Biol Chem. 1990 Jan 25;265(3):1531-6 [2153136.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):57-61 [16397216.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):420-30 [12189384.001]
  • [Cites] Int J Cancer. 1989 Nov 15;44(5):918-25 [2583871.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):18-21 [12517770.001]
  • [Cites] Lancet. 1999 May 15;353(9165):1689-94 [10335805.001]
  • [Cites] Lancet. 2000 Jul 29;356(9227):385-90 [10972371.001]
  • [Cites] Immunol Today. 1989 Nov;10(11):370-5 [2514701.001]
  • [Cites] J Clin Oncol. 1992 Jan;10(1):52-60 [1727926.001]
  • [Cites] Cancer Chemother Pharmacol. 1987;20(3):223-9 [3315281.001]
  • [Cites] J Biol Chem. 1989 Jul 15;264(20):11974-80 [2545693.001]
  • [Cites] Cancer Res. 1988 Feb 1;48(3):544-50 [3257167.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Sep;80(17):5397-401 [6193516.001]
  • [Cites] Mol Cancer Ther. 2003 May;2(5):445-51 [12748306.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1396-400 [11986770.001]
  • [Cites] J Exp Med. 1993 May 1;177(5):1391-8 [8478614.001]
  • [Cites] Ann Surg. 1891 Sep;14(3):199-220 [17859590.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1215-9 [12149200.001]
  • [Cites] Mutat Res. 2003 Feb-Mar;523-524:119-25 [12628509.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Sep;72(9):3666-70 [1103152.001]
  • [Cites] Curr Opin Immunol. 2008 Apr;20(2):241-6 [18508251.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] EMBO J. 2008 Jun 18;27(12 ):1671-81 [18511911.001]
  • [Cites] Cancer Res. 2006 Dec 1;66(23):11125-30 [17145855.001]
  • [Cites] J Immunol. 1984 May;132(5):2464-9 [6609199.001]
  • [Cites] Br J Cancer. 1987 Dec;56(6):803-8 [3435706.001]
  • [Cites] Nat Rev Immunol. 2004 Jul;4(7):499-511 [15229469.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9455-62 [17909055.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Aug;87(16):6151-5 [2166946.001]
  • [Cites] Lancet. 1994 Oct 22;344(8930):1105-10 [7934491.001]
  • [Cites] J Immunol. 2005 Jul 15;175(2):1197-205 [16002723.001]
  • [Cites] J Biol Chem. 1985 Feb 25;260(4):2345-54 [3871770.001]
  • [Cites] Nature. 1984 Dec 20-1985 Jan 2;312(5996):721-4 [6334807.001]
  • [Cites] Br J Cancer. 2000 Feb;82(4):973-80 [10732774.001]
  • [Cites] J Clin Oncol. 2007 Oct 10;25(29):4542-9 [17925549.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6563-6 [3476961.001]
  • [Cites] Nat Med. 1999 Jul;5(7):828-31 [10395330.001]
  • [Cites] Pharmacol Ther. 2008 Feb;117(2):244-79 [18155297.001]
  • [Cites] Immunity. 2005 Jan;22(1):93-104 [15664162.001]
  • [Cites] Leuk Lymphoma. 2005 Apr;46(4):509-16 [16019478.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):585-92 [17234767.001]
  • [Cites] Clin Orthop Relat Res. 1991 Jan;(262):3-11 [1984929.001]
  • [Cites] J Exp Med. 1988 Aug 1;168(2):637-47 [3411290.001]
  • [Cites] J Pathol. 2007 Mar;211(4):439-46 [17253597.001]
  • [Cites] J Immunol. 1999 Aug 1;163(3):1521-8 [10415055.001]
  • [Cites] Science. 1985 Nov 22;230(4728):943-5 [3933111.001]
  • [Cites] Cell. 1996 Nov 1;87(3):565-76 [8898208.001]
  • [Cites] Trends Immunol. 2007 Aug;28(8):333-9 [17597006.001]
  • [Cites] J Immunol. 2008 Jun 15;180(12):8176-83 [18523283.001]
  • [Cites] Eur J Cancer. 1990;26(10):1031-4 [2148875.001]
  • [Cites] Br J Cancer. 1996 Dec;74(12):1908-15 [8980389.001]
  • [Cites] Trends Immunol. 2006 Aug;27(8):352-7 [16807108.001]
  • [Cites] Exp Cell Res. 1987 Jun;170(2):428-38 [3109929.001]
  • [Cites] Acta Med Scand Suppl. 1953;276:1-103 [13039964.001]
  • [Cites] Trends Immunol. 2004 Jun;25(6):280-8 [15145317.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7380-4 [2170974.001]
  • [Cites] Nature. 2004 Sep 23;431(7007):461-6 [15329734.001]
  • [Cites] Nature. 2008 Jul 24;454(7203):436-44 [18650914.001]
  • [Cites] Br J Cancer. 1999 Apr;80(1-2):161-6 [10389992.001]
  • [Cites] Nutr Rev. 1988 Nov;46(11):389-91 [3070444.001]
  • [Cites] N Engl J Med. 2004 Feb 26;350(9):876-85 [14985485.001]
  • [Cites] J Immunol. 2000 Apr 1;164(7):3645-51 [10725721.001]
  • [Cites] J Biochem Mol Biol. 2006 Jan 31;39(1):1-8 [16466631.001]
  • [Cites] Eur J Biochem. 1985 Nov 4;152(3):515-22 [3932069.001]
  • [Cites] Cell. 2007 Aug 10;130(3):440-55 [17693255.001]
  • [Cites] Cell. 1990 Apr 20;61(2):351-9 [2158862.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5064-8 [2662193.001]
  • [Cites] J Immunol. 1968 Jul;101(1):111-20 [5690881.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):211-7 [15766659.001]
  • [Cites] J Biol Chem. 1985 Feb 25;260(4):2334-44 [3882692.001]
  • [Cites] J Exp Med. 2007 Jan 22;204(1):33-9 [17200409.001]
  • (PMID = 19343034.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endotoxins; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 171
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30. Buckstein R, Meyer RM, Seymour L, Biagi J, Mackay H, Laurie S, Eisenhauer E: Phase II testing of sunitinib: the National Cancer Institute of Canada Clinical Trials Group IND Program Trials IND.182-185. Curr Oncol; 2007 Aug;14(4):154-61
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  • Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).
  • In the present article, we discuss the biologic and clinical rationales that have recently led the Investigational New Drug Program of the National Cancer Institute of Canada Clinical Trials Group to initiate four phase ii trials testing this agent in the following four different tumour types: relapsed diffuse large cell lymphoma, malignant pleural mesothelioma, locally advanced or metastatic cervical cancer and recurrent epithelial ovarian, fallopian tube, or primary peritoneal carcinoma.

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  • [Cites] Semin Oncol. 1994 Feb;21(1):54-62 [8310310.001]
  • [Cites] N Engl J Med. 1993 Apr 8;328(14):1002-6 [7680764.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):792-5 [8622025.001]
  • [Cites] Eur J Cancer. 1997 Mar;33(3):500-2 [9155539.001]
  • [Cites] Br J Cancer. 1997;76(9):1221-7 [9365173.001]
  • [Cites] Virchows Arch. 1999 Jul;435(1):8-12 [10431840.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):504-9 [10460612.001]
  • [Cites] Br J Cancer. 1999 Sep;81(1):54-61 [10487612.001]
  • [Cites] Int J Oncol. 2000 Apr;16(4):777-82 [10717248.001]
  • [Cites] Blood. 2000 Jul 1;96(1):282-7 [10891463.001]
  • [Cites] Exp Hematol. 2000 Sep;28(9):993-1000 [11008011.001]
  • [Cites] Cancer Metastasis Rev. 2000;19(1-2):167-72 [11191056.001]
  • [Cites] J Pathol. 2001 Apr;193(4):468-75 [11276005.001]
  • [Cites] Gynecol Oncol. 2001 May;81(2):213-5 [11354055.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3658-61 [11369666.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4341-4 [11389057.001]
  • [Cites] Med Oncol. 2001;18(4):269-75 [11918453.001]
  • [Cites] Semin Oncol. 2002 Apr;29(2 Suppl 6):18-22 [12040530.001]
  • [Cites] Gynecol Oncol. 2002 Jun;85(3):469-75 [12051876.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1484-93 [12359857.001]
  • [Cites] Mol Pathol. 2002 Dec;55(6):348-59 [12456770.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):377-82 [12538491.001]
  • [Cites] Int J Cancer. 2003 May 1;104(5):603-10 [12594815.001]
  • [Cites] Adv Exp Med Biol. 2003;522:83-97 [12674213.001]
  • [Cites] Nat Med. 2003 Jun;9(6):653-60 [12778163.001]
  • [Cites] Lancet. 2003 Jun 21;361(9375):2099-106 [12826431.001]
  • [Cites] Bone Marrow Transplant. 2003 Oct;32(7):673-9 [13130314.001]
  • [Cites] Blood. 1992 Oct 15;80(8):2142-8 [1356515.001]
  • [Cites] Am J Epidemiol. 2004 Jan 15;159(2):107-12 [14718210.001]
  • [Cites] Ann Oncol. 2004 Feb;15(2):257-60 [14760119.001]
  • [Cites] Clin Exp Metastasis. 2004;21(2):107-18 [15168728.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2893-902 [15238424.001]
  • [Cites] Blood. 2005 Feb 1;105(3):986-93 [15459012.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):489-501 [15516973.001]
  • [Cites] Cancer. 2005 Feb 15;103(4):724-30 [15637689.001]
  • [Cites] Cancer Cell. 2005 Jan;7(1):101-11 [15652753.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Gynecol Oncol. 2005 Mar;96(3):902-5 [15721449.001]
  • [Cites] J Clin Oncol. 2005 Jul 20;23(21):4626-33 [15911865.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Dec;315(3):971-9 [16002463.001]
  • [Cites] Leuk Lymphoma. 2005 Sep;46(9):1345-51 [16109613.001]
  • [Cites] Curr Opin Oncol. 2005 Nov;17(6):611-6 [16224242.001]
  • [Cites] Ann Oncol. 2005;16 Suppl 8:viii13-viii19 [16239232.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5190-8 [16951238.001]
  • [Cites] Science. 2006 Sep 22;313(5794):1785-7 [16990548.001]
  • [Cites] Lancet. 2006 Oct 14;368(9544):1329-38 [17046465.001]
  • [Cites] N Engl J Med. 2007 Jan 11;356(2):115-24 [17215529.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):884-96 [17327610.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):389-93 [1999708.001]
  • [Cites] N Engl J Med. 1987 Jun 11;316(24):1493-8 [3295541.001]
  • [Cites] J Clin Oncol. 1985 Aug;3(8):1079-85 [3894589.001]
  • [Cites] Radiother Oncol. 1995 May;35(2):107-17 [7569018.001]
  • [Cites] Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):805-7 [8456884.001]
  • (PMID = 17710208.001).
  • [ISSN] 1198-0052
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1948864
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31. Siddiqui EJ, Shabbir M, Thompson CS, Mumtaz FH, Mikhailidis DP: Growth inhibitory effect of doxazosin on prostate and bladder cancer cells. Is the serotonin receptor pathway involved? Anticancer Res; 2005 Nov-Dec;25(6B):4281-6
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  • Alpha-adrenoceptor antagonists also inhibit growth and induce apoptosis in malignant prostatic cells.
  • The apoptotic activity is independent of their capacity to antagonize alpha-adrenoceptors.
  • The effect of doxazosin on the growth of prostate and bladder cancer cell lines was assessed and whether the growth inhibitory effect of doxazosin on prostate cancer cells is serotonin (5-hydroxtryptamine; 5HT)-dependent was investigated.
  • MATERIALS AND METHODS: PC3 (androgen-independent prostate cancer) and HT1376 (grade III transitional cell carcinoma) cells were plated.
  • After 72 h, cell viability was assessed (crystal violet assay).
  • Cell viability was assessed at 72 h.
  • RESULTS: Doxazosin caused a dose-dependent inhibition of PC3 and HT1376 cell growth with a maximum inhibition of 80% (n=12, p < 0.0001) and 91% (n=12, p < 0.0001), respectively, at a concentration of 10(-4)M, at 72 h.
  • CONCLUSION: Doxazosin significantly inhibited prostate (PC3) and bladder cancer (HT1376) cell growth.
  • Furthermore, prior incubation of PC3 cells with 5HT or 5HT(1B) agonist increased cell viability as compared to treatment with doxazosin alone.
  • The effect of alpha1-adrenoceptor antagonists on tumour cell growth merits further investigation.
  • [MeSH-major] Adrenergic alpha-Antagonists / pharmacology. Carcinoma, Transitional Cell / drug therapy. Doxazosin / pharmacology. Prostatic Neoplasms / drug therapy. Receptor, Serotonin, 5-HT1B / metabolism. Serotonin / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Adrenergic alpha-1 Receptor Antagonists. Humans. Male. Pyridines / pharmacology. Pyrroles / pharmacology. Serotonin 5-HT1 Receptor Agonists

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  • (PMID = 16309229.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Pyridines; 0 / Pyrroles; 0 / Receptor, Serotonin, 5-HT1B; 0 / Serotonin 5-HT1 Receptor Agonists; 127792-75-0 / 3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo(3,2-b)pyrid-5-one; 333DO1RDJY / Serotonin; NW1291F1W8 / Doxazosin
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32. Wenghoefer M, Pantelis A, Dommisch H, Reich R, Martini M, Allam JP, Novak N, Bergé S, Jepsen S, Winter J: Decreased gene expression of human beta-defensin-1 in the development of squamous cell carcinoma of the oral cavity. Int J Oral Maxillofac Surg; 2008 Jul;37(7):660-3
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  • [Title] Decreased gene expression of human beta-defensin-1 in the development of squamous cell carcinoma of the oral cavity.
  • The aim of this study was to investigate the gene expression of human beta-defensin-1, -2, -3 (hBD-1, -2, -3), interleukin-1beta, tumour necrosis factor-alpha and cyclooxygenase-2 in oral squamous cell carcinoma (OSCC) compared to benign and premalignant lesions as well as healthy controls.
  • RNA was extracted according to standard protocols and transcripts of hBD-1, -2, -3, interleukin-1beta, tumour necrosis factor-alpha and cyclooxygenase-2 were analysed by real-time polymerase chain reaction.
  • The loss of its function might contribute to the malignant progression of these tumours.
  • [MeSH-major] Anti-Infective Agents / analysis. Carcinoma, Squamous Cell / pathology. Mouth Neoplasms / pathology. beta-Defensins / analysis
  • [MeSH-minor] Cyclooxygenase 2 / analysis. Disease Progression. Fibroma / genetics. Fibroma / pathology. Gene Expression Regulation, Neoplastic / genetics. Gingiva / anatomy & histology. Humans. Interleukin-1beta / analysis. Leukoplakia, Oral / genetics. Leukoplakia, Oral / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 18346877.001).
  • [ISSN] 0901-5027
  • [Journal-full-title] International journal of oral and maxillofacial surgery
  • [ISO-abbreviation] Int J Oral Maxillofac Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / DEFB1 protein, human; 0 / DEFB4A protein, human; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 0 / beta-Defensins; 0 / beta-defensin 3, human; EC 1.14.99.1 / Cyclooxygenase 2
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33. Yamada M, Yanaba K, Hasegawa M, Matsushita Y, Horikawa M, Komura K, Matsushita T, Kawasuji A, Fujita T, Takehara K, Steeber DA, Tedder TF, Sato S: Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1. Clin Exp Immunol; 2006 Feb;143(2):216-27
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  • [Title] Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1.
  • Malignant melanoma is often accompanied by a host response of inflammatory cell infiltration that is highly regulated by multiple adhesion molecules.
  • This enhancement was associated generally with a reduced accumulation of natural killer (NK) cells, CD4+ T cells and CD8+ T cells and also with a diminished release of interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha but not interleukin (IL)-6.
  • Cytotoxicity against melanoma was not defective by the absence of ICAM-1, L-selectin or both, suggesting that the enhancement of tumour growth and metastasis caused by the loss of adhesion molecules results from an impaired migration of effector cells into the tissue rather than from a suppression of the cytotoxic response.
  • The results indicate that L-selectin and ICAM-1 contribute co-operatively to the anti-tumour reaction by regulating lymphocyte infiltration to the tumour.

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  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] Am J Pathol. 2000 Jul;157(1):237-47 [10880393.001]
  • [Cites] J Mol Diagn. 2001 May;3(2):55-61 [11333300.001]
  • [Cites] Eur J Cancer Prev. 2001 Aug;10(4):327-35 [11535875.001]
  • [Cites] J Immunol. 2002 Mar 15;168(6):2970-8 [11884469.001]
  • [Cites] J Invest Dermatol. 2002 Jun;118(6):915-22 [12060384.001]
  • [Cites] J Immunol. 2002 Aug 1;169(3):1634-9 [12133994.001]
  • [Cites] Am J Pathol. 2002 Nov;161(5):1607-18 [12414509.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2322-9 [12727857.001]
  • [Cites] Life Sci. 2003 Dec 26;74(6):781-92 [14654170.001]
  • [Cites] Br J Cancer. 2004 Mar 22;90(6):1279-84 [15026813.001]
  • [Cites] Br J Cancer. 2004 Apr 5;90(7):1457-63 [15054471.001]
  • [Cites] J Immunol. 1986 Jul 1;137(1):245-54 [3086451.001]
  • [Cites] J Immunol. 1990 Jun 15;144(12):4579-86 [1972160.001]
  • [Cites] J Invest Dermatol. 1991 Aug;97(2):197-202 [1712819.001]
  • [Cites] Cell. 1991 Dec 20;67(6):1033-6 [1760836.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3539-43 [8097319.001]
  • [Cites] Cancer Immunol Immunother. 1993 Jun;36(6):357-63 [7684652.001]
  • [Cites] Cancer Res. 1993 Sep 15;53(18):4315-21 [8364926.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8529-33 [8104338.001]
  • [Cites] J Exp Med. 1994 Jul 1;180(1):95-109 [7911822.001]
  • [Cites] Immunity. 1994 Jul;1(4):247-60 [7534203.001]
  • [Cites] J Immunol. 1995 Jun 1;154(11):6080-93 [7751650.001]
  • [Cites] Annu Rev Physiol. 1995;57:827-72 [7778885.001]
  • [Cites] Recent Results Cancer Res. 1995;139:169-82 [7597288.001]
  • [Cites] Semin Oncol. 1996 Feb;23(1):108-17 [8607021.001]
  • [Cites] J Exp Med. 1996 Feb 1;183(2):589-98 [8627170.001]
  • [Cites] Cancer Res. 1996 Oct 1;56(19):4338-42 [8813119.001]
  • [Cites] J Immunol. 1997 Jun 1;158(11):5191-9 [9164936.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6432-7 [9177235.001]
  • [Cites] Am J Physiol. 1997 Sep;273(3 Pt 1):L513-23 [9316484.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7562-7 [9636189.001]
  • [Cites] J Immunol. 1998 Jul 15;161(2):897-908 [9670968.001]
  • [Cites] J Exp Med. 1998 Dec 21;188(12):2357-68 [9858522.001]
  • [Cites] J Surg Res. 1998 Dec;80(2):143-8 [9878305.001]
  • [Cites] EMBO J. 1999 Mar 15;18(6):1516-25 [10075923.001]
  • [Cites] Am J Physiol. 1999 Jun;276(6 Pt 1):L961-70 [10362721.001]
  • [Cites] Nat Med. 1999 Jul;5(7):828-31 [10395330.001]
  • [Cites] J Appl Physiol (1985). 1999 Jul;87(1):299-307 [10409588.001]
  • [Cites] J Immunol. 1999 Aug 15;163(4):2176-86 [10438959.001]
  • [Cites] Am J Physiol. 1999 Aug;277(2 Pt 1):L310-9 [10444525.001]
  • [Cites] J Immunol. 1999 Sep 1;163(5):2809-15 [10453025.001]
  • [Cites] Crit Rev Oncol Hematol. 1996 Apr;22(3):213-28 [8793276.001]
  • [Cites] J Allergy Clin Immunol. 2001 Apr;107(4):734-8 [11295667.001]
  • (PMID = 16412045.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA54464; United States / NCI NIH HHS / CA / CA81776
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin
  • [Other-IDs] NLM/ PMC1809598
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34. Karmaniolas K, Dalamaga M, Liatis S, Kaskara A, Rigopoulos A, Migdalis IN: Hematological malignancies are associated with a lower interferon-a blocking activity than solid tumors. Res Commun Mol Pathol Pharmacol; 2005;117-118:65-75
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  • Interferon (IFN) and especially IFN-alpha exhibit clinical anti-tumor activity against various types of malignant diseases.
  • IFN inhibitors have been implicated for the ineffectiveness of IFN treatment in malignant neoplasias.
  • PATIENTS AND METHODS: Ninety patients with a clinically evident solid tumour and forty-six patients with haematological malignancies were included in the study.
  • Interferon-inhibiting activity as well as endogenous IFN-like activity were determined in all serum samples in a cell line highly sensitive to IFN.
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Line, Tumor. Cytopathogenic Effect, Viral / drug effects. Female. Humans. Interferon-alpha / antagonists & inhibitors. Interferon-alpha / blood. Male. Middle Aged. Recombinant Proteins

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  • (PMID = 18426079.001).
  • [ISSN] 1078-0297
  • [Journal-full-title] Research communications in molecular pathology and pharmacology
  • [ISO-abbreviation] Res. Commun. Mol. Pathol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon Type I; 0 / Interferon-alpha; 0 / Recombinant Proteins
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35. Dallosso AR, Hancock AL, Szemes M, Moorwood K, Chilukamarri L, Tsai HH, Sarkar A, Barasch J, Vuononvirta R, Jones C, Pritchard-Jones K, Royer-Pokora B, Lee SB, Owen C, Malik S, Feng Y, Frank M, Ward A, Brown KW, Malik K: Frequent long-range epigenetic silencing of protocadherin gene clusters on chromosome 5q31 in Wilms' tumor. PLoS Genet; 2009 Nov;5(11):e1000745
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  • [Title] Frequent long-range epigenetic silencing of protocadherin gene clusters on chromosome 5q31 in Wilms' tumor.
  • Wilms' tumour (WT) is a pediatric tumor of the kidney that arises via failure of the fetal developmental program.
  • The methylated genes all belong to alpha-, beta-, and gamma-protocadherin (PCDH) gene clusters (Human Genome Organization nomenclature PCDHA@, PCDHB@, and PCDHG@, respectively).
  • Bisulfite polymerase chain reaction analysis showed that PCDH hypermethylation is a frequent event found in all Wilms' tumor subtypes.
  • WT precursor lesions showed no PCDH hypermethylation, suggesting that de novo PCDH hypermethylation occurs during malignant progression.
  • Importantly, we show that PCDHs negatively regulate canonical Wnt signalling, as short-interfering RNA-induced reduction of PCDHG@ encoded proteins leads to elevated beta-catenin protein, increased beta-catenin/T-cell factor (TCF) reporter activity, and induction of Wnt target genes.
  • Thus PCDHs are candidate tumor suppressors that modulate regulatory pathways critical in development and disease, such as canonical Wnt signaling.
  • [MeSH-major] Cadherins / genetics. Chromosomes, Human, Pair 5 / genetics. Epigenesis, Genetic. Gene Silencing. Multigene Family. Wilms Tumor / genetics

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  • [Cites] Am J Pathol. 1998 Sep;153(3):991-1000 [9736048.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):3880-2 [10463574.001]
  • [Cites] J Biol Chem. 2005 Mar 11;280(10):9313-9 [15611067.001]
  • [Cites] J Biol Chem. 2005 Apr 22;280(16):15888-97 [15711011.001]
  • [Cites] J Biol Chem. 2005 Jun 3;280(22):21129-36 [15778498.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5263-71 [15958572.001]
  • [Cites] Mol Cell Neurosci. 2005 Aug;29(4):603-16 [15964765.001]
  • [Cites] Nat Genet. 2005 Aug;37(8):853-62 [16007088.001]
  • [Cites] Nat Rev Cancer. 2005 Sep;5(9):699-712 [16110318.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 24;103(4):982-7 [16415157.001]
  • [Cites] Nat Genet. 2006 Feb;38(2):149-53 [16444255.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):1070-80 [16247458.001]
  • [Cites] Cell. 2006 Apr 21;125(2):301-13 [16630818.001]
  • [Cites] Nat Genet. 2006 May;38(5):540-9 [16642018.001]
  • [Cites] Genome Res. 2006 Jul;16(7):890-900 [16751344.001]
  • [Cites] Cancer Res. 2006 Nov 15;66(22):10664-70 [17090521.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):232-6 [17200670.001]
  • [Cites] Cell. 2007 Mar 23;128(6):1231-45 [17382889.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5527-32 [17369352.001]
  • [Cites] Development. 2007 Jul;134(13):2533-9 [17537789.001]
  • [Cites] Development. 2007 Sep;134(17):3177-90 [17693601.001]
  • [Cites] J Clin Pathol. 2007 Sep;60(9):1013-6 [17172473.001]
  • [Cites] Nat Med. 2007 Sep;13(9):1060-9 [17694067.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9107-16 [17909015.001]
  • [Cites] Physiology (Bethesda). 2007 Oct;22:303-9 [17928543.001]
  • [Cites] Curr Opin Cell Biol. 2007 Oct;19(5):584-92 [17936607.001]
  • [Cites] Neoplasia. 2007 Nov;9(11):970-8 [18030365.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Jun;47(6):461-70 [18311776.001]
  • [Cites] Mol Cancer Res. 2008 Jul;6(7):1114-23 [18644976.001]
  • [Cites] Cell Stem Cell. 2008 Aug 7;3(2):169-81 [18682239.001]
  • [Cites] Oncogene. 2008 Aug 7;27(34):4657-65 [18408767.001]
  • [Cites] Kidney Int. 2008 Oct;74(8):1004-8 [18633347.001]
  • [Cites] Cancer Res. 2008 Oct 15;68(20):8616-25 [18922938.001]
  • [Cites] Lung Cancer. 2008 Oct;62(1):15-22 [18358560.001]
  • [Cites] Dev Cell. 2008 Nov;15(5):781-91 [19000842.001]
  • [Cites] J Biol Chem. 2009 Jan 30;284(5):2880-90 [19047047.001]
  • [Cites] Gastroenterology. 2009 Feb;136(2):640-51.e1 [19084528.001]
  • [Cites] Cancer Res. 2000 May 1;60(9):2356-60 [10811108.001]
  • [Cites] Cancer Res. 2002 Jan 1;62(1):48-52 [11782357.001]
  • [Cites] Oncogene. 2002 Sep 26;21(43):6694-702 [12242669.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7277-82 [12370819.001]
  • [Cites] Neuron. 2002 Dec 5;36(5):843-54 [12467588.001]
  • [Cites] Cancer Cell. 2003 Jan;3(1):89-95 [12559178.001]
  • [Cites] Curr Biol. 2003 Apr 15;13(8):680-5 [12699626.001]
  • [Cites] Biochim Biophys Acta. 2003 Jun 5;1653(1):1-24 [12781368.001]
  • [Cites] J Neurosci. 2003 Jun 15;23(12):5096-104 [12832533.001]
  • [Cites] J Pathol. 2003 Aug;200(5):667-74 [12898605.001]
  • [Cites] Int J Cancer. 2003 Nov 10;107(3):365-74 [14506735.001]
  • [Cites] Oncogene. 2003 Oct 2;22(43):6794-801 [14555992.001]
  • [Cites] Hum Mol Genet. 2004 Feb 15;13(4):405-15 [14681303.001]
  • [Cites] Cancer Biol Ther. 2004 Jan;3(1):36-41 [14739782.001]
  • [Cites] J Gen Virol. 1977 Jul;36(1):59-74 [886304.001]
  • [Cites] Cancer Res. 1981 May;41(5):1751-6 [7214343.001]
  • [Cites] Nature. 1993 Apr 22;362(6422):749-51 [8097018.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10330-4 [9294210.001]
  • [ErratumIn] PLoS Genet. 2009 Dec;5(12). doi: 10.1371/annotation/012d5a44-8239-4057-8c3b-3dc159ea3a02
  • (PMID = 19956686.001).
  • [ISSN] 1553-7404
  • [Journal-full-title] PLoS genetics
  • [ISO-abbreviation] PLoS Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / PCDH1 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC2776977
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36. Szlosarek PW, Grimshaw MJ, Wilbanks GD, Hagemann T, Wilson JL, Burke F, Stamp G, Balkwill FR: Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer. Int J Cancer; 2007 Jul 01;121(1):6-11
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  • [Title] Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer.
  • The pro-inflammatory cytokine, tumour necrosis factor-alpha, TNF-alpha, is dysregulated in malignant compared with normal ovarian surface epithelium (OSE).
  • Several epidemiological studies have associated inflammation with ovarian tumorigenesis, with TNF-alpha playing a key role in modulating invasion, angiogenesis and metastasis.
  • Here, we show that TNF-alpha also induces expression of arate-limiting enzyme in arginine synthesis, argininosuccinate synthetase (AS), thereby linking inflammation with several arginine-dependent metabolic pathways, implicated in accelerated carcinogenesis and tumour progression.
  • Having identified AS mRNA induction in TNF-alpha-treated IGROV-1 ovarian cancer cells, using RNA-arbitrarily primed-PCR, we then observed differential regulation of AS mRNA and protein in malignant, compared with normal, OSE cells.
  • A cDNA cancer profiling array with matched normal ovarian and ovarian tumour samples revealed increased expression of AS mRNA in the latter.
  • Moreover, AS protein co-localised with TNF-alpha in ovarian cancer cells, with significantly higher levels of AS in malignant compared with normal ovarian tissue.
  • Increased co-expression of AS and TNF-alpha mRNA was also observed in 2 other epithelial tumours, non-small cell lung and stomach cancer, compared with normal corresponding tissues.
  • In summary, high levels of AS expression, which may be required for several arginine-dependent processes in cancer, including the production of nitric oxide, proline, pyrimidines and polyamines, is regulated by TNF-alpha and may provide an important molecular pathway linking inflammation and metabolism to ovarian tumorigenesis.
  • [MeSH-major] Argininosuccinate Synthase / metabolism. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Ovarian Neoplasms / enzymology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Female. Health. Humans. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 17354225.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974; United Kingdom / Medical Research Council / / G0601867
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 6.3.4.5 / Argininosuccinate Synthase
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37. Darra E, Lenaz G, Cavalieri E, Fato R, Mariotto S, Bergamini C, Carcereri de Prati A, Perbellini L, Leoni S, Suzuki H: Alpha-bisabolol: unexpected plant-derived weapon in the struggle against tumour survival? Ital J Biochem; 2007 Dec;56(4):323-8
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  • [Title] Alpha-bisabolol: unexpected plant-derived weapon in the struggle against tumour survival?
  • Despite enormous scientific and economic effort tumour still is one of the most terrible pathologies among human population all over the world.
  • Here, we summarize the short story of the study of an extraordinary effect of one plant compound towards transformed cells derived from highly malignant tumours.
  • Alpha-bisabolol, a sesquiterpene widely present in plants, selectively kills transformed cells by apoptosis without affecting the viability of normal cells.
  • One of its intracellular targets seems to be situated on mitochondria and is possibly identified as the permeability transition pore, as judged from rapid mitochondrial membrane potential dissipation induced by alpha-bisabolol and the failure to kill cells in the presence of cyclosporine A.
  • Preferential adsorption of alpha-bisabolol into lipid rafts, rich in tumour cells, may explain the selective action of this compounds towards tumour cells.
  • Furthermore, Surface Plasmon Resonance analysis indicates that alpha-bisabolol directly interacts with Bid protein, a member of the Bcl2 family deeply involved in apoptosis, suggesting a possibility that Bid, or similar protein(s), may be involved in a putative intracellular transport system of alpha-bisabolol from plasma membrane to mitochondria.
  • Experiments with animals indicate that alpha-bisabolol is not toxic and is accumulated, through blood flow, in every tissues examined.
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Models, Biological. Signal Transduction

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  • (PMID = 19192636.001).
  • [ISSN] 0021-2938
  • [Journal-full-title] The Italian journal of biochemistry
  • [ISO-abbreviation] Ital. J. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Sesquiterpenes; 24WE03BX2T / bisabolol
  • [Number-of-references] 15
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38. Hungermann D, Buerger H, Oehlschlegel C, Herbst H, Boecker W: Adenomyoepithelial tumours and myoepithelial carcinomas of the breast--a spectrum of monophasic and biphasic tumours dominated by immature myoepithelial cells. BMC Cancer; 2005;5:92
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  • METHODS: A series of 27 adenomyoepithelial tumours of the breast was analysed immunohistochemically with antibodies directed against various cytokeratins, p63, smooth muscle alpha-actin (SMA) and vimentin.
  • With exception of one case diagnosed as myoepithelial carcinoma, all tested tumours expressed low molecular weight cytokeratin Ck18 in variable proportions of cells.
  • Double immunofluorescence revealed tumour cells exclusively staining for Ck5/Ck14 in the presence of other cell populations that co-expressed high molecular weight Ck5/Ck14 as well as either low molecular weight Ck8/18 or SMA.
  • Based on morphology, we assigned the series to three categories, benign, borderline and malignant.
  • Although categorisation of adenomyoepithelial tumours in benign, borderline and malignant was supported by results of CGH, any assessment of prognosis requires to be firmly based on morphological grounds.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma / diagnosis. Epithelial Cells / cytology. Myoepithelioma / diagnosis
  • [MeSH-minor] Actins / biosynthesis. Adult. Aged. Aged, 80 and over. Cell Proliferation. DNA-Binding Proteins. Female. Genes, Tumor Suppressor. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Immunophenotyping. Keratins / biosynthesis. Microscopy, Fluorescence. Middle Aged. Nucleic Acid Hybridization. Phosphoproteins / biosynthesis. Prognosis. Trans-Activators / biosynthesis. Transcription Factors. Tumor Suppressor Proteins. Vimentin / biosynthesis

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  • [Cites] J Pathol. 1998 Feb;184(2):197-206 [9602712.001]
  • [Cites] Histopathology. 1997 Jun;30(6):542-8 [9205858.001]
  • [Cites] Exp Cell Res. 1999 Feb 25;247(1):267-78 [10047469.001]
  • [Cites] J Pathol. 1999 Dec;189(4):521-6 [10629552.001]
  • [Cites] Virchows Arch. 2000 Feb;436(2):158-66 [10755607.001]
  • [Cites] Lab Invest. 2000 Jun;80(6):831-6 [10879734.001]
  • [Cites] J Cell Sci. 2002 Jan 1;115(Pt 1):39-50 [11801722.001]
  • [Cites] Genes Dev. 2002 Mar 15;16(6):693-706 [11914275.001]
  • [Cites] Ultrastruct Pathol. 2002 Mar-Apr;26(2):77-80 [12036095.001]
  • [Cites] Lab Invest. 2002 Nov;82(11):1525-33 [12429812.001]
  • [Cites] J Pathol. 2002 Dec;198(4):458-67 [12434415.001]
  • [Cites] J Pathol. 2002 Dec;198(4):487-94 [12434418.001]
  • [Cites] Cell Prolif. 2003 Oct;36 Suppl 1:33-44 [14521514.001]
  • [Cites] Cell Prolif. 2003 Oct;36 Suppl 1:59-72 [14521516.001]
  • [Cites] Cell Prolif. 2003 Oct;36 Suppl 1:73-84 [14521517.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15853-8 [14668450.001]
  • [Cites] Semin Diagn Pathol. 2004 Feb;21(1):57-64 [15074560.001]
  • [Cites] Curr Top Pathol. 1970;53:161-220 [4323195.001]
  • [Cites] Exp Cell Res. 1991 Jun;194(2):267-74 [1709103.001]
  • [Cites] Am J Surg Pathol. 1991 Jun;15(6):554-68 [1709559.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2156-60 [8134364.001]
  • [Cites] Dev Biol. 1999 Feb 1;206(1):88-99 [9918697.001]
  • (PMID = 16050957.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vimentin; 68238-35-7 / Keratins
  • [Other-IDs] NLM/ PMC1187882
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39. Obi N, Katabami T, Obi R, Odanaka M, Sasano K, Tanaka Y: Primary malignant hepatic glucagonoma: an autopsy case. Endocr J; 2009;56(5):715-9
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  • [Title] Primary malignant hepatic glucagonoma: an autopsy case.
  • She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml).
  • Thus, we suspected a glucagonoma causing secondary diabetes.
  • However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma.
  • At autopsy, the only tumor detected was the liver mass.
  • This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe.
  • Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases.
  • Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
  • [MeSH-major] Diabetes Mellitus, Type 2 / etiology. Glucagonoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 19367016.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amino Acids
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40. Ranza E, Bertolotti A, Facoetti A, Mariotti L, Pasi F, Ottolenghi A, Nano R: Influence of imatinib mesylate on radiosensitivity of astrocytoma cells. Anticancer Res; 2009 Nov;29(11):4575-8
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  • Imatinib mesylate (STI571), an inhibitor of alpha- and beta-platelet-derived growth factor receptors (PDGFR) and other tyrosine kinases, is a well established treatment for chronic myeloid leukaemia and gastrointestinal stromal tumours.
  • Moreover, it is under investigation for the therapy of several other malignant tumours since protein kinases are frequently mutated or otherwise deregulated in human malignancies and they serve as a target for differentiating between tumour cells and normal tissues.
  • The objective of this study was to determine whether gamma radiation could sensitize astrocytoma cell lines to the effects of imatinib in vitro.
  • The clonogenic survival assays performed with the combination of imatinib with radiation demonstrated that the drug had an additive antiproliferative effect in both cell lines considered.
  • Imatinib confered greater radiosensitivity on the T98G tumour cells effecting a significant decrease in colony formation compared with radiation alone.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Benzamides. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Combined Modality Therapy. Dose-Response Relationship, Drug. Gamma Rays. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Humans. Imatinib Mesylate

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  • (PMID = 20032406.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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41. Roesch-Ely M, Schnölzer M, Nees M, Plinkert PK, Bosch FX: Reference spectra from squamous epithelium and connective tissue allow whole section proteomics analysis. Arch Physiol Biochem; 2010 Oct-Dec;116(4-5):218-26
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  • We reasoned that micro-dissection of tumour cells for protein expression studies should be omitted since tumour-stroma interactions are an important part of the biology of solid tumours.
  • To study such interactions in head and neck squamous cell carcinoma (HNSCC) development, we generated reference protein spectra for normal squamous epithelium and connective tissue by SELDI-TOF-MS.
  • The alpha-defensins 1-3 and the haemoglobin subunits were identified in the connective tissue.
  • Tumour-distant epithelia, representing early pre-malignant lesions, showed up-regulated expression of the stromal alpha-defensins, whereas the epithelial Annexin 1 was down-regulated.
  • Thus, tumour microenvironment interactions occur very early in the carcinogenic process.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Head and Neck Neoplasms / metabolism. Neoplasm Proteins / metabolism. Protein Array Analysis. Proteomics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization / methods. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization / standards
  • [MeSH-minor] Annexins / analysis. Calgranulin A / analysis. Cluster Analysis. Connective Tissue / chemistry. Connective Tissue / metabolism. Connective Tissue / pathology. Epithelium / chemistry. Epithelium / metabolism. Epithelium / pathology. Hemoglobins / analysis. Humans. Microdissection. Reference Standards. alpha-Defensins / analysis

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  • (PMID = 21080850.001).
  • [ISSN] 1744-4160
  • [Journal-full-title] Archives of physiology and biochemistry
  • [ISO-abbreviation] Arch. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexins; 0 / Calgranulin A; 0 / Hemoglobins; 0 / Neoplasm Proteins; 0 / alpha-Defensins
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42. Ammirante M, Luo JL, Grivennikov S, Nedospasov S, Karin M: B-cell-derived lymphotoxin promotes castration-resistant prostate cancer. Nature; 2010 Mar 11;464(7286):302-5
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  • [Title] B-cell-derived lymphotoxin promotes castration-resistant prostate cancer.
  • Prostate cancer (CaP) progresses from prostatic intraepithelial neoplasia through locally invasive adenocarcinoma to castration-resistant metastatic carcinoma.
  • Curiously, castration-resistant CaP remains androgen-receptor dependent, and potent androgen-receptor antagonists induce tumour regression in castrated mice.
  • The inflammation-responsive IkappaB kinase (IKK)-beta and its target NF-kappaB have important tumour-promoting functions within malignant cells and inflammatory cells.
  • The latter, including macrophages and lymphocytes, are important elements of the tumour microenvironment, but the mechanisms underlying their recruitment remain obscure, although they are thought to depend on chemokine and cytokine production.
  • We found that CaP progression is associated with inflammatory infiltration and activation of IKK-alpha, which stimulates metastasis by an NF-kappaB-independent, cell autonomous mechanism.
  • Here we show that androgen ablation causes infiltration of regressing androgen-dependent tumours with leukocytes, including B cells, in which IKK-beta activation results in production of cytokines that activate IKK-alpha and STAT3 in CaP cells to enhance hormone-free survival.


43. Karlberg N, Karlberg S, Karikoski R, Mikkola S, Lipsanen-Nyman M, Jalanko H: High frequency of tumours in Mulibrey nanism. J Pathol; 2009 Jun;218(2):163-71
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  • In this work, the frequency and pathology of malignant and benign tumours were analysed in a national cohort of 89 Finnish MUL patients aged 0.7-76 years.
  • The results show that the MUL patients have disturbed architecture with ectopic tissues and a high frequency of both benign and malignant tumours detectable in several internal organs.
  • Fifteen malignancies occurred in 13 patients (15%), seven of them in the kidney (five Wilms' tumours), three in the thyroid gland, two gynaecological cancers, one gastrointestinal carcinoid tumour, one neuropituitary Langerhans cell histiocytosis and one case of acute lymphoblastic leukaemia (ALL).
  • The lesions showed strong expression of the endothelial cell markers CD34 and CD31 as well as the myocyte marker alpha-smooth muscle actin (alpha-SMA).
  • Our findings show that MUL is associated with frequent malignant tumours and benign adenomatous and vascular lesions, as well as disturbed organ development.
  • [MeSH-minor] Adolescent. Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / pathology. Adult. Aged. Child. Child, Preschool. Cohort Studies. Female. Finland. Heart Neoplasms / complications. Heart Neoplasms / pathology. Humans. Infant. Kidney Neoplasms / complications. Kidney Neoplasms / pathology. Liver Neoplasms / complications. Liver Neoplasms / pathology. Lung Neoplasms / complications. Lung Neoplasms / pathology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology. Prevalence. Thyroid Neoplasms / complications. Thyroid Neoplasms / pathology. Wilms Tumor / complications. Wilms Tumor / pathology


44. Jalving M, Koornstra JJ, De Jong S, De Vries EG, Kleibeuker JH: Review article: the potential of combinational regimen with non-steroidal anti-inflammatory drugs in the chemoprevention of colorectal cancer. Aliment Pharmacol Ther; 2005 Feb 15;21(4):321-39
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  • Non-steroidal anti-inflammatory drugs do not, however, offer complete protection against adenoma and carcinoma development.
  • There is increasing interest in combining non-steroidal anti-inflammatory drugs with agents that target specific cell signalling pathways in malignant and premalignant cells.
  • This review aims to describe the current knowledge regarding the efficacy of peroxisome proliferator-activated receptor-gamma ligands, cholesterol synthesis inhibitors (statins), epidermal growth factor signalling inhibitors and tumour necrosis factor-related apoptosis-inducing ligand against colorectal neoplasms and the rationale for combining these drugs with non-steroidal anti-inflammatory drugs to improve efficacy in the chemoprevention of colorectal cancer, a PUBMED computer search of the English language literature was conducted to identify relevant papers published before July 2004.
  • In vitro, tumour necrosis factor-related apoptosis-inducing ligand induces apoptosis in human colon cancer cells, but not in normal cells.
  • [MeSH-minor] Apoptosis Regulatory Proteins. Drug Therapy, Combination. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use. Ligands. Membrane Glycoproteins / therapeutic use. PPAR gamma / agonists. Receptor, Epidermal Growth Factor / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 15709983.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / PPAR gamma; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 190
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45. Lopes N, Sousa B, Martins D, Gomes M, Vieira D, Veronese LA, Milanezi F, Paredes J, Costa JL, Schmitt F: Alterations in Vitamin D signalling and metabolic pathways in breast cancer progression: a study of VDR, CYP27B1 and CYP24A1 expression in benign and malignant breast lesions. BMC Cancer; 2010;10:483
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  • [Title] Alterations in Vitamin D signalling and metabolic pathways in breast cancer progression: a study of VDR, CYP27B1 and CYP24A1 expression in benign and malignant breast lesions.
  • CONCLUSIONS: From this study, we conclude that there is a deregulation of the Vitamin D signalling and metabolic pathways in breast cancer, favouring tumour progression.
  • Thus, during mammary malignant transformation, tumour cells lose their ability to synthesize the active form of Vitamin D and respond to VDR-mediated Vitamin D effects, while increasing their ability to degrade this hormone.
  • [MeSH-major] 25-Hydroxyvitamin D3 1-alpha-Hydroxylase / metabolism. Breast / metabolism. Breast Neoplasms / metabolism. Receptors, Calcitriol / metabolism. Steroid Hydroxylases / metabolism. Vitamin D / metabolism
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Cohort Studies. Disease Progression. Female. Gene Expression Profiling. Humans. Immunoenzyme Techniques. Metabolic Networks and Pathways. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Vitamin D3 24-Hydroxylase

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  • [Cites] Clin Exp Metastasis. 1994 May;12(3):195-202 [8194194.001]
  • [Cites] Cancer Res. 1991 Jan 1;51(1):239-44 [1846309.001]
  • [Cites] J Histochem Cytochem. 1998 Nov;46(11):1335-7 [9774633.001]
  • [Cites] Am J Clin Nutr. 2004 Dec;80(6 Suppl):1721S-4S [15585794.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3579-86 [15867263.001]
  • [Cites] Am J Physiol Renal Physiol. 2005 Jul;289(1):F8-28 [15951480.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2370-6 [16214919.001]
  • [Cites] Virchows Arch. 2005 Oct;447(4):688-94 [16012853.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Oct;97(1-2):153-64 [16111884.001]
  • [Cites] Breast Cancer Res. 2005;7(6):R980-6 [16280049.001]
  • [Cites] Science. 2006 Apr 14;312(5771):233-6 [16614213.001]
  • [Cites] J Steroid Biochem Mol Biol. 2006 Aug;100(4-5):184-92 [16828283.001]
  • [Cites] Ann Oncol. 2007 Mar;18(3):581-92 [17287242.001]
  • [Cites] Virchows Arch. 2007 Jan;450(1):73-80 [17123107.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):684-700 [17721433.001]
  • [Cites] J Histochem Cytochem. 2007 Dec;55(12):1257-64 [17875655.001]
  • [Cites] Proc Nutr Soc. 2008 May;67(2):115-27 [18412986.001]
  • [Cites] J Cell Biochem. 2008 Nov 1;105(4):980-8 [18767073.001]
  • [Cites] Anticancer Res. 2009 Jan;29(1):155-7 [19331145.001]
  • [Cites] Int J Cancer. 2009 Sep 15;125(6):1328-33 [19437538.001]
  • [Cites] Mol Pharmacol. 2009 Oct;76(4):702-9 [19570947.001]
  • [Cites] J Cell Biochem. 1999 Dec 15;75(4):640-51 [10572247.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Nat Genet. 2000 Jun;25(2):144-6 [10835626.001]
  • [Cites] Circ Res. 2000 Aug 4;87(3):214-20 [10926872.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):3371-9 [10955825.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Histochem J. 2002 Jan-Feb;34(1-2):35-40 [12365798.001]
  • [Cites] Mol Cell Endocrinol. 2003 Feb 28;200(1-2):67-80 [12644300.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5367-74 [15328174.001]
  • [Cites] Lancet. 1979 Dec 22-29;2(8156-8157):1335-6 [92676.001]
  • [Cites] Cancer Res. 1984 Apr;44(4):1677-81 [6322984.001]
  • [Cites] Cancer Res. 1987 Dec 15;47(24 Pt 1):6793-9 [2824042.001]
  • [Cites] Science. 1988 May 13;240(4854):889-95 [3283939.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Sep;67(3):607-13 [2842365.001]
  • [Cites] Am J Clin Pathol. 1988 Sep;90(3):233-9 [2458030.001]
  • [Cites] J Bone Miner Res. 1998 Mar;13(3):325-49 [9525333.001]
  • (PMID = 20831823.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D; EC 1.14.- / 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / CYP24A1 protein, human; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase
  • [Other-IDs] NLM/ PMC2945944
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46. Neuzil J, Dyason JC, Freeman R, Dong LF, Prochazka L, Wang XF, Scheffler I, Ralph SJ: Mitocans as anti-cancer agents targeting mitochondria: lessons from studies with vitamin E analogues, inhibitors of complex II. J Bioenerg Biomembr; 2007 Feb;39(1):65-72
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  • Recently mitochondria in cancer cells have emerged as the Achilles heel for tumour destruction.
  • Anti-cancer agents specifically targeting cancer cell mitochondria are referred to as 'mitocans'.
  • These compounds act by destabilising these organelles, unleashing their apoptogenic potential, resulting in the efficient death of malignant cells and suppression of tumour growth.
  • Importantly, at least some mitocans are selective for cancer cells, and these are represented by the group of redox-silent vitamin E analogues, epitomised by alpha-tocopheryl succinate (alpha-TOS).
  • Moreover, alpha-TOS is selective for cancer cells with their reduced anti-oxidant defenses and lower esterase activity than the normal (non-malignant) counterparts.
  • In this mini-review we discuss the emerging significance of mitocans, as exemplified by alpha-TOS.

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  • [Cites] Free Radic Biol Med. 1996;21(3):335-48 [8855444.001]
  • [Cites] FASEB J. 2001 Feb;15(2):403-15 [11156956.001]
  • [Cites] Nat Chem Biol. 2005 Sep;1(4):223-32 [16408039.001]
  • [Cites] EMBO J. 2001 Nov 15;20(22):6306-15 [11707402.001]
  • [Cites] Biochemistry. 2003 Apr 15;42(14):4277-91 [12680782.001]
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1378-86 [16729025.001]
  • [Cites] J Biol Chem. 1995 Nov 3;270(44):26104-8 [7592812.001]
  • [Cites] J Biol Chem. 2004 Jun 25;279(26):27302-14 [15082714.001]
  • [Cites] J Biol Chem. 2006 May 12;281(19):13005-8 [16565519.001]
  • [Cites] J Cell Biol. 1997 Dec 1;139(5):1281-92 [9382873.001]
  • [Cites] Cell. 2003 Feb 21;112(4):481-90 [12600312.001]
  • [Cites] Mol Nutr Food Res. 2006 Aug;50(8):675-85 [16835868.001]
  • [Cites] Br J Cancer. 2001 Jan 5;84(1):87-9 [11139318.001]
  • [Cites] Oncogene. 1999 Apr 22;18(16):2537-46 [10353597.001]
  • [Cites] Mol Cell Biol. 1998 Oct;18(10):6083-9 [9742125.001]
  • [Cites] Blood. 2005 Jul 15;106(2):408-18 [15797997.001]
  • [Cites] Int J Cancer. 2004 Nov 10;112(3):385-92 [15382062.001]
  • [Cites] Trends Biochem Sci. 2000 Oct;25(10):502-8 [11050436.001]
  • [Cites] J Biol Chem. 2001 Apr 13;276(15):11615-23 [11136736.001]
  • [Cites] Nature. 1998 Jan 29;391(6666):449-50 [9461210.001]
  • [Cites] Lancet. 2000 Jan 29;355(9201):389-94 [10665569.001]
  • [Cites] Biochim Biophys Acta. 2004 Dec 10;1705(1):43-51 [15585172.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4812-30 [16892093.001]
  • [Cites] Biochim Biophys Acta. 2001 Sep 3;1528(1):25-30 [11514094.001]
  • [Cites] Nat Cell Biol. 2001 Feb;3(2):173-82 [11175750.001]
  • [Cites] J Biol Chem. 2005 Jun 3;280(22):21295-312 [15788391.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Nov 5;324(1):269-75 [15465013.001]
  • [Cites] Cancer Res. 2005 Mar 1;65(5):1984-93 [15753398.001]
  • [Cites] Cell. 2005 Jul 1;121(7):1043-57 [15989954.001]
  • [Cites] Cancer Lett. 2002 Dec 5;186(2):151-6 [12213284.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2483-91 [12750270.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9167-71 [9689052.001]
  • [Cites] J Biol Chem. 1996 Mar 29;271(13):7440-4 [8631771.001]
  • [Cites] FEBS Lett. 2006 May 15;580(11):2671-6 [16647070.001]
  • [Cites] Free Radic Biol Med. 1997;22(7):1145-51 [9098087.001]
  • [Cites] J Am Chem Soc. 2005 Jul 27;127(29):10191-6 [16028929.001]
  • [Cites] FEBS Lett. 2001 Dec 14;509(3):435-8 [11749969.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10587-98 [15590655.001]
  • [Cites] Oncogene. 2001 Nov 15;20(52):7579-87 [11753636.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3909-13 [12124317.001]
  • [Cites] Mol Aspects Med. 1993;14(3):253-8 [8264340.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4787-97 [16892091.001]
  • [Cites] J Biol Chem. 2006 Jun 9;281(23):16034-42 [16608847.001]
  • [Cites] Br J Cancer. 2003 Jun 16;88(12):1948-55 [12799642.001]
  • [Cites] J Biol Chem. 2006 Apr 28;281(17):11819-25 [16520381.001]
  • [Cites] Biochemistry. 2001 Apr 17;40(15):4686-92 [11294636.001]
  • [Cites] J Neurochem. 2005 Sep;94(5):1448-56 [16001965.001]
  • [Cites] J Bioenerg Biomembr. 2000 Apr;32(2):153-62 [11768748.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):613-21 [15695406.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4633-46 [16892078.001]
  • [Cites] Nat Rev Cancer. 2005 Nov;5(11):857-66 [16327764.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):647-56 [12209154.001]
  • [Cites] Drugs Today (Barc). 2003 Mar;39(3):157-74 [12730701.001]
  • [Cites] FEBS Lett. 2006 Oct 2;580(22):5125-9 [16979626.001]
  • [Cites] Int J Cancer. 2005 Nov 1;117(2):188-93 [15900584.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1259-63 [11818574.001]
  • [Cites] J Biol Chem. 2004 Aug 13;279(33):34682-90 [15178689.001]
  • [Cites] J Biol Chem. 2005 Jul 8;280(27):25369-76 [15878867.001]
  • [Cites] FEBS Lett. 2006 Apr 3;580(8):1925-31 [16529749.001]
  • [Cites] Mol Biol Cell. 2003 Aug;14(8):3082-96 [12925748.001]
  • [Cites] Cell Cycle. 2005 May;4(5):654-8 [15846094.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):203-9 [15665296.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1294-305 [15901672.001]
  • [Cites] J Biol Chem. 2006 Mar 17;281(11):7260-70 [16407291.001]
  • [Cites] Cell Death Differ. 2000 Dec;7(12):1166-73 [11175253.001]
  • [Cites] J Biol Chem. 2001 Feb 16;276(7):4588-96 [11092892.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1263-8 [15937216.001]
  • [Cites] Cancer Cell. 2003 May;3(5):497-509 [12781367.001]
  • [Cites] Cancer Cell. 2006 Sep;10(3):175-6 [16959608.001]
  • [Cites] Curr Med Res Opin. 2005 Mar;21(3):403-11 [15811209.001]
  • (PMID = 17294131.001).
  • [ISSN] 0145-479X
  • [Journal-full-title] Journal of bioenergetics and biomembranes
  • [ISO-abbreviation] J. Bioenerg. Biomembr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 1406-18-4 / Vitamin E; EC 1.3.5.1 / Electron Transport Complex II
  • [Number-of-references] 73
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47. Humphreys EH, Williams KT, Adams DH, Afford SC: Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent apoptosis, but are insensitive to direct activation with exogenous Fas ligand. PLoS One; 2010 Nov 17;5(11):e14037
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  • [Title] Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent apoptosis, but are insensitive to direct activation with exogenous Fas ligand.
  • We have shown that primary human cholangiocyte and hepatocyte survival is tightly regulated via co-operative interactions between two tumour necrosis family (TNF) receptor family members; CD40 and Fas (CD95).
  • AIMS: To determine whether malignant cholangiocytes display defects in CD40 mediated apoptosis.
  • By comparing CD40 and Fas-mediated apoptosis and intracellular signalling in primary human cholangiocytes and three cholangiocyte cell lines.
  • RESULTS: Primary cholangiocytes and cholangiocyte cell lines were relatively insensitive to direct Fas-mediated killing with exogenous FasL when compared with Jurkat cells, which readily underwent Fas-mediated apoptosis, but were extremely sensitive to CD154 stimulation.
  • The sensitivity of cells to CD40 activation was similar in magnitude in both primary and malignant cells and was STAT-3 and AP-1 dependent in both. CONCLUSIONS:.
  • 1) Both primary and malignant cholangiocytes are relatively resistant to Fas-mediated killing but show exquisite sensitivity to CD154, suggesting that the CD40 pathway is intact and fully functional in both primary and malignant cholangiocytes 2) The relative insensitivity of cholangiocytes to Fas activation demonstrates the importance of CD40 augmentation of Fas dependent death in these cells.
  • Agonistic therapies which target CD40 and associated intracellular signalling pathways may be effective in promoting apoptosis of malignant cholangiocytes.

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  • [Cites] Int J Oncol. 2007 Oct;31(4):843-50 [17786316.001]
  • [Cites] J Immunol. 2007 Sep 1;179(5):2705-12 [17709483.001]
  • [Cites] Int Immunol. 2004 Nov;16(11):1583-94 [15466914.001]
  • [Cites] Cancer Immunol Immunother. 1985;20(1):23-8 [2998589.001]
  • [Cites] EMBO J. 1989 May;8(5):1403-10 [2475341.001]
  • [Cites] In Vitro Cell Dev Biol. 1989 Dec;25(12):1189-92 [2691499.001]
  • [Cites] Cell. 1991 Jul 26;66(2):233-43 [1713127.001]
  • [Cites] Oncology. 1991;48(4):290-6 [1891170.001]
  • [Cites] Biochim Biophys Acta. 1991 Dec 10;1072(2-3):129-57 [1751545.001]
  • [Cites] Nature. 1992 May 7;357(6373):80-2 [1374165.001]
  • [Cites] J Pathol. 1993 May;170(1):1-8 [8326456.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1169-78 [7505205.001]
  • [Cites] J Exp Med. 1994 Aug 1;180(2):557-67 [7519240.001]
  • [Cites] Ann Surg. 1994 Nov;220(5):644-52 [7979612.001]
  • [Cites] Semin Immunol. 1994 Oct;6(5):337-41 [7532462.001]
  • [Cites] World J Surg. 1995 Jul-Aug;19(4):637-41 [7676713.001]
  • [Cites] J Immunol. 1995 Oct 1;155(7):3329-37 [7561026.001]
  • [Cites] J Pathol. 1995 Aug;176(4):373-80 [7562252.001]
  • [Cites] J Immunol. 1996 Jan 1;156(1):13-7 [8598453.001]
  • [Cites] J Exp Med. 1996 Jan 1;183(1):159-67 [8551219.001]
  • [Cites] J Cell Biol. 1996 Apr;133(2):335-43 [8609166.001]
  • [Cites] Gut. 1996 Apr;38(4):610-5 [8707097.001]
  • [Cites] Br J Surg. 1996 Aug;83(8):1062-64 [8869303.001]
  • [Cites] Int J Epidemiol. 1996 Oct;25(5):933-40 [8921477.001]
  • [Cites] Clin Exp Immunol. 1996 Dec;106(3):481-90 [8973616.001]
  • [Cites] J Immunol. 1997 Jan 15;158(2):977-83 [8993019.001]
  • [Cites] Hepatology. 1999 Dec;30(6):1398-404 [10573518.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5503-15 [10891490.001]
  • [Cites] Hepatology. 2000 Oct;32(4 Pt 1):761-9 [11003620.001]
  • [Cites] Mol Immunol. 2000 Jun;37(9):515-26 [11163401.001]
  • [Cites] Cell Mol Life Sci. 2001 Jan;58(1):4-43 [11229815.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4450-8 [11389075.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3280-7 [11432896.001]
  • [Cites] Endoscopy. 2001 Jul;33(7):614-9 [11473335.001]
  • [Cites] FASEB J. 2001 Nov;15(13):2345-54 [11689460.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3854-9 [11891278.001]
  • [Cites] J Natl Cancer Inst. 2002 Sep 18;94(18):1381-95 [12237284.001]
  • [Cites] Crit Rev Oncol Hematol. 2002 Nov;44(2):143-61 [12413632.001]
  • [Cites] Tumori. 2002 Sep-Oct;88(5):361-6 [12487551.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):587-96 [12547716.001]
  • [Cites] Biochem Pharmacol. 2003 Oct 15;66(8):1403-8 [14555214.001]
  • [Cites] Transplantation. 2004 Mar 15;77(5):717-26 [15021835.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1931-6 [9050882.001]
  • [Cites] Br J Haematol. 1997 May;97(2):409-17 [9163608.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):652-5 [9207415.001]
  • [Cites] Hepatology. 1997 Dec;26(6):1399-405 [9397977.001]
  • [Cites] Int J Cancer. 1998 Sep 11;77(6):849-53 [9714053.001]
  • [Cites] Breast Cancer Res Treat. 1998 Jul;50(1):27-36 [9802617.001]
  • [Cites] Immunity. 1998 Nov;9(5):711-20 [9846492.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):751-63 [9858598.001]
  • [Cites] J Exp Med. 1999 Jan 18;189(2):441-6 [9892626.001]
  • [Cites] J Immunol. 1999 Feb 15;162(4):2024-34 [9973474.001]
  • [Cites] Eur J Immunol. 1999 Jul;29(7):2148-55 [10427977.001]
  • [Cites] J Gastrointest Surg. 1999 Jul-Aug;3(4):374-81; discussion 382 [10482689.001]
  • [Cites] Genes Dev. 1999 Oct 1;13(19):2604-16 [10521404.001]
  • [Cites] Lancet. 2005 Oct 8;366(9493):1303-14 [16214602.001]
  • [Cites] Gut. 2005 Nov;54(11):1518-20 [16227354.001]
  • [Cites] Oncogene. 2005 Nov 24;24(53):7913-23 [16091748.001]
  • [Cites] Cell Signal. 2006 Apr;18(4):456-68 [15970430.001]
  • [Cites] Prostate. 2006 Jun 1;66(8):831-8 [16491482.001]
  • [Cites] PLoS One. 2007;2(1):e159 [17225862.001]
  • [Cites] Hepatology. 2008 Feb;47(2):552-62 [17999420.001]
  • (PMID = 21103345.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E017096/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / STAT3 Transcription Factor; 0 / Transcription Factor AP-1; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 147205-72-9 / CD40 Ligand
  • [Other-IDs] NLM/ PMC2984448
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48. Moriya T, Kozuka Y, Kanomata N, Tse GM, Tan PH: The role of immunohistochemistry in the differential diagnosis of breast lesions. Pathology; 2009 Jan;41(1):68-76
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  • [Title] The role of immunohistochemistry in the differential diagnosis of breast lesions.
  • Immunohistochemistry may be helpful in the diagnosis of various breast lesions.
  • It can be used to assist in distinguishing benign and malignant conditions, or to clarify the histological subtype of invasive carcinomas.
  • Myoepithelial markers (p63, alpha-SMA, smooth muscle myosin heavy chain, and others) are useful to highlight myoepithelial cells.
  • They are employed to verify myoepithelial cell lining in intraductal papillary lesions, or to recognise peripheral myoepithelial cells for non-invasive carcinoma, although their staining results are not always excellent.
  • High molecular weight cytokeratins (CK5/6, CK14, 34betaE12) typically show a mosaic-like pattern of expression in benign papillary/hyperplastic lesions, and are mostly negative in ductal in situ carcinoma, but some exceptions exist.
  • Negative E-cadherin staining is used for making confirmative diagnosis of lobular carcinoma, with a specificity and sensitivity of approximately 90%.
  • Cytokeratins, especially the antibody 34betaE12, are of value to differentiate spindle cell carcinoma from phyllodes tumour.
  • Nevertheless, for accurate diagnosis, it is essential to correlate the immmunohistochemical staining results with the histological findings.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Breast Neoplasms / diagnosis. Breast Neoplasms / metabolism. Immunohistochemistry / methods
  • [MeSH-minor] Carcinoma, Intraductal, Noninfiltrating / diagnosis. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / diagnosis. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Diagnosis, Differential. Female. Humans. Myoepithelioma / diagnosis. Myoepithelioma / metabolism. Myoepithelioma / pathology


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

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  • (PMID = 16079290.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alpha2beta1; 0 / Protease Inhibitors; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; 9007-34-5 / Collagen; EC 3.4.- / Metalloproteases
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50. Fillies T, Werkmeister R, van Diest PJ, Brandt B, Joos U, Buerger H: HIF1-alpha overexpression indicates a good prognosis in early stage squamous cell carcinomas of the oral floor. BMC Cancer; 2005;5:84
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  • [Title] HIF1-alpha overexpression indicates a good prognosis in early stage squamous cell carcinomas of the oral floor.
  • BACKGROUND: Hypoxia-inducible factor 1 (HIF-1) is a transcription factor, which plays a central role in biologic processes under hypoxic conditions, especially concerning tumour angiogenesis.
  • HIF-1alpha is the relevant, oxygen-dependent subunit and its overexpression has been associated with a poor prognosis in a variety of malignant tumours.
  • METHODS: 85 patients with histologically proven surgically treated T1/2 squamous cell carcinoma (SCC) of the oral floor were eligible for the study.
  • Tumor specimens were investigated by means of tissue micro arrays (TMAs) and immunohistochemistry for the expression of HIF-1.
  • The expression of HIF-1alpha was related with a significantly improved 5-year survival rate (p < 0.01) and a significantly increased disease free period (p = 0.01) independent from nodal status and tumour size.
  • [MeSH-major] Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / metabolism. Gene Expression Regulation, Neoplastic. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Mouth Neoplasms / diagnosis. Mouth Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anoxia. Biomarkers, Tumor / biosynthesis. Disease-Free Survival. Female. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models. Regression Analysis. Treatment Outcome

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  • [Cites] Int J Cancer. 2003 Jun 10;105(2):176-81 [12673675.001]
  • [Cites] Cancer. 2003 Mar 15;97(6):1573-81 [12627523.001]
  • [Cites] Oncol Rep. 2003 Jul-Aug;10(4):797-802 [12792726.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):721-32 [13130303.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5679-84 [14522883.001]
  • [Cites] Fortschr Kiefer Gesichtschir. 1992;37:43-5 [1639309.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5510-4 [7539918.001]
  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] J Clin Pathol. 2005 Feb;58(2):172-7 [15677538.001]
  • [Cites] J Clin Pathol. 2005 Mar;58(3):335; author reply 336 [15735177.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4693-6 [10987269.001]
  • [Cites] J Natl Cancer Inst. 2001 Feb 21;93(4):309-14 [11181778.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2911-6 [11306467.001]
  • [Cites] Br J Cancer. 2001 Sep 14;85(6):881-90 [11556841.001]
  • [Cites] Cancer Lett. 2002 Feb 25;176(2):215-23 [11804750.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1020-4 [11861376.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2493-7 [11980639.001]
  • [Cites] Gen Dent. 2001 Jan-Feb;49(1):72-82 [12004680.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2002 Jul;128(7):751-8 [12117328.001]
  • [Cites] J Clin Pathol. 2002 Aug;55(8):613-5 [12147657.001]
  • [Cites] J Korean Med Sci. 2003 Apr;18(2):196-203 [12692416.001]
  • (PMID = 16035955.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
  • [Other-IDs] NLM/ PMC1190162
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51. Willhauck-Fleckenstein M, Moehler TM, Merling A, Pusunc S, Goldschmidt H, Schwartz-Albiez R: Transcriptional regulation of the vascular endothelial glycome by angiogenic and inflammatory signalling. Angiogenesis; 2010 Mar;13(1):25-42
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  • Vascular endothelial cells undergo many molecular changes during pathological processes such as inflammation and tumour development.
  • Tumours such as malignant lymphomas affecting bone marrow are dependent on interactions with endothelial cells for (1) site-specific homing and (2) tumour-induced angiogenesis.
  • In order to gain a comprehensive insight into the regulation of the endothelial glycome, comprising genes encoding for sugar transporters (sugar s/t), glycosyltransferases (GT), glycan-degrading enzymes (GD) and lectins (GBP), we performed gene profiling analysis of the human bone marrow-derived microvascular endothelial cell line HBMEC-60 that resembles closely in its biological behaviour primary bone marrow endothelial cells.
  • [MeSH-minor] Biomarkers / metabolism. Bone Marrow Cells / cytology. Cell Line. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Glycoconjugates / chemistry. Glycoconjugates / metabolism. Glycoproteins / genetics. Glycoproteins / metabolism. Glycosyltransferases / metabolism. Humans. N-Acetylneuraminic Acid / metabolism. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 20162350.001).
  • [ISSN] 1573-7209
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Glycoconjugates; 0 / Glycoproteins; 0 / Polysaccharides; 0 / Receptors, Cell Surface; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; EC 2.4.- / Glycosyltransferases; GZP2782OP0 / N-Acetylneuraminic Acid
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52. Ludwig A, Schulte A, Schnack C, Hundhausen C, Reiss K, Brodway N, Held-Feindt J, Mentlein R: Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells. J Neurochem; 2005 Jun;93(5):1293-303
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  • In cultivated human glioma cells as well as in activated mouse astroglial cells, CXCL16 mRNA and protein is constitutively expressed and further up-regulated by tumour necrosis factor alpha (TNFalpha) and interferon-gamma (IFNgamma).
  • Thus, the transmembrane chemokine CXCL16 is expressed in the brain by malignant and inflamed astroglial cells, shed to a soluble form and targets not only activated T cells but also glial cells themselves.
  • [MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL6. Humans. Interferon-gamma / pharmacology. Metalloproteases / metabolism. Mice. Microglia / metabolism. Neuroglia / metabolism. RNA, Messenger / metabolism. Receptors, Scavenger. Recombinant Proteins / pharmacology. Solubility. Tissue Culture Techniques. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation

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  • (PMID = 15934948.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL16 protein, human; 0 / Chemokine CXCL6; 0 / Chemokines, CXC; 0 / Cxcl16 protein, mouse; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Immunologic; 0 / Receptors, Scavenger; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 3.4.- / Metalloproteases
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53. 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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54. Klabatsa A, Sheaff MT, Steele JP, Evans MT, Rudd RM, Fennell DA: Expression and prognostic significance of hypoxia-inducible factor 1alpha (HIF-1alpha) in malignant pleural mesothelioma (MPM). Lung Cancer; 2006 Jan;51(1):53-9
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  • [Title] Expression and prognostic significance of hypoxia-inducible factor 1alpha (HIF-1alpha) in malignant pleural mesothelioma (MPM).
  • Malignant pleural mesothelioma (MPM) is a highly chemoresistant cancer with a poor prognosis.
  • Hypoxia-inducible factor 1alpha (HIF-1alpha) is a subunit of a heterodimeric transcription complex that regulates several genes associated with tumour progression and anti-apoptosis.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Mesothelioma / metabolism. Pleural Neoplasms / metabolism
  • [MeSH-minor] Antigens, CD31 / biosynthesis. Apoptosis. Cell Nucleus / metabolism. Cytoplasm / metabolism. Disease Progression. Humans. Immunohistochemistry. In Vitro Techniques. Prognosis

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  • (PMID = 16169121.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
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55. Charalambous MP, Lightfoot T, Speirs V, Horgan K, Gooderham NJ: Expression of COX-2, NF-kappaB-p65, NF-kappaB-p50 and IKKalpha in malignant and adjacent normal human colorectal tissue. Br J Cancer; 2009 Jul 7;101(1):106-15
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  • [Title] Expression of COX-2, NF-kappaB-p65, NF-kappaB-p50 and IKKalpha in malignant and adjacent normal human colorectal tissue.
  • We hypothesised an association between COX-2 expression and NF-kappaB-p65, NF-kappaB-p50 and IkappaB-kinase-alpha (IKKalpha) in both epithelial and stromal cells in human colorectal cancer.
  • METHODS: Using immunohistochemistry, we measured COX-2, NF-kappaB-p65, NF-kappaB-p65 nuclear localisation sequence (NLS), NF-kappaB-p50, NF-kappaB-p50 NLS and IKKalpha protein expression in matched colorectal biopsy samples comprising both non-tumour and adjacent tumour tissue from 32 patients with colorectal cancer.
  • RESULTS: We have shown that stromal cells of malignant and surrounding normal colorectal tissue express COX-2.
  • In all cell types of malignant tissue, and in vascular endothelial cells (VECs) of neighbouring normal tissue, COX-2 expression was strongly associated with NF-kappaB-p65 expression (Pearson's correlation, P=0.019 for macrophages, P=0.001 for VECs, P=0.002 for fibroblasts (malignant tissue), and P=0.011 for VECs (non-malignant tissue)) but not NF-kappaB-p50 or IKKalpha.
  • Finally, the lack of association between COX-2, NF-kappaB-p65 or IKKalpha in stromal cells with the clinical severity of colorectal cancer as determined by Duke's stage, suggests that COX-2, NF-kappaB-p65 and IKKalpha expression are possibly early post-initiation events, which could be involved in tumour progression.

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  • [Cites] Br J Cancer. 2000 Aug;83(3):324-8 [10917546.001]
  • [Cites] J Clin Invest. 2000 Jun;105(11):1589-94 [10841517.001]
  • [Cites] Nat Immunol. 2002 Mar;3(3):221-7 [11875461.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1676-81 [11912139.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):6846-9 [12460897.001]
  • [Cites] J Gastroenterol. 2003;38(1):69-73 [12560924.001]
  • [Cites] Br J Cancer. 2003 May 19;88(10):1598-604 [12771929.001]
  • [Cites] Cancer Biol Ther. 2005 Feb;4(2):175-80 [15655349.001]
  • [Cites] Eur J Pharmacol. 2005 Jul 25;518(1):47-55 [15993407.001]
  • [Cites] J Exp Clin Cancer Res. 2005 Jun;24(2):279-87 [16110762.001]
  • [Cites] Pathol Res Pract. 2005;201(6):427-33 [16136748.001]
  • [Cites] Anticancer Res. 2005 May-Jun;25(3B):2065-8 [16158946.001]
  • [Cites] J Cancer Res Clin Oncol. 2006 Feb;132(2):76-84 [16215757.001]
  • [Cites] Cell Signal. 2006 Aug;18(8):1262-9 [16326073.001]
  • [Cites] Cancer Lett. 2006 Aug 8;239(2):246-53 [16216410.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):4013-21 [16849420.001]
  • [Cites] Cancer Gene Ther. 2006 Dec;13(12):1093-104 [16841079.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7613-8 [14633677.001]
  • [Cites] Hum Pathol. 2003 Dec;34(12):1242-6 [14691908.001]
  • [Cites] Clin Cancer Res. 2004 Sep 1;10(17):5870-9 [15355919.001]
  • [Cites] J Surg Oncol. 1983 Sep;24(1):83-7 [6887943.001]
  • [Cites] N Engl J Med. 1991 Dec 5;325(23):1593-6 [1669840.001]
  • [Cites] Cancer Res. 1992 Oct 15;52(20):5575-89 [1394181.001]
  • [Cites] N Engl J Med. 1993 May 6;328(18):1313-6 [8385741.001]
  • [Cites] J Biol Chem. 1993 Apr 25;268(12):9049-54 [8473346.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Aug 30;203(1):190-9 [8074655.001]
  • [Cites] Gastroenterology. 1994 Oct;107(4):1183-8 [7926468.001]
  • [Cites] Gut. 1994 Sep;35(9):1258-61 [7959233.001]
  • [Cites] N Engl J Med. 1995 Sep 7;333(10):609-14 [7637720.001]
  • [Cites] Arthritis Rheum. 1997 Feb;40(2):226-36 [9041934.001]
  • [Cites] Cancer Res. 1997 Apr 1;57(7):1276-80 [9102213.001]
  • [Cites] J Exp Med. 1998 Jan 19;187(2):143-6 [9432972.001]
  • [Cites] Anticancer Res. 1998 Jul-Aug;18(4A):2397-403 [9703885.001]
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3761-4 [9731479.001]
  • [Cites] Lancet. 1999 Jan 30;353(9150):391-9 [9950460.001]
  • [Cites] Cancer Lett. 1999 Jun 1;140(1-2):27-35 [10403538.001]
  • [Cites] Mod Pathol. 2005 Feb;18(2):212-20 [15475936.001]
  • [Cites] J Clin Oncol. 2005 Apr 20;23(12):2840-55 [15837998.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):6013-20 [10557090.001]
  • [Cites] J Immunol. 2000 Dec 15;165(12):7180-8 [11120850.001]
  • (PMID = 19513071.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B p50 Subunit; 0 / Transcription Factor RelA; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.10 / I-kappa B Kinase
  • [Other-IDs] NLM/ PMC2713702
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56. Ko CW, Cuthbert RJ, Orsi NM, Brooke DA, Perry SL, Markham AF, Coletta PL, Hull MA: Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice. J Pathol; 2008 Apr;214(5):603-9
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  • [Title] Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice.
  • Interleukin (IL)-4 receptor (IL-4R) alpha chain-dependent signalling by IL-4 and IL-13 promotes tumour growth and metastasis in mouse models of colorectal cancer.
  • However, the role of IL-4R alpha-dependent signalling during the early, pre-malignant stages of colorectal carcinogenesis has not been investigated.
  • Therefore, we investigated the effect of deletion of the IL-4R alpha gene on azoxymethane-induced colorectal aberrant crypt focus (ACF) multiplicity and size in Balb/c mice.
  • IL-4R alpha(-/-) mice developed significantly more ACFs [median 8, inter-quartile range (IQR) 4-11.5; n = 9] than wild-type (WT) animals (median 4, IQR 1-6; n = 9; p = 0.04, Mann-Whitney U-test).
  • There were significantly higher levels of IL-4 in serum from azoxymethane- and sham-treated IL-4R alpha(-/-) mice than WT animals, but no difference in serum IL-13 levels.
  • We found that mucosal TGFbeta mRNA levels and intestinal epithelial cell TGFbeta immunoreactivity were significantly higher in IL-4R alpha(-/-) mice than in WT animals.
  • In summary, IL-4R alpha-dependent signalling has a protective, anti-neoplastic role during the post-initiation phase of azoxymethane-induced colorectal carcinogenesis in Balb/c mice.
  • Our data should prompt thorough investigation of the role of IL-4R alpha-dependent signalling during human colorectal carcinogenesis, particularly as antagonism of IL-4R signalling represents a therapeutic strategy for asthma and other allergic diseases.
  • [MeSH-major] Colorectal Neoplasms / immunology. Precancerous Conditions / immunology. Receptors, Cell Surface / immunology
  • [MeSH-minor] Animals. Azoxymethane. Carcinogens. Cell Transformation, Neoplastic / immunology. Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Female. Interleukin-13 / blood. Interleukin-4 / blood. Intestinal Mucosa / immunology. Intestinal Mucosa / pathology. Mice. Mice, Inbred BALB C. Mice, Knockout. Signal Transduction / immunology. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / blood

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  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland
  • (PMID = 18220315.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/146; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; MO0N1J0SEN / Azoxymethane
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57. Iida H, Honda M, Kawai HF, Yamashita T, Shirota Y, Wang BC, Miao H, Kaneko S: Ephrin-A1 expression contributes to the malignant characteristics of {alpha}-fetoprotein producing hepatocellular carcinoma. Gut; 2005 Jun;54(6):843-51
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  • [Title] Ephrin-A1 expression contributes to the malignant characteristics of {alpha}-fetoprotein producing hepatocellular carcinoma.
  • BACKGROUND AND AIMS: alpha-Fetoprotein (AFP), a tumour marker for hepatocellular carcinoma (HCC), is associated with poor prognosis.
  • Using cDNA microarray analysis, we previously found that ephrin-A1, an angiogenic factor, is the most differentially overexpressed gene in AFP producing hepatoma cell lines.
  • METHODS: We examined ephrin-A1 expression and its effect on cell proliferation and gene expression in five AFP producing hepatoma cell lines, three AFP negative hepatoma cell lines, and 20 human HCC specimens.
  • Thus ephrin-A1 affects hepatoma cell growth. cDNA microarray analysis showed that ephrin-A1 induced expression of genes related to the cell cycle (p21), angiogenesis (angiopoietin 1 and thrombospondin 1), and cell-cell interactions (Rho, integrin, and matrix metalloproteinases) in cultured hepatoma cells.
  • CONCLUSION: These findings suggest that the poor prognosis of patients with AFP producing HCC is partially caused by ephrin-A1 expression, which induces expression of genes related to tumour cell growth, angiogenesis, invasion, and metastasis.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Ephrin-A1 / metabolism. Liver Neoplasms / metabolism. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. DNA, Complementary / analysis. Dose-Response Relationship, Drug. Gene Expression. Humans. Immunohistochemistry / methods. Oligonucleotide Array Sequence Analysis. Oligonucleotides, Antisense / pharmacology. Prognosis. RNA, Messenger / metabolism

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  • [Cites] Prostate. 1999 Dec 1;41(4):275-80 [10544301.001]
  • [Cites] Int J Cancer. 1999 Oct 22;84(5):494-501 [10502726.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):62-9 [10655584.001]
  • [Cites] Oncogene. 2000 Dec 7;19(52):6043-52 [11146556.001]
  • [Cites] Hepatology. 2001 Mar;33(3):676-91 [11230749.001]
  • [Cites] Gastroenterology. 2001 Mar;120(4):955-66 [11231949.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2301-6 [11280802.001]
  • [Cites] Hepatology. 2001 Apr;33(4):832-40 [11283847.001]
  • [Cites] Nat Cell Biol. 2001 May;3(5):527-30 [11331884.001]
  • [Cites] Oncol Rep. 2001 Jul-Aug;8(4):763-6 [11410779.001]
  • [Cites] Exp Biol Med (Maywood). 2001 Sep;226(8):726-33 [11520937.001]
  • [Cites] Cancer Lett. 2002 Jan 25;175(2):187-95 [11741747.001]
  • [Cites] Cytokine Growth Factor Rev. 2002 Feb;13(1):75-85 [11750881.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):1009-19 [11891198.001]
  • [Cites] Oncogene. 2002 Oct 10;21(46):7011-26 [12370823.001]
  • [Cites] Science. 1987 Dec 18;238(4834):1717-20 [2825356.001]
  • [Cites] Mol Cell Biol. 1988 Sep;8(9):3770-6 [3221865.001]
  • [Cites] Histopathology. 1989 May;14(5):503-13 [2472345.001]
  • [Cites] Cancer. 1989 Oct 15;64(8):1700-7 [2477133.001]
  • [Cites] Oncogene. 1990 Mar;5(3):445-7 [2314900.001]
  • [Cites] Int J Cancer. 1992 Jul 30;51(6):862-8 [1322376.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5123-7 [7685115.001]
  • [Cites] Nature. 1993 Dec 16;366(6456):701-4 [8259214.001]
  • [Cites] Hepatology. 1994 Jan;19(1):61-6 [7506227.001]
  • [Cites] Hepatology. 1994 Jun;19(6):1513-20 [8188183.001]
  • [Cites] Int J Cancer. 1994 Oct 15;59(2):191-5 [7927918.001]
  • [Cites] Science. 1994 Nov 4;266(5186):816-9 [7973638.001]
  • [Cites] Int J Cancer. 1995 Jan 3;60(1):129-36 [7814145.001]
  • [Cites] Cancer Res. 1995 Jun 15;55(12):2528-32 [7780963.001]
  • [Cites] Gastroenterology. 1996 Oct;111(4):996-1001 [8831594.001]
  • [Cites] Hepatology. 1997 Mar;25(3):575-9 [9049201.001]
  • [Cites] Gastroenterology. 1997 Apr;112(4):1290-6 [9098015.001]
  • [Cites] Carcinogenesis. 1997 Jul;18(7):1291-7 [9230270.001]
  • [Cites] Curr Opin Cell Biol. 1997 Oct;9(5):608-15 [9330863.001]
  • [Cites] Am J Physiol. 1997 Oct;273(4 Pt 1):G824-32 [9357823.001]
  • [Cites] J Biochem. 1997 Oct;122(4):717-22 [9399573.001]
  • [Cites] Anticancer Res. 1998 Jan-Feb;18(1B):555-64 [9568177.001]
  • [Cites] Int J Cancer. 1998 Aug 21;79(4):424-8 [9699537.001]
  • [Cites] Hepatology. 1998 Dec;28(6):1512-7 [9828214.001]
  • [Cites] J Clin Invest. 1999 Feb;103(3):341-5 [9927494.001]
  • [Cites] Jpn J Clin Oncol. 1999 Feb;29(2):58-62 [10089944.001]
  • [Cites] Int J Cancer. 1999 Dec 22;84(6):604-8 [10567906.001]
  • (PMID = 15888795.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA, Complementary; 0 / Ephrin-A1; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / alpha-Fetoproteins; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Other-IDs] NLM/ PMC1774523
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58. Koehn H, Magan N, Isaacs RJ, Stowell KM: Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin. Anticancer Drugs; 2007 Apr;18(4):419-25
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  • [Title] Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin.
  • Radiotherapy and chemotherapy often induce DNA double-strand breaks in both normal and malignant cells.
  • The proteins involved in the repair of such lesions are central to cancer prognosis and treatment, as they can be overexpressed in many cancers, accelerating malignant transformation and increasing repair capacity, potentially leading to cellular resistance.
  • If malignant cells can be selectively targeted repair proteins could also be candidates for targeted therapy.
  • In this study, two keyplayers in eukaryotic DNA double-strand break repair, Rad51 and DNA-dependent protein kinase catalytic subunit, were analysed in noncancerous human breast cells (MCF12A) and the breast cancer cell lines (MDA MB 231 and MCF7) in response to treatment with doxorubicin.
  • A cell cycle-independent increase in Rad51 protein levels (a recombinase involved in homologous recombination repair) was observed 24 and 48 h after treatment in MDA MB 231 and MCF12A when exposed to low levels of doxorubicin, whereas MCF7 cells displayed a continuous decrease in Rad51 protein with increasing drug concentration.
  • Topoisomerase II-alpha protein, the primary target of doxorubicin, was upregulated at low concentrations of doxorubicin in all cell lines tested.
  • Here we show that Rad51 protein levels can be differentially regulated in normal and malignant breast cell lines in response to doxorubicin, independent of cell cycle state.
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA Damage. Dose-Response Relationship, Drug. Female. Flow Cytometry. Genes, p53 / genetics. Humans. Receptors, Estrogen / genetics. Receptors, Estrogen / physiology. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / physiology

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  • (PMID = 17351394.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Receptors, Estrogen; 0 / Transforming Growth Factor beta; 80168379AG / Doxorubicin; EC 2.7.7.- / Rad51 Recombinase
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59. Huang L, Verstrepen L, Heyninck K, Wullaert A, Revets H, De Baetselier P, Beyaert R: ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells. Oncogene; 2008 Oct 16;27(47):6131-40
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  • [Title] ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells.
  • The epidermal growth factor receptor (EGFR) is frequently overexpressed in various tumours of epidermal origin and is held responsible for tumourigenicity and tumour persistence.
  • Increased nuclear factor (NF)-kappaB activity has been suggested to be involved in the malignant behaviour of EGFR-overexpressing cells.
  • Moreover, EGF-induced NF-kappaB activation could be inhibited by overexpression of ABINs, which were previously identified as intracellular inhibitors of tumour necrosis factor, interleukin-1 and lipopolysaccharide-induced NF-kappaB activation.
  • Adenoviral gene transfer of ABINs reduced constitutive NF-kappaB activity as well as the proliferation of EGFR-overexpressing A431 and DU145 human carcinoma cells.
  • Altogether, these results demonstrate an important role for an ABIN-sensitive non-classical NF-kappaB signalling pathway in the proliferation of EGFR-overexpressing tumour cells, and indicate a potential use for ABIN gene therapy in the treatment of cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cyclin D1 / genetics. Epidermal Growth Factor / pharmacology. Genetic Therapy. Humans. I-kappa B Proteins / metabolism. NF-kappa B p52 Subunit / metabolism. Phosphorylation. Protein Structure, Tertiary. RNA Interference. Signal Transduction

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  • (PMID = 18622428.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / NF-kappa B p52 Subunit; 0 / TNIP1 protein, human; 0 / TNIP2 protein, human; 136601-57-5 / Cyclin D1; 139874-52-5 / NF-kappaB inhibitor alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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60. Monteagudo C, Martin JM, Jorda E, Llombart-Bosch A: CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors. J Clin Pathol; 2007 Jun;60(6):596-9
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  • [Title] CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors.
  • BACKGROUND: A role for CXCR3, the receptor for chemokines Mig, IP-10 and interferon-inducible T cell alpha-chemoattractant, in tumour cell migration during melanoma progression has been proposed.
  • AIMS: To analyse CXCR3 expression in primary cutaneous malignant melanomas and its comparison with clinicopathological and prognostic factors.
  • Melanomas were categorised by age, sex, primary site, tumour thickness, growth phase, ulceration, lymphocytic infiltration, recurrence, lymph node and distant metastasis, and survival.
  • In univariate analysis, a significant association of CXCR3-positive tumour cell immunostaining with tumour thickness >1 mm (p = 0.003), absence of lymphocytic infiltration (p = 0.04) and the presence of distant metastasis (p = 0.048) was found.
  • Multivariate analysis found tumour thickness as the only independent factor with considerable association with distant metastases.
  • CONCLUSIONS: Our findings of a positive correlation of CXCR3 tumour cell immunoreactivity in human primary cutaneous melanoma with tumour thickness >1 mm and absence of intratumoral lymphocytic infiltration support the biological implication of CXCR3 in the tumour progression of cutaneous malignant melanoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Melanoma / metabolism. Receptors, Chemokine / metabolism. Skin Neoplasms / metabolism

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  • [Cites] Arch Dermatol. 1999 Dec;135(12):1451-6 [10606049.001]
  • [Cites] Int J Cancer. 2005 Dec 10;117(5):861-5 [15981210.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):24-5 [11242022.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):50-6 [11242036.001]
  • [Cites] Am J Pathol. 2001 May;158(5):1703-11 [11337368.001]
  • [Cites] N Engl J Med. 2001 Sep 13;345(11):833-5 [11556308.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45098-105 [11571298.001]
  • [Cites] Cancer Control. 2002 Jan-Feb;9(1):9-15 [11907461.001]
  • [Cites] Am J Respir Crit Care Med. 2002 May 15;165(10):1404-9 [12016104.001]
  • [Cites] Am J Clin Pathol. 2002 Oct;118(4):504-11 [12375635.001]
  • [Cites] Br J Dermatol. 2004 Feb;150(2):179-85 [14996086.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):4010-7 [15173015.001]
  • [Cites] Arch Pathol Lab Med. 1985 Aug;109(8):716-21 [3893381.001]
  • [Cites] J Immunol Methods. 1998 Nov 1;220(1-2):1-17 [9839921.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2673-81 [11023497.001]
  • (PMID = 16522748.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCR3 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, CXCR3; 0 / Receptors, Chemokine
  • [Other-IDs] NLM/ PMC1955073
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61. Baumeister P, Schwenk-Zieger S, Reiter M, Welz C, Harréus U: Transforming Growth Factor-alpha reduces carcinogen-induced DNA damage in mini-organ cultures from head-and-neck cancer patients. Mutat Res; 2009 Jun-Jul;677(1-2):42-5
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  • [Title] Transforming Growth Factor-alpha reduces carcinogen-induced DNA damage in mini-organ cultures from head-and-neck cancer patients.
  • EGFR is over-expressed in up to 90-100% of head-and-neck squamous cell carcinomas (HNSCC), and increased expression of EGFR and its ligand Transforming Growth Factor-alpha (TGF-alpha) is not limited to malignant cells, but also detected in histologically normal mucosa of HNSCC patients, supporting the hypothesis of field carcinogenesis.
  • Our study evaluates the impact of stimulation by TGF-alpha on carcinogen-induced and oxidative DNA damage in mucosa tissue cultures of macroscopically normal biopsies from tumour patients and controls.
  • Effects of TGF-alpha on DNA-repair capacity were investigated.
  • To assess DNA fragmentation, alkaline single-cell gel electrophoresis (comet assay) was used.
  • Stimulation of cultures during 24 h with TGF-alpha decreased benzo(a)pyrene diolepoxide (BPDE)-induced DNA damage by 36% in the tumour group (p < 0.001) and by 7% in controls (n = 30).
  • The exact mechanism by which TGF-alpha stimulation reduces BPDE-induced DNA fragmentation remains unclear.
  • However, our results show a strong DNA-stabilizing effect of stimulation by TGF-alpha in mucosa tissue cultures of tumour patients and may therefore be seen as a physiological response to continued carcinogenic impact on the epithelium of the upper aerodigestive tract.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. DNA Damage / drug effects. Head and Neck Neoplasms / genetics. Transforming Growth Factor alpha / pharmacology

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  • (PMID = 19539778.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Transforming Growth Factor alpha; 55097-80-8 / 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide; BBX060AN9V / Hydrogen Peroxide
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62. Brennan PA, Mackenzie N, Quintero M: Hypoxia-inducible factor 1alpha in oral cancer. J Oral Pathol Med; 2005 Aug;34(7):385-9
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  • It contributes to local and systemic tumour progression as well as potentially compromising radiotherapy and chemotherapy.
  • It targets the transcription of over 60 genes involved in many aspects of cancer biology including cell survival, glucose metabolism, cell invasion and angiogenesis.
  • RESULTS: Although there are a few conflicting reports of its prognostic significance, over expression of HIF-1alpha seems to play an adverse role in the malignant progression of head and neck cancer by facilitating the adaptation of cells to hypoxia as well as contributing to the invasive properties and angiogenesis in these tumours.
  • The pharmacological manipulation of HIF-1alpha has marked effects on tumour growth, and it could prove to be an important target for drug therapy, both in oral cancer and in other hypoxia-dependent disease states.
  • [MeSH-major] Cell Hypoxia / physiology. Mouth Neoplasms / metabolism. Nitric Oxide / physiology. Transcription Factors / physiology
  • [MeSH-minor] Humans. Hypoxia-Inducible Factor 1, alpha Subunit

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  • (PMID = 16011605.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 40
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63. Milicevic Z, Bogojevic D, Mihailovic M, Petrovic M, Krivokapic Z: Molecular characterization of hsp90 isoforms in colorectal cancer cells and its association with tumour progression. Int J Oncol; 2008 Jun;32(6):1169-78
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  • [Title] Molecular characterization of hsp90 isoforms in colorectal cancer cells and its association with tumour progression.
  • As determined by Western blot assay all hsp90 isoforms studied, alpha (84 kDa), beta (86 kDa) and hsp90N (75 kDa), were up-regulated and differentially expressed in various stages of colorectal carcinoma.
  • The expression of hsp90beta is definitely higher in poorly-differentiated carcinomas than in well-differentiated cancers, suggesting an involvement of hsp90beta in the inhibition of cancer cell differentiation.
  • Especially, the expression of cytosolic hsp90N isoform in malignant cells points to the possibility that induction or overexpression of hsp90N might be causally related to tumour formation.
  • In this way, the hsp90 would be at the crossroads of both signalling and cell migration events.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Differentiation. Cell Membrane / metabolism. Cell Movement. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Protein Isoforms. Signal Transduction

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  • (PMID = 18497978.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 0 / Protein Isoforms
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64. Jackson IL, Batinic-Haberle I, Sonveaux P, Dewhirst MW, Vujaskovic Z: ROS production and angiogenic regulation by macrophages in response to heat therapy. Int J Hyperthermia; 2006 Jun;22(4):263-73
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  • PURPOSE: It has been well established that inadequate blood supply combined with high metabolic rates of oxygen consumption results in areas of low oxygen tension (<1%) within malignant tumours and that elevating tumour temperatures above 39 degrees Celsius results in significant improvement in tumour oxygenation.
  • Macrophages play a dual role in tumour initiation and progression having both pro-tumour and anti-tumour effects.
  • [MeSH-minor] Animals. Cell Line. Cytokines / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / analysis. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Mice. Neoplasms / metabolism. Neoplasms / therapy. Oxygen Consumption / physiology. Respiratory Burst / physiology. Superoxides / metabolism. Temperature. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16754348.001).
  • [ISSN] 0265-6736
  • [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 / Cytokines; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Reactive Oxygen Species; 0 / Vascular Endothelial Growth Factor A; 11062-77-4 / Superoxides
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65. Aggelis V, Craven RA, Peng J, Harnden P, Cairns DA, Maher ER, Tonge R, Selby PJ, Banks RE: Proteomic identification of differentially expressed plasma membrane proteins in renal cell carcinoma by stable isotope labelling of a von Hippel-Lindau transfectant cell line model. Proteomics; 2009 Apr;9(8):2118-30
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  • [Title] Proteomic identification of differentially expressed plasma membrane proteins in renal cell carcinoma by stable isotope labelling of a von Hippel-Lindau transfectant cell line model.
  • The von Hippel-Lindau (VHL) tumour suppressor gene plays a central role in development of clear cell renal cell carcinoma (RCC).
  • Using a cell line pair generated from the VHL-defective RCC cell line UMRC2 by transfection with vector control or VHL (-/+VHL) and stable isotope labelling with amino acids in cell culture (SILAC) followed by enrichment of plasma membrane proteins by cell surface biotinylation/avidin-affinity chromatography and analysis by GeLC-MS/MS, VHL-associated changes in plasma membrane proteins were analysed.
  • These included several proteins previously reported to be VHL targets, such as transferrin receptor 1 and the alpha 3 and beta1 integrin subunits and novel findings including upregulation of CD166 and CD147 in VHL-defective cells.
  • Analysis of patient-matched normal and malignant renal tissues confirmed these differences were also present in vivo in a subset of clear cell RCCs.
  • [MeSH-major] Carcinoma, Renal Cell / metabolism. Membrane Proteins / biosynthesis. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Antigens, CD / biosynthesis. Antigens, CD147 / biosynthesis. Biomarkers / metabolism. Cell Adhesion Molecules, Neuronal / biosynthesis. Cell Line, Tumor. Fetal Proteins / biosynthesis. Glycosylation. Humans. Isotope Labeling. Kidney Neoplasms / chemistry. Kidney Neoplasms / metabolism. Kidney Neoplasms / ultrastructure. Mass Spectrometry. Proteomics. Transfection. Up-Regulation

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  • (PMID = 19337990.001).
  • [ISSN] 1615-9861
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ALCAM protein, human; 0 / Antigens, CD; 0 / Biomarkers; 0 / Cell Adhesion Molecules, Neuronal; 0 / Fetal Proteins; 0 / Membrane Proteins; 136894-56-9 / Antigens, CD147; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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66. Katori H, Nozawa A, Tsukuda M: Markers of malignant transformation of sinonasal inverted papilloma. Eur J Surg Oncol; 2005 Oct;31(8):905-11
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  • [Title] Markers of malignant transformation of sinonasal inverted papilloma.
  • AIM: To measure HPV status, epidermal growth factor receptor (EGFR) and transforming growth factor-alpha (TGF-alpha) expression and Ki-67 index in exophytic papilloma (EP), inverted papilloma (IP) with dysplasia, IP with carcinoma and invasive squamous cell carcinoma (SCC).
  • The nasal tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • RESULTS: Significant increase of EGFR and TGF-alpha was observed in IP with severe dysplasia, IP with carcinoma and invasive SCC compared to IP with mild dysplasia and control nasal mucosa.
  • Among IP, HPV 6/11-positive was present in 42% tumour and HPV 16/18-positive was present in 31% of tumours.
  • CONCLUSION: Pre-cancerous lesions of IP exhibited elevated levels of EGFR and TGF-alpha and these expression may be associated with early events in IP carcinogenesis.
  • HPV infection may be an early event in a multistep process of malignant formation of IP.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic / pathology. Nose Neoplasms / pathology. Papilloma, Inverted / pathology. Paranasal Sinus Neoplasms / pathology
  • [MeSH-minor] Antibodies, Monoclonal. Carcinoma / pathology. Carcinoma, Squamous Cell / pathology. Female. Humans. In Situ Hybridization. Ki-67 Antigen / analysis. Male. Middle Aged. Nasal Mucosa / pathology. Neoplasm Invasiveness. Papilloma / pathology. Papillomaviridae / classification. Papillomaviridae / isolation & purification. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / analysis. Transforming Growth Factor alpha / analysis

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  • (PMID = 16005600.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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67. Przybyło M, Lityńska A, Pocheć E: Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation. Biochimie; 2005 Feb;87(2):133-42
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  • [Title] Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation.
  • In tumour cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • This study used cell lines having very different behaviour in vivo: HCV29 non-malignant transitional epithelium and T24 bladder transitional cell carcinoma.
  • The functional role of carbohydrates was studied by treating these cells with swainsonine, an inhibitor of Golgi alpha-mannosidase II, and in vitro adhesion and migration assays.
  • Swainsonine treatment reduced the rate of T24 cell migration by 20%.
  • We concluded that beta1-6 branched tri- and tetraantennary complex-type glycans have an important function in adhesion and migration in the studied cell lines.
  • [MeSH-major] Cell Movement. Epithelial Cells / metabolism. Polysaccharides / biosynthesis. Ureter / metabolism. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Glycosylation / drug effects. Humans. Male. Species Specificity. Swainsonine / pharmacology

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  • (PMID = 15760705.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Polysaccharides; RSY4RK37KQ / Swainsonine
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68. Tajima N, Schönherr K, Niedling S, Kaatz M, Kanno H, Schönherr R, Heinemann SH: Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1alpha and the von Hippel-Lindau protein. J Physiol; 2006 Mar 1;571(Pt 2):349-59
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  • Under chronic hypoxia, tumour cells undergo adaptive changes involving hypoxia-inducible factors (HIFs).
  • This increase involves the HIF system as confirmed by overexpression of HIF-1alpha or the von Hippel-Lindau tumour suppressor gene.
  • Hypoxia increased cell proliferation, but the K(Ca) channel blockers apamin and charybdotoxin slowed down cell growth, particularly under hypoxic conditions.
  • Similar results were obtained for the cell line IGR39 and for acutely isolated cells from a biopsy of a melanoma metastasis.
  • Thus, up-regulation of K(Ca) channels may be a novel mechanism by which HIFs can contribute to the malignant phenotype of human tumour cells.
  • [MeSH-major] Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Intermediate-Conductance Calcium-Activated Potassium Channels / metabolism. Melanoma / metabolism. Potassium Channels, Calcium-Activated / metabolism. Small-Conductance Calcium-Activated Potassium Channels / metabolism. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Apamin / pharmacology. Cell Hypoxia. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Transfection. Tumor Cells, Cultured. Up-Regulation

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  • [Cites] Physiology (Bethesda). 2004 Oct;19:285-92 [15381757.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Apr;77(4):2200-4 [6929546.001]
  • [Cites] J Neurochem. 1992 Apr;58(4):1538-46 [1347783.001]
  • [Cites] Physiol Rev. 1992 Apr;72(2):449-89 [1557429.001]
  • [Cites] J Membr Biol. 1993 Mar;132(3):201-9 [7684087.001]
  • [Cites] J Biol Chem. 1994 Feb 11;269(6):4355-9 [8308005.001]
  • [Cites] Nat Genet. 1994 May;7(1):85-90 [7915601.001]
  • [Cites] J Biol Chem. 1994 Sep 23;269(38):23757-63 [8089148.001]
  • [Cites] Nature. 1996 Jan 4;379(6560):88-91 [8538748.001]
  • [Cites] Cancer Res. 1996 Mar 1;56(5):941-3 [8640781.001]
  • [Cites] J Membr Biol. 1996 May;151(2):149-57 [8661503.001]
  • [Cites] Cancer Res. 1996 Oct 1;56(19):4509-15 [8813149.001]
  • [Cites] J Membr Biol. 1996 Nov;154(2):91-107 [8929284.001]
  • [Cites] J Physiol. 1997 Jul 15;502 ( Pt 2):293-305 [9263911.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11651-6 [9326665.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):11013-8 [9380751.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2347-53 [9410914.001]
  • [Cites] Cancer Res. 1998 Apr 1;58(7):1408-16 [9537241.001]
  • [Cites] Mol Cell Biol. 1998 May;18(5):2845-54 [9566903.001]
  • [Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):2820-4 [10850421.001]
  • [Cites] Nat Cell Biol. 2000 Jul;2(7):423-7 [10878807.001]
  • [Cites] EMBO J. 2000 Aug 15;19(16):4298-309 [10944113.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2001 Apr;280(4):L801-12 [11238022.001]
  • [Cites] Science. 2001 Apr 20;292(5516):464-8 [11292862.001]
  • [Cites] Science. 2001 Apr 20;292(5516):468-72 [11292861.001]
  • [Cites] Receptors Channels. 2001;7(5):345-56 [11697078.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2350-5 [11854528.001]
  • [Cites] Br J Cancer. 2002 Jan 21;86(2):301-8 [11870523.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]
  • [Cites] J Membr Biol. 2002 Jul 15;188(2):137-49 [12172639.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):7004-11 [12460920.001]
  • [Cites] J Biol Chem. 2003 Jun 20;278(25):22316-24 [12679337.001]
  • [Cites] Cancer Treat Rev. 2003 Aug;29(4):297-307 [12927570.001]
  • [Cites] Ann Neurol. 2003 Sep;54(3):352-9 [12953267.001]
  • [Cites] Nat Rev Drug Discov. 2003 Oct;2(10):803-11 [14526383.001]
  • [Cites] J Appl Physiol (1985). 2004 Mar;96(3):1187-95; discussion 1170-2 [14766769.001]
  • [Cites] Neuropharmacology. 2004 Mar;46(3):318-30 [14975687.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2004 Apr;286(4):R608-23 [15003941.001]
  • [Cites] Pflugers Arch. 2004 Jun;448(3):274-86 [15048575.001]
  • [Cites] J Membr Biol. 1999 Sep 15;171(2):107-15 [10489423.001]
  • [Cites] Am J Physiol Cell Physiol. 2004 Jul;287(1):C125-34 [14985237.001]
  • [Cites] Biol Reprod. 2004 Jul;71(1):331-9 [15031145.001]
  • [Cites] Physiology (Bethesda). 2004 Aug;19:176-82 [15304631.001]
  • [Cites] Cell Physiol Biochem. 1999;9(3):126-32 [10494026.001]
  • [Cites] EMBO J. 1999 Oct 15;18(20):5540-7 [10523298.001]
  • [Cites] Oncologist. 2004;9 Suppl 5:10-7 [15591418.001]
  • [Cites] J Physiol. 2005 Jul 15;566(Pt 2):491-503 [15890701.001]
  • [Cites] Circulation. 2005 Aug 30;112(9):1309-15 [16116057.001]
  • [Cites] J Membr Biol. 2005 Jun;205(3):175-84 [16362505.001]
  • (PMID = 16396931.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intermediate-Conductance Calcium-Activated Potassium Channels; 0 / Potassium Channels, Calcium-Activated; 0 / Small-Conductance Calcium-Activated Potassium Channels; 24345-16-2 / Apamin; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC1796787
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69. Woodward JK, Rennie IG, Elshaw SR, Burn JL, Sisley K: Invasive and noninvasive uveal melanomas have different adhesive properties. Eye (Lond); 2005 Mar;19(3):342-8
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  • METHODS: Cells from an invasive and noninvasive uveal melanoma cell line and hepatic and dermal microvascular endothelial cells were assessed by flow cytometry for adhesion molecule expression.
  • Tumour cell adhesion to ECM substrates (collagens I and IV, fibronectin, laminin, and vitronectin) and endothelial cells was also investigated using a commercially available assay or a fluorescence-based in vitro assay, respectively.
  • The significance of results comparing cell lines was determined using a Student's t-test, whereby P-values of less than 0.05 were taken as significant.
  • The invasive cell line also expressed higher levels of other integrins than the noninvasive line.
  • CONCLUSIONS: Successful attachment to and migration through the ECM, basement membrane, and endothelium are vital processes involved in malignant progression.
  • [MeSH-minor] Cell Adhesion. Cell Adhesion Molecules / metabolism. Endothelial Cells / pathology. Endothelium, Vascular / pathology. Extracellular Matrix / pathology. Extracellular Matrix Proteins / metabolism. Humans. Integrin alpha Chains / metabolism. Neoplasm Invasiveness. Neoplasm Proteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 15258612.001).
  • [ISSN] 0950-222X
  • [Journal-full-title] Eye (London, England)
  • [ISO-abbreviation] Eye (Lond)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Extracellular Matrix Proteins; 0 / Integrin alpha Chains; 0 / Neoplasm Proteins
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70. Oremek GM, Sauer-Eppel H, Bruzdziak TH: Value of tumour and inflammatory markers in lung cancer. Anticancer Res; 2007 Jul-Aug;27(4A):1911-5
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  • [Title] Value of tumour and inflammatory markers in lung cancer.
  • The aim of this study was to evaluate the individual diagnostic utility of tumour and inflammatory markers in patients with different pulmonary diseases.
  • The usefulness of neuron-specific enolase (NSE), carcino-embryonic antigen (CEA), serum pro-gastrin releasing peptide (ProGRP) and CYFRA 21-1, as tumour markers, and C-reactive protein (CRP) and tumour necrosis factor-alpha (TNFalpha) as inflammatory markers for diagnosis, treatment and monitoring of patients with different pulmonary afflictions was investigated.
  • Moreover, serum marker levels were analyzed in 139 patients with different pulmonary malignancies: 29 patients with adenocarcinoma, 30 patients with squamous cell carcinoma, 80 patients with small cell lung cancer (SCLC).
  • All tumour markers showed significantly elevated values in malignant diseases.
  • The acute phase response had a wide range in patients with malignant tumours.
  • In conclusion, when serum tumour markers are abnormally elevated in patients with lung cancer, CEA, CYFRA 21-1, NSE and ProGRP are useful clinical markers, good indicators of disease extent and may have important prognostic value.
  • [MeSH-major] Biomarkers, Tumor / blood. Inflammation / blood. Lung Neoplasms / diagnosis
  • [MeSH-minor] Antigens, Neoplasm / blood. Area Under Curve. C-Reactive Protein / analysis. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Small Cell / blood. Carcinoma, Small Cell / diagnosis. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / diagnosis. Humans. Immunoassay. Keratin-19. Keratins / blood. Lung Diseases / blood. Lung Diseases / diagnosis. Peptide Fragments / blood. Peptides / blood. Phosphopyruvate Hydratase / blood. ROC Curve. Recombinant Proteins / blood. Sensitivity and Specificity. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17649794.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / antigen CYFRA21.1; 0 / pro-gastrin-releasing peptide (31-98); 68238-35-7 / Keratins; 9007-41-4 / C-Reactive Protein; EC 4.2.1.11 / Phosphopyruvate Hydratase
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71. Lansigan F, Foss FM: Current and emerging treatment strategies for cutaneous T-cell lymphoma. Drugs; 2010 Feb 12;70(3):273-86
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  • [Title] Current and emerging treatment strategies for cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCLs) are a rare group of mature T-cell lymphomas presenting primarily in the skin.
  • Other than an allogeneic stem cell transplant, there are no curative therapies for this disease.
  • These therapies include biological immune enhancers such as interferon alpha and extracorporeal photopheresis that exert their effect by stimulating an immune response to the tumour cells.
  • The fusion toxin denileukin diftitox targets the interleukin-2 receptor expressed on malignant T cells.
  • Forodesine is a novel inhibitor of purine nucleoside phosphorylase and leads to apoptosis of malignant T cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Lymphoma, T-Cell, Cutaneous / drug therapy. Lymphoma, T-Cell, Cutaneous / therapy. Skin Neoplasms / drug therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Clinical Protocols. Drug Administration Routes. Hematopoietic Stem Cell Transplantation / methods. Humans

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  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):376-88 [11208829.001]
  • [Cites] J Clin Oncol. 2007 Jul 20;25(21):3109-15 [17577020.001]
  • [Cites] Arch Dermatol. 2007 Jul;143(7):854-9 [17638728.001]
  • [Cites] Arch Dermatol. 1977 Oct;113(10):1387-9 [911166.001]
  • [Cites] Br J Dermatol. 2007 Jun;156(6):1379-81 [17459033.001]
  • [Cites] Clin Lymphoma Myeloma. 2006 Jul;7(1):51-8 [16879770.001]
  • [Cites] Blood. 1992 Aug 1;80(3):587-92 [1353380.001]
  • [Cites] Photodermatol Photoimmunol Photomed. 2007 Oct;23(5):163-71 [17803594.001]
  • [Cites] J Am Acad Dermatol. 1984 Feb;10(2 Pt 1):238-45 [6609177.001]
  • [Cites] N Engl J Med. 1987 Feb 5;316(6):297-303 [3543674.001]
  • [Cites] J Am Acad Dermatol. 1992 Nov;27(5 Pt 1):729-36 [1430395.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2865-8 [11675364.001]
  • [Cites] Bone Marrow Transplant. 2004 Sep;34(6):521-5 [15286686.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4267-72 [12543862.001]
  • [Cites] Cancer. 1999 May 1;85(9):1985-95 [10223240.001]
  • [Cites] Blood. 2005 May 15;105(10):3768-85 [15692063.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2456-71 [11331325.001]
  • [Cites] Ann Intern Med. 1988 Sep 1;109(5):372-82 [3408055.001]
  • [Cites] Arch Dermatol. 1999 Nov;135(11):1377-80 [10566837.001]
  • [Cites] Arch Dermatol. 1987 Jul;123(7):897-901 [3606168.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Jul 15;38(5):1027-35 [9276369.001]
  • [Cites] J Am Acad Dermatol. 2008 Oct;59(4):589-95 [18656282.001]
  • [Cites] J Am Acad Dermatol. 2002 Jan;46(1):95-106 [11756953.001]
  • [Cites] J Am Acad Dermatol. 2002 Aug;47(2):191-7 [12140464.001]
  • [Cites] Br J Haematol. 2001 Sep;114(3):624-31 [11552988.001]
  • [Cites] Hum Cell. 1995 Sep;8(3):121-6 [8652448.001]
  • [Cites] Br J Ophthalmol. 2006 Aug;90(8):1070-1 [16854841.001]
  • [Cites] Arch Dermatol. 1992 Jul;128(7):931-3 [1626959.001]
  • [Cites] Ann N Y Acad Sci. 2001 Sep;941:1-11 [11594563.001]
  • [Cites] Blood. 1996 Feb 1;87(3):906-11 [8562961.001]
  • [Cites] J Clin Oncol. 1992 Dec;10 (12 ):1907-13 [1453206.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Jul 15;32(4):987-95 [7607973.001]
  • [Cites] Yale J Biol Med. 1985 Nov-Dec;58(6):519-34 [3832664.001]
  • [Cites] Arch Dermatol. 1998 Aug;134(8):949-54 [9722724.001]
  • [Cites] Br J Dermatol. 2008 Apr;158(4):659-78 [18241274.001]
  • [Cites] Front Radiat Ther Oncol. 1991;25:80-9; discussion 132-3 [1908426.001]
  • [Cites] Cancer Treat Rep. 1979 Apr;63(4):725-8 [445521.001]
  • [Cites] Blut. 1987 Apr;54(4):247-50 [3493819.001]
  • [Cites] J Am Acad Dermatol. 1989 Mar;20(3):416-28 [2537348.001]
  • [Cites] Blood. 2007 Sep 15;110(6):1713-22 [17540844.001]
  • [Cites] Eur J Cancer. 2006 May;42(8):1014-30 [16574401.001]
  • [Cites] Dermatologica. 1987;175 Suppl 1:145-50 [3500880.001]
  • [Cites] Cancer. 2003 Sep 1;98(5):993-1001 [12942567.001]
  • [Cites] J Am Acad Dermatol. 2006 Nov;55(5):807-13 [17052486.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3117-21 [10506607.001]
  • [Cites] Eur J Haematol. 2003 Oct;71(4):250-6 [12950233.001]
  • [Cites] J Invest Dermatol. 2005 Dec;125(6):xvi-xvii [16354175.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1991 Apr;20(4):809-13 [2004959.001]
  • [Cites] Lancet. 1997 Jul 5;350(9070):32-3 [9217723.001]
  • [Cites] J Natl Cancer Inst. 1990 Aug 15;82(16):1353-5 [1696322.001]
  • [Cites] J Clin Oncol. 1987 Nov;5(11):1796-803 [3681368.001]
  • [Cites] Cancer. 2005 Dec 1;104(11):2437-41 [16216001.001]
  • [Cites] J Clin Oncol. 2000 Jul;18(13):2603-6 [10893292.001]
  • [Cites] Adv Cancer Res. 2004;91:137-68 [15327890.001]
  • [Cites] Nat Rev Drug Discov. 2002 Apr;1(4):287-99 [12120280.001]
  • [Cites] Ann Intern Med. 1984 Oct;101(4):484-7 [6332565.001]
  • [Cites] Blood. 2005 Jul 15;106(2):454-7 [15811959.001]
  • [Cites] J Clin Oncol. 2007 Sep 20;25(27):4293-7 [17709797.001]
  • [Cites] Cancer. 1999 Oct 1;86(7):1368-76 [10506727.001]
  • [Cites] J Am Acad Dermatol. 1989 Mar;20(3):395-407 [2783939.001]
  • [Cites] Nat Rev Drug Discov. 2006 Sep;5(9):769-84 [16955068.001]
  • [Cites] Blood. 1994 Aug 1;84(3):733-8 [7913841.001]
  • [Cites] J Am Acad Dermatol. 1992 Jun;26(6):960-7 [1607416.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1631-8 [15161670.001]
  • [Cites] J Am Acad Dermatol. 1996 Jun;34(6):1022-9 [8647968.001]
  • [Cites] Blood. 2007 Jan 1;109(1):31-9 [16960145.001]
  • [Cites] J Am Acad Dermatol. 2000 Jul;43(1 Pt 1):54-60 [10863224.001]
  • [Cites] Dermatol Ther. 2003;16(4):311-21 [14686974.001]
  • [Cites] Arch Dermatol. 2000 Jun;136(6):748-52 [10871938.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2929-39 [11929784.001]
  • [Cites] Blood. 2001 Jan 15;97(2):523-7 [11154232.001]
  • [Cites] Arch Dermatol. 2005 Sep;141(9):1176-8 [16172331.001]
  • [Cites] Ther Apher. 1999 Feb;3(1):50-62 [10079806.001]
  • [Cites] Oncology (Williston Park). 2007 Feb;21(2 Suppl 1):29-32 [17474357.001]
  • [Cites] Arch Dermatol. 2002 Mar;138(3):325-32 [11902983.001]
  • [Cites] Hematol Oncol Clin North Am. 2003 Dec;17(6):1485-507 [14710899.001]
  • [Cites] Curr Opin Investig Drugs. 2007 Jun;8(6):493-8 [17621880.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4655-62 [17311990.001]
  • [Cites] J Am Acad Dermatol. 1996 Jul;35(1):69-73 [8682967.001]
  • (PMID = 20166766.001).
  • [ISSN] 1179-1950
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 90
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72. Lau YS, Sabokbar A, Giele H, Cerundolo V, Hofstetter W, Athanasou NA: Malignant melanoma and bone resorption. Br J Cancer; 2006 May 22;94(10):1496-503
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  • [Title] Malignant melanoma and bone resorption.
  • The cellular and humoral mechanisms accounting for osteolysis in skeletal metastases of malignant melanoma are uncertain.
  • We isolated tumour-associated macrophages (TAMs) from metastatic (lymph node/skin) melanomas and cultured them in the presence and absence of osteoclastogenic cytokines and growth factors.
  • The effect of tumour-derived fibroblasts and melanoma cells on osteoclast formation and resorption was also analysed.
  • Tumour-associated macrophage-osteoclast differentiation also occurred via a RANKL-independent pathway when TAMs were cultured with tumour necrosis factor-alpha and interleukin (IL)-1alpha.
  • Our findings indicate that TAMs in metastatic melanomas can differentiate into osteoclasts and that melanoma fibroblasts and melanoma tumour cells can induce osteoclast formation by RANKL-dependent and RANKL-independent mechanisms, respectively.
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Carrier Proteins / metabolism. Cell Differentiation. Cells, Cultured. Culture Media, Conditioned / pharmacology. Female. Fibroblasts. Glycoproteins / pharmacology. Humans. Interleukin-1 / pharmacology. Lymphatic Metastasis. Male. Membrane Glycoproteins / metabolism. Middle Aged. Osteolysis / pathology. Osteoprotegerin. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Receptors, Cytoplasmic and Nuclear. Receptors, Tumor Necrosis Factor. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology

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  • [Cites] J Immunol. 2001 Jun 1;166(11):6483-90 [11359798.001]
  • [Cites] Arch Ophthalmol. 2001 May;119(5):670-6 [11346394.001]
  • [Cites] Eur J Cancer. 2002 Mar;38 Suppl 4:S120-4 [11858977.001]
  • [Cites] J Pathol. 2002 Oct;198(2):220-7 [12237882.001]
  • [Cites] Bone. 2003 Jan;32(1):1-7 [12584029.001]
  • [Cites] Bone. 2003 Jul;33(1):28-37 [12919697.001]
  • [Cites] Histol Histopathol. 2004 Jan;19(1):189-99 [14702187.001]
  • [Cites] Bone. 2004 Jan;34(1):57-64 [14751563.001]
  • [Cites] Melanoma Res. 2004 Apr;14(2):91-5 [15057037.001]
  • [Cites] Calcif Tissue Int. 1982 May;34(3):285-90 [6809291.001]
  • [Cites] Am J Pathol. 1985 Mar;118(3):419-24 [3976845.001]
  • [Cites] Cancer Res. 1987 Aug 1;47(15):4141-5 [3300960.001]
  • [Cites] J Cell Biol. 1989 Oct;109(4 Pt 1):1817-26 [2477382.001]
  • [Cites] J Clin Pathol. 1990 Dec;43(12):997-1003 [2266187.001]
  • [Cites] Lab Invest. 1992 Aug;67(2):166-74 [1501443.001]
  • [Cites] J Cell Sci. 1992 Mar;101 ( Pt 3):681-6 [1522150.001]
  • [Cites] Lab Invest. 1994 Oct;71(4):465-71 [7526033.001]
  • [Cites] Calcif Tissue Int. 1995;56 Suppl 1:S8-10 [7719993.001]
  • [Cites] J Orthop Res. 1996 Jan;14(1):2-6 [8618161.001]
  • [Cites] Clin Orthop Relat Res. 1996 Feb;(323):277-83 [8625592.001]
  • [Cites] Endocrinology. 1996 Sep;137(9):4058-60 [8756585.001]
  • [Cites] Cell. 1997 Apr 18;89(2):309-19 [9108485.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3597-602 [9520411.001]
  • [Cites] J Pathol. 1998 Jan;184(1):31-6 [9582524.001]
  • [Cites] J Orthop Res. 2005 May;23(3):511-9 [15885469.001]
  • [Cites] Hum Pathol. 2005 Sep;36(9):945-54 [16153456.001]
  • [Cites] J Interferon Cytokine Res. 2005 Nov;25(11):674-83 [16318581.001]
  • [Cites] J Pathol. 2006 May;209(1):114-20 [16482498.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Nov 2;264(3):751-8 [10544003.001]
  • [Cites] Int J Cancer. 2000 Jan 15;85(2):182-8 [10629075.001]
  • [Cites] J Exp Med. 2000 Jan 17;191(2):275-86 [10637272.001]
  • [Cites] J Bone Miner Res. 2000 Jan;15(1):2-12 [10646108.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jan 19;267(2):632-7 [10631114.001]
  • [Cites] Br J Cancer. 2000 Mar;82(5):1058-62 [10737389.001]
  • [Cites] Clin Orthop Relat Res. 2000 Apr;(373):104-14 [10810467.001]
  • [Cites] Cytokine. 2000 Jun;12(6):547-54 [10843728.001]
  • [Cites] J Bone Miner Res. 2000 Aug;15(8):1459-66 [10934644.001]
  • [Cites] Eur J Cancer. 2001 Mar;37(5):629-40 [11290439.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):893-903 [11549582.001]
  • (PMID = 16641914.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Culture Media, Conditioned; 0 / Glycoproteins; 0 / Interleukin-1; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2361270
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73. Kang KB, Zhu C, Yong SK, Gao Q, Wong MC: Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy. Mol Cancer; 2009;8:66
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  • [Title] Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy.
  • BACKGROUND: Selective cyclooxygenase (COX)-2 inhibitors elicit anti-proliferative responses in various tumours, however the underlying anti-tumour mechanisms are unclear.
  • Mutational inactivation of the tumour suppressor p53 gene is frequent in malignant gliomas.
  • The role of p53 mutation in the anti-tumour responses of the selective COX-2 inhibitor celecoxib in human glioblastoma cells is unknown.
  • Inhibition of p53 was achieved in U87MG cells transfected with E6 oncoprotein (U87MG-E6) and treated with pifithrin-alpha, a reversible inhibitor of p53 (U87MG-PFT).
  • We investigated whether the anti-glioblastoma responses of celecoxib were p53-dependent, and whether celecoxib induced DNA damage leading to p53-dependent G1 cell cycle arrest, followed by autophagy or apoptosis.
  • RESULTS: Our findings demonstrated that celecoxib concentration-dependently reduced glioblastoma cell viability, following 24 and 72 hours of treatment.
  • Celecoxib induced G1-phase cell cycle arrest, accompanied with p21 activation in U87MG cells.
  • Cell cycle progression of U87MG-E6 and U87MG-PFT cells was not affected by celecoxib.
  • In parallel, celecoxib induced G1 cell cycle arrest in LN229 cells, but not in U373MG cells.
  • Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.
  • [MeSH-major] Autophagy / drug effects. DNA Damage. G1 Phase / drug effects. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Analysis of Variance. Benzothiazoles / pharmacology. Blotting, Western. Celecoxib. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Comet Assay. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase Inhibitors / pharmacology. Dose-Response Relationship, Drug. G0 Phase / drug effects. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction. Toluene / analogs & derivatives. Toluene / pharmacology