[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 1437
1. Akagi T, Shih LY, Kato M, Kawamata N, Yamamoto G, Sanada M, Okamoto R, Miller CW, Liang DC, Ogawa S, Koeffler HP: Hidden abnormalities and novel classification of t(15;17) acute promyelocytic leukemia (APL) based on genomic alterations. Blood; 2009 Feb 19;113(8):1741-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Acute promyelocytic leukemia (APL) is a hematopoietic malignant disease characterized by the chromosomal translocation t(15;17), resulting in the formation of the PML-RARA gene.

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Haematologica. 2009 Feb;94(2):213-23 [19144660.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3188-97 [12515727.001]
  • [Cites] Cancer. 2003 Sep 15;98(6):1206-16 [12973844.001]
  • [Cites] Blood. 1984 Feb;63(2):254-9 [6362749.001]
  • [Cites] Nature. 1990 Oct 11;347(6293):558-61 [2170850.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] Cell. 1991 Aug 23;66(4):675-84 [1652369.001]
  • [Cites] Haematologica. 2000 Jan;85(1):31-4 [10629588.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Br J Haematol. 2002 Mar;116(4):744-57 [11886377.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2985-91 [11929790.001]
  • [Cites] N Engl J Med. 1993 Jul 15;329(3):177-89 [8515790.001]
  • [Cites] Blood. 1997 Jan 15;89(2):376-87 [9002938.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2551-6 [9122233.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):815-8 [9486655.001]
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Blood. 2005 May 1;105(9):3699-706 [15650056.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4792-9 [15718420.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4129-37 [15806161.001]
  • [Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1153-60 [15889156.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2113-9 [15951308.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Oncogene. 2006 Mar 13;25(11):1594-601 [16550159.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1708-15 [16675706.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1202-10 [17053054.001]
  • [Cites] Br J Haematol. 2007 Apr;137(1):64-75 [17359372.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Br J Haematol. 2007 Sep;138(5):603-15 [17686054.001]
  • [Cites] Blood. 2008 Jan 15;111(2):776-84 [17890455.001]
  • [Cites] Cancer. 2008 Mar 15;112(6):1296-305 [18246537.001]
  • [Cites] Blood. 2008 Aug 1;112(3):814-21 [18490517.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Sep;47(9):729-39 [18506749.001]
  • [Cites] Leuk Lymphoma. 2008 Jun;49(6):1178-83 [18452069.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Nov;35(3):261-70 [12353268.001]
  • (PMID = 19109227.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / 5R01CA026038-30
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2647673
  •  go-up   go-down


2. Normandin K, Péant B, Le Page C, de Ladurantaye M, Ouellet V, Tonin PN, Provencher DM, Mes-Masson AM: Protease inhibitor SERPINA1 expression in epithelial ovarian cancer. Clin Exp Metastasis; 2010;27(1):55-69
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This is in stark contrast to the 95% 5 years survival rate in ovarian cancer patients diagnosed with low malignant potential (LMP) disease.
  • The progression from localized tumor to invasive metastasis involves matrix proteolysis.
  • To study the effects of its over expression on different tumorigenic parameters, SERPINA1 was cloned in the pcDNA3.1+ plasmid which was subsequently used to derive stable clones from two invasive ovarian cancer cell lines, TOV-112D and TOV-1946.
  • We found no effect of SERPINA1 over expression on tumor growth in SCID mice although cell migration and invasion were affected in in vitro assays.
  • SERPINA1 remains an interesting candidate since protein homeostasis, regulated by proteases and their inhibitors, should be studied holistically in order to assess their full impact in tumor progression.
  • [MeSH-major] Ovarian Neoplasms / metabolism. alpha 1-Antitrypsin / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Humans. Mice. Mice, SCID. Tissue Array Analysis

  • Genetic Alliance. consumer health - Ovarian cancer.
  • Genetic Alliance. consumer health - Ovarian epithelial cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2005 Oct 10;23 (29):7257-64 [16087957.001]
  • [Cites] Hum Pathol. 2004 Aug;35(8):934-48 [15297961.001]
  • [Cites] Science. 1994 Jan 28;263(5146):526-9 [8290962.001]
  • [Cites] Biochem Soc Trans. 2002 Apr;30(2):93-8 [12023832.001]
  • [Cites] Mol Cell Endocrinol. 2002 Feb 22;187(1-2):29-38 [11988309.001]
  • [Cites] J Clin Invest. 1986 Dec;78(6):1427-31 [3537008.001]
  • [Cites] Clin Cancer Res. 1996 Apr;2(4):613-8 [9816210.001]
  • [Cites] J Biol Chem. 2001 Sep 7;276(36):33293-6 [11435447.001]
  • [Cites] Genome Biol. 2006;7(5):216 [16737556.001]
  • [Cites] Biol Chem Hoppe Seyler. 1996 May;377(5):301-11 [8828821.001]
  • [Cites] J Pathol. 2008 Jul;215(3):222-30 [18438953.001]
  • [Cites] Br J Cancer. 1992 Feb;65(2):300-2 [1739634.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Nov;60(2):159-79 [17018256.001]
  • [Cites] Cancer Res. 2007 Jun 1;67(11):5117-25 [17545589.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] Clin Cancer Res. 2002 Sep;8(9):2924-32 [12231537.001]
  • [Cites] J Cell Biol. 2003 Jan 20;160(2):267-77 [12527751.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8657-65 [15574774.001]
  • [Cites] Int J Cancer. 1990 Feb 15;45(2):244-50 [2303291.001]
  • [Cites] Histopathology. 2007 May;50(6):773-9 [17493241.001]
  • [Cites] Bioessays. 2005 Nov;27(11):1181-91 [16237672.001]
  • [Cites] Cancer. 1993 Feb 15;71(4):1368-83 [8435813.001]
  • [Cites] Curr Opin Obstet Gynecol. 2007 Feb;19(1):3-9 [17218844.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Methods Mol Biol. 2009;472:413-37 [19107446.001]
  • [Cites] Nat Rev Cancer. 2003 May;3(5):362-74 [12724734.001]
  • [Cites] Clin Med Res. 2007 Mar;5(1):35-44 [17456833.001]
  • [Cites] Annu Rev Biochem. 1983;52:655-709 [6193754.001]
  • [Cites] Surg Oncol. 2006 Dec;15(4):217-22 [17320378.001]
  • [Cites] J Clin Invest. 1988 Jul;82(1):26-36 [3260605.001]
  • [Cites] Clin Exp Metastasis. 1992 May;10(3):145-55 [1582084.001]
  • [Cites] BMC Cancer. 2008 May 28;8:152 [18507860.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Jul;25(3):290-300 [10379876.001]
  • [Cites] Int J Cancer. 2009 Oct 1;125(7):1542-50 [19569240.001]
  • [Cites] Nat Cell Biol. 2007 Aug;9(8):893-904 [17618273.001]
  • [Cites] Am J Surg Pathol. 2005 Feb;29(2):218-24 [15644779.001]
  • [Cites] Nat Rev Cancer. 2008 Jul;8(7):535-45 [18548086.001]
  • [Cites] Genomics. 2002 Jan;79(1):104-13 [11827463.001]
  • [Cites] Oncogene. 2005 Jul 7;24(29):4672-87 [15940270.001]
  • [Cites] PLoS Med. 2008 Dec 2;5(12):e232 [19053170.001]
  • [Cites] Prostate. 2009 May 15;69(7):706-18 [19170126.001]
  • [Cites] Am J Med. 2008 Jan;121(1):3-9 [18187064.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Mar;82(3):745-52 [9062476.001]
  • [Cites] Expert Opin Biol Ther. 2006 Mar;6(3):257-79 [16503735.001]
  • [Cites] Neoplasia. 2007 Oct;9(10):820-9 [17971902.001]
  • [Cites] BMC Cancer. 2008 Nov 26;8:346 [19032793.001]
  • [Cites] Chem Rev. 2002 Dec;102(12):4751-804 [12475206.001]
  • [Cites] Cell Cycle. 2006 Apr;5(8):812-7 [16627996.001]
  • [Cites] Int J Biochem Cell Biol. 2003 Nov;35(11):1536-47 [12824063.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 2000 Jun;36(6):357-61 [10949993.001]
  • [Cites] J Clin Invest. 1981 Jan;67(1):281-91 [6161137.001]
  • [Cites] Curr Oncol Rep. 2008 Nov;10(6):519-23 [18928667.001]
  • [Cites] J Cell Physiol. 2006 Dec;209(3):617-24 [17001697.001]
  • [Cites] Mod Pathol. 2005 Feb;18 Suppl 2:S19-32 [15761464.001]
  • [Cites] Clin Exp Metastasis. 1998 Jan;16(1):62-73 [9502078.001]
  • [Cites] Mol Cancer. 2004 Oct 07;3:27 [15471544.001]
  • [Cites] Cancer. 2003 May 15;97(10 Suppl):2631-42 [12733128.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10602-12 [16288054.001]
  • [Cites] J Natl Cancer Inst. 2003 Mar 19;95(6):484-6 [12644542.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Clin Chim Acta. 2005 Feb;352(1-2):1-13 [15653097.001]
  • (PMID = 20049513.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  •  go-up   go-down


3. Eyüpoglu IY, Hahnen E, Heckel A, Siebzehnrübl FA, Buslei R, Fahlbusch R, Blümcke I: Malignant glioma-induced neuronal cell death in an organotypic glioma invasion model. Technical note. J Neurosurg; 2005 Apr;102(4):738-44
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant glioma-induced neuronal cell death in an organotypic glioma invasion model. Technical note.
  • Rapid growth and diffuse brain infiltration are hallmarks of malignant gliomas.
  • The authors present a novel glioma invasion model that allows researchers to monitor consecutively tumor cell proliferation and migration in an organotypic brain environment.
  • Enhanced green fluorescent protein-labeled F98 rat glioma cells were implanted into slice cultures obtained from a rat hippocampus, and tumor growth was microscopically documented up to 20 days in vitro.
  • Following implantation of F98 glioma cells into the entorhinal cortex, cell death was observed within the infiltrated brain parenchyma as well as in the neuroanatomically connected dentate gyrus.
  • Application of the N-methyl-D-aspartate receptor antagonist MK801 to the culture medium significantly reduced neuronal degeneration in the dentate gyrus, whereas the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor antagonist GYKI 52466 inhibited peritumoral cytotoxicity.
  • This new model allows researchers to address in a systematic manner the molecular pathways of brain invasion as well as specific tumor-host interactions such as necrosis.
  • [MeSH-major] Brain Neoplasms / physiopathology. Cell Death. Glioma / physiopathology
  • [MeSH-minor] Animals. Benzodiazepines / pharmacology. Cell Movement. Cell Proliferation. Dentate Gyrus / pathology. Disease Models, Animal. Dizocilpine Maleate / pharmacology. Hippocampus / pathology. Humans. Mice. Neuroprotective Agents / pharmacology. Rats. Transplantation, Heterologous. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • Hazardous Substances Data Bank. DIZOCILPINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15871520.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuroprotective Agents; 102771-26-6 / GYKI 52466; 12794-10-4 / Benzodiazepines; 6LR8C1B66Q / Dizocilpine Maleate
  •  go-up   go-down


Advertisement
4. Azevedo Rde S, Pires FR, Della Coletta R, de Almeida OP, Kowalski LP, Lopes MA: Oral myofibromas: report of two cases and review of clinical and histopathologic differential diagnosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2008 Jun;105(6):e35-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral myofibromas: report of two cases and review of clinical and histopathologic differential diagnosis.
  • Differential diagnosis included benign and malignant mesenchymal neoplasms, salivary gland tumors, and reactive processes.
  • Microscopic analysis of both lesions revealed a spindle cell tumor with immunoreactivity for vimentin, muscle-specific actin, and specific smooth muscle isoform alpha-actin, rendering the diagnoses of myofibroma.
  • Myofibroma presents a wide range of differential diagnosis, including benign and malignant neoplasms.
  • Therefore, accurate diagnosis may avoid an unnecessary aggressive therapy.
  • [MeSH-minor] Actins / analysis. Child. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Vimentin / analysis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18417385.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Vimentin
  •  go-up   go-down


5. Bexell D, Gunnarsson S, Tormin A, Darabi A, Gisselsson D, Roybon L, Scheding S, Bengzon J: Bone marrow multipotent mesenchymal stroma cells act as pericyte-like migratory vehicles in experimental gliomas. Mol Ther; 2009 Jan;17(1):183-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We implanted enhanced green fluorescent protein-expressing rat MSCs directly into rat malignant gliomas to address their migratory capacity, phenotype, and effects on tumor neovascularization and animal survival.
  • A single intratumoral injection of MSCs infiltrated the majority of invasive glioma extensions (72 +/- 14%) and a substantial fraction of distant tumor microsatellites (32 +/- 6%).
  • MSC migration was highly specific for tumor tissue.
  • Grafted MSCs integrated into tumor vessel walls and expressed pericyte markers alpha-smooth muscle actin, neuron-glia 2, and platelet-derived growth factor receptor-beta but not endothelial cell markers.
  • MSC grafting did not influence tumor microvessel density or survival of tumor-bearing animals.
  • Intratumorally grafted pericyte-like MSCs might represent a particularly well-suited vector system for delivering molecules to affect tumor angiogenesis and for targeting cancer stem cells within the perivascular niche.
  • [MeSH-minor] Animals. Antigens / metabolism. Cell Line, Tumor. Cell Movement / drug effects. Dermoscopy. Female. Flow Cytometry. Immunohistochemistry. In Situ Hybridization, Fluorescence. Indoles / pharmacology. Male. Proteoglycans / metabolism. Pyrroles / pharmacology. Rats. Receptors, Platelet-Derived Growth Factor / metabolism. Stromal Cells / cytology. Stromal Cells / physiology

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gene Ther. 2004 May;11(10):811-8 [15057261.001]
  • [Cites] J Clin Invest. 2006 Mar;116(3):642-51 [16470244.001]
  • [Cites] Gene Ther. 2004 Jul;11(14):1155-64 [15141157.001]
  • [Cites] J Histochem Cytochem. 1989 Mar;37(3):315-21 [2918221.001]
  • [Cites] Am J Pathol. 1990 Jun;136(6):1393-405 [1694058.001]
  • [Cites] Nat Med. 2000 Apr;6(4):447-50 [10742153.001]
  • [Cites] Neoplasia. 2000 Jul-Aug;2(4):306-14 [11005565.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12846-51 [11070094.001]
  • [Cites] Nat Med. 2001 Nov;7(11):1194-201 [11689883.001]
  • [Cites] Microvasc Res. 2002 Jan;63(1):129-34 [11749079.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):341-5 [11809675.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3603-8 [12097260.001]
  • [Cites] Circ Res. 2003 Apr 4;92(6):692-9 [12609969.001]
  • [Cites] J Clin Invest. 2003 May;111(9):1287-95 [12727920.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1835-40 [12897053.001]
  • [Cites] J Clin Invest. 2003 Oct;112(8):1142-51 [14561699.001]
  • [Cites] J Exp Med. 2006 May 15;203(5):1235-47 [16636132.001]
  • [Cites] Exp Neurol. 2006 Jun;199(2):301-10 [16574102.001]
  • [Cites] Exp Dermatol. 2006 Nov;15(11):865-74 [17002683.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] J Neurooncol. 2007 Jul;83(3):241-7 [17570034.001]
  • [Cites] Neuroscience. 2007 Jul 13;147(3):824-32 [17583435.001]
  • [Cites] Nature. 2007 Oct 4;449(7162):557-63 [17914389.001]
  • [Cites] Stem Cells Dev. 2008 Feb;17(1):11-8 [18240955.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6620-5 [18443294.001]
  • [Cites] Nature. 2008 May 15;453(7193):410-4 [18418378.001]
  • [Cites] Cancer Immunol Immunother. 1993 Jul;37(1):67-74 [8513454.001]
  • [Cites] Cell. 1996 Aug 9;86(3):353-64 [8756718.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] J Clin Invest. 1999 Jan;103(2):159-65 [9916127.001]
  • [Cites] Cell Mol Life Sci. 1999 Apr;55(4):663-7 [10357234.001]
  • [Cites] Curr Opin Investig Drugs. 2004 Dec;5(12):1329-39 [15648955.001]
  • [Cites] Nat Med. 2005 Mar;11(3):261-2 [15723071.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3307-18 [15833864.001]
  • [Cites] Nat Rev Cancer. 2005 Jun;5(6):436-46 [15928674.001]
  • [Cites] Cancer Gene Ther. 2005 Sep;12(9):757-68 [15832173.001]
  • [Cites] Nat Cell Biol. 2005 Sep;7(9):870-9 [16113679.001]
  • [Cites] Mol Ther. 2005 Oct;12(4):585-98 [16095972.001]
  • [Cites] Neuro Oncol. 2005 Oct;7(4):452-64 [16212810.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):18111-6 [16326806.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2630-8 [16510582.001]
  • [Cites] Brain Res Brain Res Rev. 2004 Jul;45(3):143-63 [15210301.001]
  • (PMID = 18985030.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Indoles; 0 / Proteoglycans; 0 / Pyrroles; 0 / chondroitin sulfate proteoglycan 4; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; V99T50803M / sunitinib
  • [Other-IDs] NLM/ PMC2834971
  •  go-up   go-down


6. Kim KK, Lee JJ, Yang Y, You KH, Lee JH: Macrophage inhibitory cytokine-1 activates AKT and ERK-1/2 via the transactivation of ErbB2 in human breast and gastric cancer cells. Carcinogenesis; 2008 Apr;29(4):704-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Collectively, these results show that MIC-1 may participate in the malignant progression of certain human cancer cells that overexpress ErbB2 through the transactivation of ErbB2 tyrosine kinase.
  • [MeSH-minor] Breast Neoplasms / genetics. Breast Neoplasms / pathology. Cell Line, Tumor. DNA Primers. Female. Gene Expression Regulation, Neoplastic. Growth Differentiation Factor 15. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Mitogen-Activated Protein Kinase 3. Neoplasm Invasiveness. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology. Transcriptional Activation


7. Wu Z, Xu Y: IL-15R alpha-IgG1-Fc enhances IL-2 and IL-15 anti-tumor action through NK and CD8+ T cells proliferation and activation. J Mol Cell Biol; 2010 Aug;2(4):217-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IL-15R alpha-IgG1-Fc enhances IL-2 and IL-15 anti-tumor action through NK and CD8+ T cells proliferation and activation.
  • Natural killer (NK) cells-based immunotherapy is one of the most promising treatments for incurable malignant tumors.
  • NK cells in combination with monoclonal antibodies to surface antigens of the tumor cell have been proved to be effective in a number of clinical trials.
  • We then measured the cytotoxicity of expanded NK and CD8(+) T cells against tumor cell lines and primary tumor cells.
  • Expanded NK and CD8(+) T cell populations had cytotoxic function against the PC3, LNCaP, K562 and chronic lymphocytic leukemia (CLL) patient primary B cell lymphoma.
  • We concluded that IL-2/IL-15Ralpha-IgG1-Fc significantly enhanced NK, CD8(+) T and NKT cells expansion, which possess strong anti-tumor activity.
  • [MeSH-major] Antineoplastic Agents / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Proliferation. Immunoglobulin Fc Fragments / immunology. Interleukin-15 / immunology. Interleukin-15 Receptor alpha Subunit / immunology. Interleukin-2 / immunology. Killer Cells, Natural / immunology
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Humans. Immunoglobulin G / genetics. Immunoglobulin G / immunology. Lymphocyte Activation. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20671116.001).
  • [ISSN] 1759-4685
  • [Journal-full-title] Journal of molecular cell biology
  • [ISO-abbreviation] J Mol Cell Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin G; 0 / Interleukin-15; 0 / Interleukin-15 Receptor alpha Subunit; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins
  •  go-up   go-down


8. Nikiforov MA, Riblett M, Tang WH, Gratchouck V, Zhuang D, Fernandez Y, Verhaegen M, Varambally S, Chinnaiyan AM, Jakubowiak AJ, Soengas MS: Tumor cell-selective regulation of NOXA by c-MYC in response to proteasome inhibition. Proc Natl Acad Sci U S A; 2007 Dec 4;104(49):19488-93
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor cell-selective regulation of NOXA by c-MYC in response to proteasome inhibition.
  • Therefore, it is puzzling that proteasome inhibitors such as bortezomib can display a preferential toxicity toward malignant cells.
  • In fact, proteasome inhibitors have the salient feature of promoting a dramatic induction of the proapoptotic protein NOXA in a tumor cell-restricted manner.
  • This requirement for c-MYC was found in a variety of tumor cell types, in marked contrast with dispensable roles of p53, HIF-1alpha, and E2F-1 (classical proteasomal targets that can regulate NOXA mRNA under stress).
  • Down-regulation of the endogenous levels of c-MYC abrogated the induction of NOXA in proteasome-defective tumor cells.
  • Conversely, forced expression of c-MYC enabled normal cells to accumulate NOXA and subsequently activate cell death programs in response to proteasome blockage. c-MYC is itself a proteasomal target whose levels or function are invariably up-regulated during tumor progression.
  • Our data provide an unexpected function of c-MYC in the control of the apoptotic machinery, and reveal a long sought-after oncogenic event conferring sensitivity to proteasome inhibition.

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6282-93 [16024630.001]
  • [Cites] Mol Cell. 2005 Feb 18;17(4):525-35 [15721256.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):635-45 [16064138.001]
  • [Cites] Nature. 2005 Aug 11;436(7052):807-11 [16094360.001]
  • [Cites] Blood. 2006 Jan 1;107(1):257-64 [16166592.001]
  • [Cites] J Biol Chem. 2006 Jan 13;281(2):1107-18 [16278210.001]
  • [Cites] Annu Rev Med. 2006;57:33-47 [16409135.001]
  • [Cites] Apoptosis. 2006 Apr;11(4):627-41 [16673057.001]
  • [Cites] EMBO J. 2006 Jun 21;25(12):2723-34 [16724113.001]
  • [Cites] Nat Cell Biol. 2006 Jul;8(7):764-70 [16767079.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Jul;3(7):374-87 [16826218.001]
  • [Cites] Mol Cell. 2006 Aug 4;23(3):289-96 [16885019.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Aug;3(8):448-57 [16894390.001]
  • [Cites] Semin Cancer Biol. 2006 Aug;16(4):253-64 [16904903.001]
  • [Cites] Semin Cancer Biol. 2006 Aug;16(4):318-30 [16934487.001]
  • [Cites] Semin Cancer Biol. 2006 Aug;16(4):242-52 [16935524.001]
  • [Cites] Semin Cancer Biol. 2006 Aug;16(4):288-302 [16938463.001]
  • [Cites] Semin Cancer Biol. 2006 Aug;16(4):275-87 [16945552.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9636-45 [17018621.001]
  • [Cites] J Biol Chem. 2006 Oct 20;281(42):31440-7 [16928686.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):425-35 [17097564.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 21;103(47):17834-9 [17093053.001]
  • [Cites] Nat Cell Biol. 2006 Dec;8(12):1348-58 [17115033.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4936-43 [17284530.001]
  • [Cites] Oncogene. 2008 Mar 20;27(13):1905-15 [17906696.001]
  • [Cites] Mol Cell Biol. 2007 Nov;27(21):7381-93 [17785433.001]
  • [Cites] Science. 2000 May 12;288(5468):1053-8 [10807576.001]
  • [Cites] Immunity. 2001 Jan;14(1):45-55 [11163229.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(15):5063-70 [11438662.001]
  • [Cites] Mol Cell Biol. 2002 Sep;22(17):6158-69 [12167710.001]
  • [Cites] Nat Cell Biol. 2002 Nov;4(11):859-64 [12389032.001]
  • [Cites] Curr Opin Cell Biol. 2003 Apr;15(2):172-83 [12648673.001]
  • [Cites] Genes Dev. 2003 Jun 15;17(12):1475-86 [12783855.001]
  • [Cites] Oncogene. 2003 Jul 24;22(30):4675-8 [12879012.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2233-8 [12952892.001]
  • [Cites] Science. 2003 Nov 7;302(5647):1036-8 [14500851.001]
  • [Cites] J Exp Med. 2004 Jan 5;199(1):113-24 [14699081.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):8627-34 [14684737.001]
  • [Cites] Cancer Cell. 2004 May;5(5):417-21 [15144949.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5923-36 [15199147.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4912-8 [15256463.001]
  • [Cites] J Virol. 1990 Oct;64(10):4632-9 [2398525.001]
  • [Cites] Mol Cell Biol. 1993 Sep;13(9):5216-24 [8395000.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4342-8 [9766662.001]
  • [Cites] EMBO J. 1998 Dec 15;17(24):7151-60 [9857172.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jan;6(1):79-87 [15688069.001]
  • [Cites] Mol Cell. 2005 Feb 4;17(3):393-403 [15694340.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6294-304 [16024631.001]
  • (PMID = 18042711.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107237; United States / NCI NIH HHS / CA / R01 CA120244; United States / NCI NIH HHS / CA / CA120244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / E2F1 Transcription Factor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / PMAIP1 protein, human; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyrazines; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; 69G8BD63PP / Bortezomib
  • [Other-IDs] NLM/ PMC2148316
  •  go-up   go-down


9. Blum R, Jacob-Hirsch J, Amariglio N, Rechavi G, Kloog Y: Ras inhibition in glioblastoma down-regulates hypoxia-inducible factor-1alpha, causing glycolysis shutdown and cell death. Cancer Res; 2005 Feb 1;65(3):999-1006
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ras inhibition in glioblastoma down-regulates hypoxia-inducible factor-1alpha, causing glycolysis shutdown and cell death.
  • Active Ras and phosphatidylinositol-3-kinase-dependent pathways contribute to the malignant phenotype of glioblastoma multiformes (GBM).
  • Consequently, U87 cell growth was arrested and the cells died.
  • [MeSH-minor] Cell Death / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Down-Regulation / drug effects. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Glycolysis / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Phosphatidylinositol 3-Kinases / metabolism


10. Engbring JA, Hossain R, VanOsdol SJ, Kaplan-Singer B, Wu M, Hibino S, Koblinski JE: The laminin alpha-1 chain derived peptide, AG73, increases fibronectin levels in breast and melanoma cancer cells. Clin Exp Metastasis; 2008;25(3):241-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The laminin alpha-1 chain derived peptide, AG73, increases fibronectin levels in breast and melanoma cancer cells.
  • Laminin-111 promotes the malignant phenotype, and a 12-mer synthetic peptide (AG73, RKRLQVQLSIRT) from the carboxyl terminus of the alpha1 chain increases B16F10 melanoma metastasis to the lung and liver.
  • The increased fibronectin is cell-associated with no increase in soluble fibronectin.
  • The AG73 peptide increased the number and size of bone metastases with both B16F10 melanoma and MDA-231 breast carcinoma cells in an intracardiac injection model.
  • [MeSH-minor] Animals. Cell Adhesion. Female. Fluorescent Antibody Technique. Immunoblotting. Mice. Mice, Inbred C57BL. Mice, Nude. Protein Array Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Clin Nutr. 1989 Feb;49(2):314-9 [2916450.001]
  • [Cites] Int J Cancer. 1998 Aug 12;77(4):632-9 [9679769.001]
  • [Cites] Arch Biochem Biophys. 1994 Feb 15;309(1):117-22 [8117101.001]
  • [Cites] Nature. 2000 Aug 3;406(6795):532-5 [10952316.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):22077-85 [11304538.001]
  • [Cites] Biochemistry. 2003 Nov 4;42(43):12625-33 [14580209.001]
  • [Cites] Breast Cancer Res Treat. 1994;32(1):73-84 [7819589.001]
  • [Cites] Surg Oncol Clin N Am. 2001 Apr;10(2):329-38, ix [11382590.001]
  • [Cites] Am J Physiol. 1995 Dec;269(6 Pt 1):L766-75 [8572238.001]
  • [Cites] Science. 1987 Nov 20;238(4830):1132-4 [2961059.001]
  • [Cites] J Cell Biol. 2000 Mar 6;148(5):1075-90 [10704455.001]
  • [Cites] FASEB J. 2001 Jun;15(8):1389-97 [11387236.001]
  • [Cites] Cell. 2003 Feb 21;112(4):453-65 [12600310.001]
  • [Cites] Dev Dyn. 2000 Jun;218(2):213-34 [10842354.001]
  • [Cites] Int J Cancer. 1997 May 2;71(3):436-41 [9139881.001]
  • [Cites] Int J Oncol. 2001 May;18(5):913-21 [11295035.001]
  • [Cites] Int J Cancer. 1995 Sep 27;63(1):92-9 [7558459.001]
  • [Cites] J Cell Sci. 2003 Aug 15;116(Pt 16):3269-76 [12857786.001]
  • [Cites] Cell. 1987 Mar 27;48(6):989-96 [2951015.001]
  • [Cites] Am J Pathol. 1999 Sep;155(3):739-52 [10487832.001]
  • [Cites] Br J Cancer. 2002 Apr 8;86(7):1169-73 [11953867.001]
  • [Cites] Cancer Lett. 2005 Jun 1;223(1):1-10 [15890231.001]
  • [Cites] Nat New Biol. 1973 Apr 4;242(118):148-9 [4512654.001]
  • [Cites] Cancer Res. 1988 Dec 1;48(23):6876-81 [3180096.001]
  • [Cites] Cancer Res. 1993 Jan 15;53(2):423-8 [8417834.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Sep;4(9):700-11 [14506473.001]
  • [Cites] Exp Cell Res. 2003 May 1;285(2):189-95 [12706114.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Mar;87(6):2279-83 [2156266.001]
  • [Cites] Matrix Biol. 2005 Aug;24(5):326-32 [15979864.001]
  • [Cites] J Biol Chem. 2006 Oct 27;281(43):32929-40 [16945929.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3549-54 [12068003.001]
  • [Cites] Arch Biochem Biophys. 2007 Mar 15;459(2):249-55 [17286955.001]
  • [Cites] Cancer Res. 1993 May 1;53(9):1998-2004 [8481902.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19):5395-9 [1394144.001]
  • [Cites] Science. 1997 May 23;276(5316):1268-72 [9157888.001]
  • [Cites] Cancer Res. 1991 Feb 1;51(3):903-6 [1703042.001]
  • (PMID = 18185912.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AG 73; 0 / Fibronectins; 0 / Laminin; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 151186-83-3 / laminin A
  •  go-up   go-down


11. Perez-Torres M, Valle BL, Maihle NJ, Negron-Vega L, Nieves-Alicea R, Cora EM: Shedding of epidermal growth factor receptor is a regulated process that occurs with overexpression in malignant cells. Exp Cell Res; 2008 Oct 1;314(16):2907-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Shedding of epidermal growth factor receptor is a regulated process that occurs with overexpression in malignant cells.
  • Soluble isoforms of the epidermal growth factor receptor (sEGFR) previously have been identified in the conditioned culture media (CCM) of the vulvar adenocarcinoma cell line, A431 and within exosomes of the keratinocyte cell line HaCaT.
  • Here, we report that the extracellular domain (ECD) of EGFR is shed from the cell surface of human carcinoma cell lines that express 7x10(5) receptors/cell or more.
  • The release of PI-sEGFR from MDA-MB-468 cells is enhanced by phorbol 12-myristate 13-acetate, heat-inactivated fetal bovine serum, pervanadate, and EGFR ligands (i.e., EGF and TGF-alpha).
  • Our results further suggest that when proteolytic shedding of EGFR does occur, it is correlated with a highly malignant phenotype.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cattle. Cell Line, Tumor. Enzyme Activation. Epidermal Growth Factor / metabolism. Humans. Molecular Sequence Data. Peptides / chemistry. Peptides / genetics. Peptides / metabolism. Phenylmercuric Acetate / analogs & derivatives. Phenylmercuric Acetate / metabolism. Protease Inhibitors / metabolism. Protein Kinase C / metabolism. Protein Structure, Tertiary. Sequence Alignment. Spectrometry, Mass, Electrospray Ionization. Tetradecanoylphorbol Acetate / metabolism. Transforming Growth Factor alpha / metabolism. Vanadates / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • Hazardous Substances Data Bank. PHENYLMERCURIC ACETATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18687326.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 096297; United States / NCI NIH HHS / CA / CA73859; United States / NCI NIH HHS / CA / CA85133; United States / NCRR NIH HHS / RR / P20RR016439; United States / NIGMS NIH HHS / GM / S06GM08225
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptides; 0 / Protease Inhibitors; 0 / Protein Isoforms; 0 / Transforming Growth Factor alpha; 0 / pervanadate; 3WHH0066W5 / Vanadates; 62229-50-9 / Epidermal Growth Factor; 6283-24-5 / 4-aminophenylmercuriacetate; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.13 / Protein Kinase C; NI40JAQ945 / Tetradecanoylphorbol Acetate; OSX88361UX / Phenylmercuric Acetate
  •  go-up   go-down


12. Riganti C, Doublier S, Aldieri E, Orecchia S, Betta PG, Gazzano E, Ghigo D, Bosia A: Asbestos induces doxorubicin resistance in MM98 mesothelioma cells via HIF-1alpha. Eur Respir J; 2008 Aug;32(2):443-51
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Human malignant mesothelioma (HMM), which is strongly related to asbestos exposure, exhibits high resistance to many anticancer drugs.
  • These effects were prevented by the co-incubation with the cell-permeating iron salt ferric nitrilotriacetate, which caused an increase of intracellular iron bioavailability, measured as increased activity of the iron regulatory protein-1.
  • Crocidolite, dexrazoxane and hypoxia induce doxorubicin resistance in human malignant mesothelioma cells by increasing hypoxia-inducible factor-1alpha activity, through an iron-sensitive mechanism.
  • [MeSH-major] Asbestos / toxicity. Drug Resistance, Neoplasm. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Lung Neoplasms / drug therapy. Mesothelioma / drug therapy
  • [MeSH-minor] Anoxia. Antineoplastic Agents / pharmacology. Asbestos, Crocidolite / pharmacology. Cell Line, Tumor. Doxorubicin / pharmacology. Humans. Iron / metabolism. Lung / pathology. P-Glycoprotein / metabolism. Razoxane / pharmacology

  • MedlinePlus Health Information. consumer health - Asbestos.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Mesothelioma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ASBESTOS .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. IRON, ELEMENTAL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18385176.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / P-Glycoprotein; 12001-28-4 / Asbestos, Crocidolite; 1332-21-4 / Asbestos; 5AR83PR647 / Razoxane; 80168379AG / Doxorubicin; E1UOL152H7 / Iron
  •  go-up   go-down


13. Landmeier S, Altvater B, Pscherer S, Juergens H, Varnholt L, Hansmeier A, Bollard CM, Moosmann A, Bisping G, Rossig C: Activated human gammadelta T cells as stimulators of specific CD8+ T-cell responses to subdominant Epstein Barr virus epitopes: potential for immunotherapy of cancer. J Immunother; 2009 Apr;32(3):310-21
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activated human gammadelta T cells as stimulators of specific CD8+ T-cell responses to subdominant Epstein Barr virus epitopes: potential for immunotherapy of cancer.
  • Coincubation of activated gammadelta T cells pulsed with human leukocyte antigen-restricted epitopes of either the highly stimulatory EBV lytic cycle antigen Bam H1 Z fragment leftward open reading frame or the tumor-associated latent EBV antigen latent membrane protein 2a (LMP2a) with autologous peripheral blood lymphocytes induced selective expansion of peptide-specific, fully functional CD3CD8 cytolytic effector memory T cells.
  • In summary, bisphosphonate-activated human gammadelta T cells stimulate expansion of cytotoxic effector T cells specific for both subdominant and dominant viral epitopes and thus show promise as a novel source of efficient APCs for immunotherapy of viral and malignant disease.
  • [MeSH-major] Antigens, Viral / immunology. CD8-Positive T-Lymphocytes / immunology. Epitopes / immunology. Epstein-Barr Virus Infections / therapy. Herpesvirus 4, Human / immunology. Immunotherapy. Receptors, Antigen, T-Cell, gamma-delta / immunology
  • [MeSH-minor] Antigen-Presenting Cells / immunology. Antigen-Presenting Cells / virology. Cell Line, Tumor. Diphosphonates / pharmacology. Humans. Imidazoles / pharmacology. Transduction, Genetic. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / immunology

  • Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Med. 1996 May;2(5):551-5 [8616714.001]
  • [Cites] J Rheumatol. 1996 Jan;23(1):124-9 [8838520.001]
  • [Cites] Hum Gene Ther. 1996 Aug 1;7(12):1405-13 [8844199.001]
  • [Cites] Crit Rev Immunol. 1997;17(1):89-118 [9034725.001]
  • [Cites] Annu Rev Immunol. 1997;15:405-31 [9143694.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1664-72 [9269787.001]
  • [Cites] J Clin Invest. 1997 Dec 1;100(11):2757-65 [9389740.001]
  • [Cites] Clin Immunol Immunopathol. 1998 Feb;86(2):121-33 [9473374.001]
  • [Cites] N Engl J Med. 1999 Mar 4;340(9):737-8 [10068336.001]
  • [Cites] J Virol. 2005 Jan;79(2):1296-307 [15613356.001]
  • [Cites] J Exp Med. 2005 Feb 7;201(3):349-60 [15684323.001]
  • [Cites] Nat Rev Immunol. 2005 Apr;5(4):296-306 [15803149.001]
  • [Cites] Science. 2005 Jul 8;309(5732):264-8 [15933162.001]
  • [Cites] J Immunol. 2005 Sep 15;175(6):4137-47 [16148164.001]
  • [Cites] Nat Med. 2006 Feb;12(2):214-9 [16444265.001]
  • [Cites] Nat Med. 2006 Feb;12(2):207-13 [16444266.001]
  • [Cites] Leukemia. 2006 Apr;20(4):645-9 [16498391.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4109-17 [16931630.001]
  • [Cites] J Immunother. 2007 Jan;30(1):96-107 [17198088.001]
  • [Cites] J Immunol. 2007 May 1;178(9):5465-72 [17442927.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1441-51 [17535975.001]
  • [Cites] J Immunother. 2007 Jul-Aug;30(5):506-16 [17589291.001]
  • [Cites] Cancer Res. 2007 Aug 1;67(15):7450-7 [17671215.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8335-43 [17804749.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2838-45 [17609424.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2793-802 [17638856.001]
  • [Cites] Nat Med. 2000 Sep;6(9):1018-23 [10973322.001]
  • [Cites] Mol Pathol. 2000 Oct;53(5):248-54 [11091848.001]
  • [Cites] Nat Med. 2001 Apr;7(4):452-8 [11283672.001]
  • [Cites] Int J Cancer. 2001 Sep 1;93(5):706-13 [11477583.001]
  • [Cites] Int J Cancer. 2001 Oct 15;94(2):228-36 [11668503.001]
  • [Cites] Nat Biotechnol. 2002 Feb;20(2):143-8 [11821859.001]
  • [Cites] J Exp Med. 2002 Apr 1;195(7):893-905 [11927633.001]
  • [Cites] J Exp Med. 2003 Jan 20;197(2):163-8 [12538656.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2704-10 [12433692.001]
  • [Cites] Nat Med. 2003 May;9(5):619-24 [12704385.001]
  • [Cites] Blood. 2003 Jul 1;102(1):200-6 [12623838.001]
  • [Cites] J Immunol Methods. 2003 Jul;278(1-2):57-66 [12957396.001]
  • [Cites] Nat Rev Immunol. 2003 Oct;3(10):801-12 [14523386.001]
  • [Cites] J Exp Med. 2004 May 17;199(10):1409-20 [15148339.001]
  • [Cites] Br J Haematol. 2004 Aug;126(4):583-92 [15287953.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1801-7 [15178578.001]
  • [Cites] Science. 1990 Nov 30;250(4985):1269-73 [1978758.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4766-70 [1647016.001]
  • [Cites] Eur J Immunol. 1992 Mar;22(3):679-87 [1312472.001]
  • [Cites] J Virol. 1993 Dec;67(12):7428-35 [7693972.001]
  • [Cites] Science. 1994 May 13;264(5161):961-5 [7513904.001]
  • [Cites] Lancet. 1995 Jan 7;345(8941):9-13 [7799740.001]
  • [Cites] Nature. 1995 May 11;375(6527):155-8 [7753173.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6733-7 [7624312.001]
  • (PMID = 19242369.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA126752; United States / NCI NIH HHS / CA / P50 CA126752-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Diphosphonates; 0 / Epitopes; 0 / Imidazoles; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Tumor Necrosis Factor-alpha; 6XC1PAD3KF / zoledronic acid
  • [Other-IDs] NLM/ NIHMS322084; NLM/ PMC3176339
  •  go-up   go-down


14. Miyake M, Fujimoto K, Matsushita C, Chihara Y, Tanaka M, Hirayama A, Hirao Y, Uemura H: [Tumor thrombus arising from the superior vena cava and extending into the right atrium in a patient with advanced testicular germ cell tumor]. Hinyokika Kiyo; 2009 Jun;55(6):371-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Tumor thrombus arising from the superior vena cava and extending into the right atrium in a patient with advanced testicular germ cell tumor].
  • Ultrasonography detected right testicular tumor and computerized tomography scanning revealed a left supraclavicular lymph node mass and bulky retroperitoneal lymph node mass.
  • He initially underwent right high orchiectomy, combination chemotherapy and retroperitoneal lymph node dissection for advanced testicular non-seminomatous germ cell tumor.
  • After complete remission of the lung metastasis with chemotherapy, the serum alpha-fetoprotein began to increase because of superior vena caval thrombus extending into the right atrium.
  • Emergency surgical excision was performed successfully using extracorporeal circulation to prevent pulmonary embolism and the resected specimen pathologically revealed adenocarcinoma interpreted as teratoma malignant transformation.
  • We report herein an extremely uncommon case of advanced testicular germ cell tumor with development of superior vena caval thrombus extending into the right atrium.
  • [MeSH-major] Heart Atria / pathology. Neoplasms, Germ Cell and Embryonal / pathology. Neoplastic Cells, Circulating / pathology. Testicular Neoplasms / pathology. Thrombosis / pathology. Vena Cava, Superior / pathology

  • MedlinePlus Health Information. consumer health - Blood Clots.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19588874.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human
  • [Number-of-references] 22
  •  go-up   go-down


15. Paner GP, Luthringer DJ, Amin MB: Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies. Arch Pathol Lab Med; 2008 Sep;132(9):1388-96
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies.
  • CONTEXT: The unrelenting challenge encountered when differentiating limited-volume prostate carcinoma and sometimes subtle variants from its many morphologic mimics has increased the use of ancillary immunohistochemistry in routine prostate needle biopsies.
  • The availability of prostate cancer-associated and basal cell-associated markers has been an invaluable addition to diagnostic surgical pathology.
  • OBJECTIVE: To review commonly used immunohistochemical stains, including innovative combinations, for confirmation or differential diagnosis of prostate carcinoma, and to propose appropriately constructed panels using morphologic patterns in prostate needle biopsies.
  • CONCLUSIONS: Basal cell-associated markers p63, high-molecular-weight cytokeratin 34 beta E12, cytokeratin 5/6 or a cocktail containing p63 and high-molecular-weight cytokeratin 34 beta E12 or cytokeratin 5/6 and prostate carcinoma-specific marker alpha-methylacyl coenzyme A (coA) racemase alone or in combination are useful adjuncts in confirming prostatic carcinoma that either lacks diagnostic, qualitative or quantitative features or that has an unusual morphologic pattern (eg, atrophic, pseudohyperplastic) or is in the setting of prior treatment.
  • The combination of alpha-methylacyl coA racemase positivity with negative staining for basal cell-associated markers supports a malignant diagnosis in the appropriate morphologic context.
  • Dual chromogen basal cell- associated markers (p63 [nuclear] and high-molecular-weight cytokeratin 34 beta E12/cytokeratin 5/6 [cytoplasmic]) and alpha-methylacyl coA racemase in an antibody cocktail provide greater sensitivity for the basal cell layer, easing evaluation and minimizing loss of representation of the focal area interest because the staining is performed on one slide.
  • Prostate-specific antigen and prostatic acid phosphatase markers are helpful in excluding secondary malignancies involving the prostate, such as urothelial carcinoma, and occasionally in excluding nonprostatic benign mimickers, such as nephrogenic adenoma, mesonephric gland hyperplasia, and Cowper glands.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biopsy, Needle. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Male

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18788849.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 47
  •  go-up   go-down


16. Voss RH, Kuball J, Engel R, Guillaume P, Romero P, Huber C, Theobald M: Redirection of T cells by delivering a transgenic mouse-derived MDM2 tumor antigen-specific TCR and its humanized derivative is governed by the CD8 coreceptor and affects natural human TCR expression. Immunol Res; 2006;34(1):67-87
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Redirection of T cells by delivering a transgenic mouse-derived MDM2 tumor antigen-specific TCR and its humanized derivative is governed by the CD8 coreceptor and affects natural human TCR expression.
  • Retroviral transfer of T cell antigen receptor (TCR) genes selected by circumventing tolerance to broad tumor- and leukemia-associated antigens in human leukocyte antigen (HLA)-A*0201 (A2.1) transgenic (Tg) mice allows the therapeutic reprogramming of human T lymphocytes.
  • Using a human CD8 x A2.1/Kb mouse derived TCR specific for natural peptide-A2.1 (pA2.1) complexes comprising residues 81-88 of the human homolog of the murine double-minute 2 oncoprotein, MDM2(81-88), we found that the heterodimeric CD8 alpha beta coreceptor, but not normally expressed homodimeric CD8 alpha alpha, is required for tetramer binding and functional redirection of TCR- transduced human T cells.
  • They were, however, sufficiently effective in recognizing malignant targets including fresh leukemia cells.
  • We further observed a reciprocal relationship between the level of Tg WT mouse relative to natural human TCR expression, resulting in T cells with decreased normal human cell surface TCR.
  • These results provide important insights into the molecular basis of TCR gene therapy of malignant disease.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Epitopes, T-Lymphocyte / immunology. Proto-Oncogene Proteins c-mdm2 / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Flow Cytometry. HLA-A2 Antigen / immunology. Humans. Mice. Mice, Transgenic. Reverse Transcriptase Polymerase Chain Reaction. Self Tolerance / immunology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Immunol. 2003 Jan;4(1):55-62 [12469116.001]
  • [Cites] J Immunol. 1999 Jan 15;162(2):989-94 [9916724.001]
  • [Cites] Nature. 1992 Jul 2;358(6381):80-3 [1614537.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2840-8 [15238416.001]
  • [Cites] Nature. 2003 Feb 20;421(6925):852-6 [12594515.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14578-83 [11121060.001]
  • [Cites] Immunol Lett. 2004 May 15;93(2-3):123-30 [15158607.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3456-64 [11719388.001]
  • [Cites] J Exp Med. 1996 Mar 1;183(3):731-41 [8642277.001]
  • [Cites] Nat Med. 2004 Nov;10(11):1234-9 [15467726.001]
  • [Cites] J Immunol. 1999 Jul 1;163(1):507-13 [10384155.001]
  • [Cites] Gene Ther. 2002 Jul;9(13):833-43 [12080377.001]
  • [Cites] J Exp Med. 2004 Apr 5;199(7):885-94 [15051765.001]
  • [Cites] J Immunol. 2004 Nov 15;173(10):5923-8 [15528325.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):1-7 [9892174.001]
  • [Cites] Science. 1992 Oct 30;258(5083):815-8 [1439792.001]
  • [Cites] J Immunol. 2005 Apr 1;174(7):3986-91 [15778355.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):8052-6 [15520215.001]
  • [Cites] J Virol. 2001 Jan;75(2):799-808 [11134293.001]
  • [Cites] Nat Immunol. 2001 Oct;2(10):957-61 [11577349.001]
  • [Cites] J Immunol. 2003 Dec 15;171(12):6650-60 [14662868.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3530-40 [12869497.001]
  • [Cites] Immunity. 2005 Jan;22(1):117-29 [15664164.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 31;102(22):7934-9 [15908507.001]
  • [Cites] Nat Immunol. 2001 Oct;2(10 ):962-70 [11577350.001]
  • [Cites] J Exp Med. 1998 Nov 2;188(9):1641-50 [9802976.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1261-9 [14563634.001]
  • [Cites] Int J Cancer. 2004 Feb 10;108(4):571-9 [14696122.001]
  • [Cites] J Clin Invest. 2002 Nov;110(10):1415-7 [12438439.001]
  • [Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):145-60 [12620409.001]
  • [Cites] Lancet. 2000 Feb 26;355(9205):735-40 [10703815.001]
  • [Cites] J Immunol. 2005 Apr 1;174(7):4415-23 [15778407.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):386-90 [14729649.001]
  • [Cites] J Immunol. 2003 Mar 1;170(5):2582-9 [12594285.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1570-6 [15735047.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):982-7 [12461571.001]
  • [Cites] Gene Ther. 2005 Jan;12(2):140-6 [15496961.001]
  • [Cites] J Immunol. 2002 Jul 1;169(1):531-9 [12077285.001]
  • [Cites] Science. 2002 Oct 25;298(5594):850-4 [12242449.001]
  • [Cites] J Immunol. 2003 Sep 15;171(6):3287-95 [12960359.001]
  • [Cites] Curr Opin Immunol. 2004 Jun;16(3):264-70 [15134773.001]
  • [Cites] Adv Immunol. 2000;75:235-82 [10879286.001]
  • [Cites] J Immunol. 2003 Aug 15;171(4):1844-9 [12902485.001]
  • [Cites] J Exp Med. 1997 Aug 29;186(5):695-704 [9271585.001]
  • [Cites] Nat Immunol. 2004 Sep;5(9):927-33 [15300249.001]
  • [Cites] Cell Immunol. 1999 Feb 1;191(2):90-6 [9973530.001]
  • [Cites] J Exp Med. 1997 Mar 3;185(5):833-41 [9120389.001]
  • [Cites] Cell. 2002 Dec 27;111(7):967-79 [12507424.001]
  • [Cites] Blood. 2004 Jul 15;104(2):478-86 [15044252.001]
  • [Cites] EMBO J. 1998 Jan 15;17 (2):554-64 [9430646.001]
  • [Cites] Science. 1996 Oct 11;274(5285):209-19 [8824178.001]
  • [Cites] Nat Immunol. 2003 Mar;4(3):225-34 [12563257.001]
  • [Cites] Int Immunol. 2002 Jan;14(1):39-44 [11751750.001]
  • (PMID = 16720899.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, T-Lymphocyte; 0 / HLA-A2 Antigen; 0 / Receptors, Antigen, T-Cell, alpha-beta; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
  •  go-up   go-down


17. Greco S, Elia MG, Muscella A, Romano S, Storelli C, Marsigliante S: Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. J Endocrinol; 2005 Aug;186(2):291-301
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture.
  • We here investigated the mitogenic effects and the signalling pathways of BK in primary cultured human epithelial breast cells obtained from a tumour and from the histologically proven non-malignant tissue adjacent to the tumour.
  • BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2).
  • In conclusion, the mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression.
  • [MeSH-minor] Analysis of Variance. Calcium / analysis. Cell Proliferation / drug effects. Enzyme Activation. Female. Humans. Immunoblotting / methods. Intracellular Fluid / chemistry. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / metabolism. Receptors, Bradykinin / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16079255.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mitogens; 0 / Receptors, Bradykinin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
  •  go-up   go-down


18. Rendon BE, Willer SS, Zundel W, Mitchell RA: Mechanisms of macrophage migration inhibitory factor (MIF)-dependent tumor microenvironmental adaptation. Exp Mol Pathol; 2009 Jun;86(3):180-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of macrophage migration inhibitory factor (MIF)-dependent tumor microenvironmental adaptation.
  • Since its activity was first reported in the mid-1960s, macrophage migration inhibitory factor (MIF) has gone from a cytokine activity modulating monocyte motility to a pleiotropic regulator of a vast array of cellular and biological processes.
  • Studies in recent years suggest that MIF contributes to malignant disease progression on several different levels.
  • Additionally, MIF expression positively correlates with angiogenic growth factor expression, microvessel density and tumor-associated neovascularization.
  • This review summarizes recent literature on the contributions of MIF to tumor-associated angiogenic growth factor expression, neovascularization and hypoxic adaptation.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Exp Med. 2003 Jun 2;197(11):1467-76 [12782713.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9354-9 [12878730.001]
  • [Cites] Cardiovasc Res. 2008 Feb 1;77(3):463-70 [18006459.001]
  • [Cites] Nature. 2008 Jan 31;451(7178):578-82 [18235500.001]
  • [Cites] Cancer Lett. 2008 Mar 18;261(2):147-57 [18171602.001]
  • [Cites] Cell Death Differ. 2008 Apr;15(4):686-90 [18259200.001]
  • [Cites] Clin Exp Immunol. 2008 May;152(2):372-80 [18341611.001]
  • [Cites] PLoS One. 2008;3(5):e2215 [18493321.001]
  • [Cites] Clin Orthop Relat Res. 2008 Sep;466(9):2107-13 [18563508.001]
  • [Cites] J Immunol. 2008 Aug 15;181(4):2330-7 [18684922.001]
  • [Cites] Cancer Res. 2008 Sep 15;68(18):7253-7 [18794110.001]
  • [Cites] Immunology. 2008 Sep;125(1):101-10 [18355244.001]
  • [Cites] Clin Breast Cancer. 2008 Oct;8(5):402-10 [18952553.001]
  • [Cites] Curr Opin Neurol. 2008 Dec;21(6):717-9 [18989118.001]
  • [Cites] FASEB J. 2009 Mar;23(3):720-30 [18952710.001]
  • [Cites] J Immunol. 2008 Jan 1;180(1):601-8 [18097062.001]
  • [Cites] Circulation. 2004 Jun 29;109(25):3149-53 [15197138.001]
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):43013-8 [15299027.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 May 28;93(11):5191-6 [8643551.001]
  • [Cites] FEBS Lett. 1996 Jul 1;389(2):145-8 [8766818.001]
  • [Cites] Mol Med. 1996 Jan;2(1):143-9 [8900542.001]
  • [Cites] FEBS Lett. 1997 Nov 3;417(1):85-8 [9395080.001]
  • [Cites] Biochemistry. 1997 Dec 9;36(49):15356-62 [9398265.001]
  • [Cites] Genes Dev. 1998 Jan 15;12(2):149-62 [9436976.001]
  • [Cites] EMBO J. 1998 Jun 1;17(11):3005-15 [9606183.001]
  • [Cites] Diagn Mol Pathol. 1998 Feb;7(1):44-50 [9646034.001]
  • [Cites] Nat Cell Biol. 2003 Dec;5(12):1029-33 [14647295.001]
  • [Cites] Science. 2004 Mar 19;303(5665):1813-8 [15031495.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3534-41 [9649424.001]
  • [Cites] Plant Cell. 1998 Nov;10(11):1779-90 [9811788.001]
  • [Cites] J Exp Med. 1999 Jan 18;189(2):341-6 [9892616.001]
  • [Cites] J Biol Chem. 1999 Feb 5;274(6):3268-71 [9920865.001]
  • [Cites] Mol Med. 1998 Nov;4(11):707-14 [9932108.001]
  • [Cites] Biochemistry. 1999 Jun 1;38(22):7346-54 [10353846.001]
  • [Cites] Atherosclerosis. 2005 Jan;178(1):83-94 [15585204.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4991-5004 [15611513.001]
  • [Cites] Mol Cell. 2005 Jan 7;17(1):11-21 [15629713.001]
  • [Cites] Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):92-107 [15650399.001]
  • [Cites] Cancer. 2005 Feb 1;103(3):588-98 [15612021.001]
  • [Cites] World J Gastroenterol. 2005 Jun 28;11(24):3767-71 [15968736.001]
  • [Cites] Ann Surg. 2005 Jul;242(1):55-63 [15973102.001]
  • [Cites] Mol Cell Biol. 2005 Aug;25(15):6415-26 [16024780.001]
  • [Cites] Biochemistry. 2005 Aug 9;44(31):10510-9 [16060660.001]
  • [Cites] J Neuroimmunol. 2005 Nov;168(1-2):168-74 [16171874.001]
  • [Cites] J Biol Chem. 2005 Nov 4;280(44):36541-4 [16115897.001]
  • [Cites] Gastroenterology. 2005 Nov;129(5):1485-503 [16285950.001]
  • [Cites] Mol Cancer Res. 2005 Dec;3(12):645-53 [16380502.001]
  • [Cites] J Exp Med. 2006 May 15;203(5):1185-96 [16636133.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Sep 8;347(4):895-903 [16854377.001]
  • [Cites] Immunity. 2006 Oct;25(4):595-606 [17045821.001]
  • [Cites] J Immunol. 2006 Dec 15;177(12):8730-9 [17142775.001]
  • [Cites] Genes Dev. 2006 Dec 15;20(24):3366-71 [17142669.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):186-93 [17210698.001]
  • [Cites] EMBO J. 2007 Feb 21;26(4):987-97 [17290223.001]
  • [Cites] Mol Cancer Ther. 2007 Jul;6(7):1993-2002 [17620429.001]
  • [Cites] Oncogene. 2007 Aug 2;26(35):5046-59 [17310986.001]
  • [Cites] BMC Cancer. 2007;7:135 [17650334.001]
  • [Cites] J Biol Chem. 2007 Oct 12;282(41):29910-8 [17709373.001]
  • [Cites] Annu Rev Pathol. 2006;1:97-117 [18039109.001]
  • [Cites] Mol Cell Biochem. 2008 Jan;307(1-2):265-71 [17786542.001]
  • [Cites] Genes Dev. 2004 Apr 1;18(7):739-44 [15082527.001]
  • [Cites] Curr Biol. 1999 Oct 21;9(20):1187-90 [10531038.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Nov 2;264(3):751-8 [10544003.001]
  • [Cites] J Exp Med. 1999 Nov 15;190(10):1375-82 [10562313.001]
  • [Cites] Genes Dev. 2000 Jan 1;14(1):34-44 [10640274.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):883-7 [10706099.001]
  • [Cites] Cancer. 2000 Jul 15;89(2):334-41 [10918163.001]
  • [Cites] Prostate. 2000 Sep 15;45(1):51-7 [10960842.001]
  • [Cites] Nature. 2000 Nov 9;408(6809):211-6 [11089976.001]
  • [Cites] J Med Chem. 2001 Feb 15;44(4):540-7 [11170644.001]
  • [Cites] Physiol Genomics. 2001 Feb 7;5(1):21-33 [11161003.001]
  • [Cites] Nat Immunol. 2001 Nov;2(11):1061-6 [11668338.001]
  • [Cites] Cardiovasc Res. 2001 Dec;52(3):438-45 [11738060.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):345-50 [11756671.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):144-9 [11773615.001]
  • [Cites] J Biol Chem. 2002 Jan 18;277(3):2302-10 [11704659.001]
  • [Cites] Cancer. 2002 Mar 1;94(5):1449-56 [11920501.001]
  • [Cites] Jpn J Cancer Res. 2002 Apr;93(4):389-96 [11985788.001]
  • [Cites] J Interferon Cytokine Res. 2002 Mar;22(3):351-63 [12034043.001]
  • [Cites] J Med Chem. 2002 Jun 6;45(12):2410-6 [12036350.001]
  • [Cites] Nature. 2002 Jun 27;417(6892):975-8 [12050673.001]
  • [Cites] Nat Med. 2002 Jul;8(7):702-10 [12053176.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):24976-82 [11997397.001]
  • [Cites] Development. 2002 Oct;129(19):4399-409 [12223399.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13681-6 [12271144.001]
  • [Cites] Clin Cancer Res. 2002 Dec;8(12):3755-60 [12473586.001]
  • [Cites] Am J Pathol. 2003 Jan;162(1):11-7 [12507885.001]
  • [Cites] Curr Opin Genet Dev. 2003 Feb;13(1):55-60 [12573436.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):853-60 [12576459.001]
  • [Cites] Virchows Arch. 2003 May;442(5):444-52 [12692724.001]
  • (PMID = 19186177.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102285-05; United States / NCI NIH HHS / CA / CA102301-04; United States / NCI NIH HHS / CA / R01 CA129967; United States / NCI NIH HHS / CA / R01 CA102301-04; United States / NCRR NIH HHS / RR / 5P20RR018733; United States / NCRR NIH HHS / RR / RR018733-030002; United States / NCI NIH HHS / CA / R01 CA102301-02; United States / NCRR NIH HHS / RR / P20 RR018733; United States / NCI NIH HHS / CA / R01 CA102301-03; United States / NCI NIH HHS / CA / CA102301-01A1; United States / NCI NIH HHS / CA / R01 CA102301; United States / NCI NIH HHS / CA / R01 CA102301-01A1; United States / NCRR NIH HHS / RR / P20 RR018733-030002; United States / NCI NIH HHS / CA / 5R01CA102285; United States / NCI NIH HHS / CA / CA102301-03; United States / NCI NIH HHS / CA / CA102301-02; United States / NCI NIH HHS / CA / R01 CA102285; United States / NCI NIH HHS / CA / R01 CA102285-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Macrophage Migration-Inhibitory Factors; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.2.1 / MIF protein, human
  • [Number-of-references] 90
  • [Other-IDs] NLM/ NIHMS87090; NLM/ PMC2680445
  •  go-up   go-down


19. Wehbe H, Henson R, Lang M, Meng F, Patel T: Pifithrin-alpha enhances chemosensitivity by a p38 mitogen-activated protein kinase-dependent modulation of the eukaryotic initiation factor 4E in malignant cholangiocytes. J Pharmacol Exp Ther; 2006 Dec;319(3):1153-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pifithrin-alpha enhances chemosensitivity by a p38 mitogen-activated protein kinase-dependent modulation of the eukaryotic initiation factor 4E in malignant cholangiocytes.
  • Pifithrin-alpha is the lead compound for a novel group of small molecules that are being developed for use as anticancer agents.
  • We examined the utility of pifithrin-alpha as an adjunct to therapy for the treatment of human cholangiocarcinoma, a tumor that is highly refractory to therapy, and we assessed the involvement of p53-dependent eIF-4E regulation in cellular responses to pifithrin-alpha.
  • Preincubation of KMCH cells with pifithrin-alpha enhanced gemcitabine-induced cytotoxicity in an eIF-4E-dependent manner.
  • Furthermore, pifithrin-alpha increased eIF-4E phosphorylation at serine 209 via activation of p38 mitogen-activated protein kinase (MAPK).
  • Pifithrin-alpha was shown to activate aryl hydrocarbon receptor (AhR) signaling and p38 MAPK activation.
  • Sequencing analysis indicated the presence of a functionally inactivating p53 mutation in KMCH cells, and small interfering RNA to p53 did not modulate chemosensitization by pifithrin-alpha.
  • Pifithrin-alpha enhanced chemosensitivity by a mechanism independent of p53 and involving AhR and p38 MAPK deregulation of eIF-4E phosphorylation.
  • Thus, pifithrin-alpha may prove useful for enhancing chemosensitivity in tumors with mutated p53.

  • MedlinePlus Health Information. consumer health - Bile Duct Cancer.
  • COS Scholar Universe. author profiles.
  • PhosphoSitePlus. gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource .
  • Hazardous Substances Data Bank. TOLUENE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16982703.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK069370-01; United States / NIDDK NIH HHS / DK / R01 DK069370; United States / NIDDK NIH HHS / DK / DK069370; United States / NIDDK NIH HHS / DK / R01 DK069370-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Benzothiazoles; 0 / DNA, Neoplasm; 0 / Eukaryotic Initiation Factor-4E; 0 / Receptors, Aryl Hydrocarbon; 0 / pifithrin; 0W860991D6 / Deoxycytidine; 3FPU23BG52 / Toluene; B76N6SBZ8R / gemcitabine; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  •  go-up   go-down


20. Qiuping Z, Jie X, Youxin J, Qun W, Wei J, Chun L, Jin W, Yan L, Chunsong H, Mingzhen Y, Qingping G, Qun L, Kejian Z, Zhimin S, Junyan L, Jinquan T: Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia. Oncogene; 2005 Jan 20;24(4):573-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia.
  • We investigated CD4(+)CD34(+), CD8(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells from cord blood and from typical patients with T-cell-lineage acute lymphocytic leukemia and T-cell-lineage chronic lymphocytic leukemia in terms of expression and functions of CXCR5/CXCL13.
  • We found that CXCR5 was selectively frequently expressed on T-cell-lineage acute (chronic) lymphocytic leukemia (T-ALL) CD8(+)CD34(+) T cells, but not on T-ALL CD4(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells.
  • CXCL13/B cells attracting chemokine 1 induced significant resistance to TNF-alpha-mediated apoptosis in T-ALL CD8(+)CD34(+) T cells, instead of induction of chemotactic and adhesive responsiveness.
  • A proliferation-inducing ligand expression in T-ALL CD8(+)CD34(+) T cells was upregulated by CXCL13/BCA-1 (B-cell attracting chemokine 1).
  • In this process, cell-cell contact in culture was necessary.
  • Normal lymphocytes, especially naive B and T cells, utilized CXCR5/CXCL13 for migration, homing, maturation, and cell homeostasis, as well as secondary lymphoid tissue organogenesis.
  • Meanwhile, certain malignant cells took advantages of CXCR5/CXCL13 for infiltration, resistance to apoptosis, and inappropriate proliferation.
  • [MeSH-major] Antigens, CD34 / metabolism. Apoptosis. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Cytokine / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Cell Adhesion / drug effects. Cell Line. Cell Lineage / drug effects. Chemokine CXCL13. Chemokines, CXC / metabolism. Chemokines, CXC / pharmacology. Chemotaxis / drug effects. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Nuclear Proteins / pharmacology. Receptors, CXCR5. Receptors, Chemokine / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / genetics

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [RetractionIn] Oncogene. 2011 Jun 16;30(24):2798 [21677655.001]
  • (PMID = 15580304.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ANP32B protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD34; 0 / BIRC7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CXCL13; 0 / Chemokines, CXC; 0 / Inhibitor of Apoptosis Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, Cytokine; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


21. Hamamura K, Furukawa K, Hayashi T, Hattori T, Nakano J, Nakashima H, Okuda T, Mizutani H, Hattori H, Ueda M, Urano T, Lloyd KO, Furukawa K: Ganglioside GD3 promotes cell growth and invasion through p130Cas and paxillin in malignant melanoma cells. Proc Natl Acad Sci U S A; 2005 Aug 2;102(31):11041-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ganglioside GD3 promotes cell growth and invasion through p130Cas and paxillin in malignant melanoma cells.
  • Although ganglioside GD3 levels are highly elevated in malignant melanomas, the role of GD3 in melanomas' malignant properties has not been clearly shown.
  • GD3+ cells showed markedly increased cell growth and invasive characteristics.
  • Two bands that underwent stronger tyrosine phosphorylation in GD3+ cell lines than in controls after treatment with FCS were found with molecular masses of 130 and 68 kDa.
  • Their roles in cell growth and invasion were analyzed with a small interfering RNA (siRNA) approach.
  • Cell growth, as analyzed by BrdUrd uptake, was strongly suppressed in GD3+ cells to near the levels of GD3- cells when treated with siRNA for p130Cas but not when treated with siRNA for paxillin.
  • These results suggested that these two molecules function as effectors of GD3-mediated signaling, leading to such malignant properties as rapid cell growth and invasion.
  • [MeSH-minor] Cell Division. Cell Line, Tumor. Crk-Associated Substrate Protein. Humans. Neoplasm Invasiveness. Paxillin. Phenotype. Phosphorylation. RNA, Small Interfering / genetics. Retinoblastoma-Like Protein p130. Sialyltransferases / genetics. Transfection. Tyrosine / chemistry

  • MedlinePlus Health Information. consumer health - Melanoma.
  • Hazardous Substances Data Bank. L-TYROSINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1996 Jun 15;56(12):2844-8 [8665524.001]
  • [Cites] J Exp Med. 1993 Aug 1;178(2):489-95 [8340755.001]
  • [Cites] J Invest Dermatol. 1996 Oct;107(4):543-8 [8823358.001]
  • [Cites] J Biol Chem. 1997 Feb 28;272(9):5501-9 [9038154.001]
  • [Cites] J Cell Biol. 1998 Jan 12;140(1):211-21 [9425168.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):361-5 [9697697.001]
  • [Cites] Exp Cell Res. 1999 Aug 1;250(2):548-57 [10413607.001]
  • [Cites] J Biol Chem. 1996 Feb 9;271(6):3247-54 [8621727.001]
  • [Cites] Trends Cell Biol. 2000 Mar;10(3):111-9 [10675905.001]
  • [Cites] J Biol Chem. 2000 Feb 25;275(8):5832-8 [10681573.001]
  • [Cites] Int J Cancer. 2000 Oct 1;88(1):53-7 [10962439.001]
  • [Cites] J Cell Sci. 2000 Dec;113 Pt 23:4139-40 [11069756.001]
  • [Cites] Nat Cell Biol. 2000 Dec;2(12):E231-6 [11146675.001]
  • [Cites] Cancer Res. 2000 Dec 1;60(23):6670-6 [11118051.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):4244-52 [11358851.001]
  • [Cites] J Biol Chem. 2002 Mar 15;277(11):9405-14 [11756413.001]
  • [Cites] Int J Cancer. 2003 Jan 10;103(2):169-76 [12455030.001]
  • [Cites] J Cell Biol. 2003 Mar 3;160(5):753-67 [12615911.001]
  • [Cites] J Cell Sci. 2003 Nov 15;116(Pt 22):4605-13 [14576354.001]
  • [Cites] J Cell Biol. 2004 May 10;165(3):371-81 [15138291.001]
  • [Cites] Mol Cell. 2004 Oct 22;16(2):257-67 [15494312.001]
  • [Cites] Eur J Biochem. 1979 Feb 15;94(1):19-23 [436839.001]
  • [Cites] J Natl Cancer Inst. 1979 Sep;63(3):623-34 [381752.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Oct;77(10):6114-8 [6934537.001]
  • [Cites] J Exp Med. 1982 Apr 1;155(4):1133-47 [7061953.001]
  • [Cites] Cancer Res. 1984 Feb;44(2):806-10 [6362854.001]
  • [Cites] Biochem Biophys Res Commun. 1984 Apr 30;120(2):500-4 [6732768.001]
  • [Cites] Cancer Res. 1984 Nov;44(11):5262-5 [6488184.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Feb;82(4):1242-6 [3883355.001]
  • [Cites] J Immunol. 1993 Sep 1;151(5):2667-75 [8360485.001]
  • [Cites] EMBO J. 1994 Aug 15;13(16):3748-56 [8070403.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10455-9 [7937974.001]
  • [Cites] Vaccine. 1994 Nov;12(14):1275-80 [7856291.001]
  • [Cites] J Biol Chem. 1995 Jun 23;270(25):15398-402 [7541040.001]
  • [Cites] Biochemistry. 1995 Oct 24;34(42):13760-7 [7577968.001]
  • [Cites] J Biol Chem. 1996 Mar 29;271(13):7375-80 [8631760.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10231-3 [12149519.001]
  • [Cites] Int J Cancer. 1986 Jan 15;37(1):123-32 [3000950.001]
  • [Cites] J Cell Biol. 1986 Mar;102(3):688-96 [3005335.001]
  • [Cites] Cancer Res. 1987 Mar 15;47(6):1724-30 [3493067.001]
  • [Cites] J Neurochem. 1988 Jun;50(6):1825-9 [3131485.001]
  • [Cites] J Natl Cancer Inst. 1989 Mar 15;81(6):440-4 [2918552.001]
  • [Cites] J Immunol. 1992 Jan 15;148(2):451-6 [1729365.001]
  • [Cites] J Biol Chem. 1992 Aug 15;267(23):16283-7 [1379593.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Mar 1;90(5):1972-6 [8095337.001]
  • [Cites] Glycoconj J. 1995 Dec;12(6):894-900 [8748167.001]
  • (PMID = 16040804.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCAR1 protein, human; 0 / Crk-Associated Substrate Protein; 0 / Cytoskeletal Proteins; 0 / Gangliosides; 0 / PXN protein, human; 0 / Paxillin; 0 / Phosphoproteins; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Retinoblastoma-Like Protein p130; 42HK56048U / Tyrosine; 62010-37-1 / ganglioside, GD3; EC 2.4.99.- / Sialyltransferases; EC 2.4.99.8 / alpha-N-acetylneuraminate alpha-2,8-sialyltransferase
  • [Other-IDs] NLM/ PMC1180226
  •  go-up   go-down


22. Marín-Hernández A, Gallardo-Pérez JC, Ralph SJ, Rodríguez-Enríquez S, Moreno-Sánchez R: HIF-1alpha modulates energy metabolism in cancer cells by inducing over-expression of specific glycolytic isoforms. Mini Rev Med Chem; 2009 Aug;9(9):1084-101
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • One such factor is hypoxia-inducible factor-1alpha (HIF-1alpha), a transcription factor induced by low oxygen conditions and found in high levels in malignant solid tumors, but not in normal tissues or slow-growing tumors.
  • In cancer cells, HIF-1alpha induces over-expression and increased activity of several glycolytic protein isoforms that differ from those found in non-malignant cells, including transporters (GLUT1, GLUT3) and enzymes (HKI, HKII, PFK-L, ALD-A, ALD-C, PGK1, ENO-alpha, PYK-M2, LDH-A, PFKFB-3).
  • The enhanced tumor glycolytic flux triggered by HIF-1alpha also involves changes in the kinetic patterns of expressed isoforms of key glycolytic enzymes.
  • Some of the HIF1alpha-induced glycolytic isoforms also participate in survival pathways, including transcriptional activation of H2B histone (by LDH-A), inhibition of apoptosis (by HKII) and promotion of cell migration (by ENO-alpha).
  • HIF-1alpha action may also modulate mitochondrial function and oxygen consumption by inactivating the pyruvate dehydrogenase complex in some tumor types, or by modulating cytochrome c oxidase subunit 4 expression to increase oxidative phosphorylation in other cancer cell lines.
  • In this review, the roles of HIF-1alpha and HIF1alpha-induced glycolytic enzymes are examined and it is concluded that targeting the HIF1alpha-induced glucose transporter and hexokinase, important to glycolytic flux control, might provide better therapeutic targets for inhibiting tumor growth and progression than targeting HIF1alpha itself.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Glycolysis. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Neoplasms / genetics. Neoplasms / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19689405.001).
  • [ISSN] 1389-5575
  • [Journal-full-title] Mini reviews in medicinal chemistry
  • [ISO-abbreviation] Mini Rev Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Protein Isoforms
  • [Number-of-references] 166
  •  go-up   go-down


23. Leucci E, De Falco G, Onnis A, Cerino G, Cocco M, Luzzi A, Crupi D, Tigli C, Bellan C, Tosi P, Leoncini L, Giordano A: The role of the Cdk9/Cyclin T1 complex in T cell differentiation. J Cell Physiol; 2007 Aug;212(2):411-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of the Cdk9/Cyclin T1 complex in T cell differentiation.
  • The Cdk9/Cyclin T1 complex is very important in controlling specific differentiative pathways of several cell types, including muscle cells and neurons.
  • We recently demonstrated the involvement of this complex in B cell activation/differentiation.
  • To check whether the Cdk9/Cyclin T1 complex is also involved in the T cell activation/differentiation process, we isolated different T cell populations by magnetic separation, based on their surface antigens.
  • These preliminary results suggest that the Cdk9/Cyclin T1 complex may be important in the activation and differentiation program of lymphoid cells and that its upregulation, which is due to still unknown mechanisms, may contribute to malignant transformation.
  • [MeSH-major] Cell Differentiation. Cell Transformation, Neoplastic / metabolism. Cyclin-Dependent Kinase 9 / metabolism. Cyclins / metabolism. Lymphocyte Activation. T-Lymphocyte Subsets / metabolism
  • [MeSH-minor] Antigens, CD27 / analysis. Antigens, CD38 / analysis. Antigens, CD45 / analysis. Cyclin T. Gene Expression. Humans. Immunologic Memory. Interleukin-2 Receptor alpha Subunit / analysis. Interleukin-7 / metabolism. Ionomycin / pharmacology. Ionophores / pharmacology. Jurkat Cells. Membrane Glycoproteins / analysis. Phorbol Esters / pharmacology. RNA, Messenger / metabolism. TCF Transcription Factors / metabolism. Time Factors. Transcription Factor 7-Like 1 Protein. Up-Regulation

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17352406.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / CCNT1 protein, human; 0 / Cyclin T; 0 / Cyclins; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Interleukin-7; 0 / Ionophores; 0 / Membrane Glycoproteins; 0 / Phorbol Esters; 0 / RNA, Messenger; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Transcription Factor 7-Like 1 Protein; 56092-81-0 / Ionomycin; EC 2.7.11.22 / CDK9 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 9; EC 3.1.3.48 / Antigens, CD45; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
  •  go-up   go-down


24. Baderca F, Lighezan R, Dema A, Alexa A, Raica M: Angiogenesis in urothelial tumors of the upper urinary tract. Rom J Morphol Embryol; 2005;46(4):263-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angiogenesis is an essential process in the progression of malignant tumors.
  • We tried to demonstrate angiogenesis by using three endothelial markers CD31, CD34, von Willebrand factor and one pericytes marker (alpha-smooth muscle actin) in 26 cases.
  • In non-invasive tumors we observed that angiogenesis process is limited to connective tissue of tumor stroma.
  • In the tumor area, the blood vessels stained with anti-CD31 had large lumen, thin walls and numerous branches, some of them being very thin.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16688360.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / von Willebrand Factor
  •  go-up   go-down


25. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


26. Chong YM, Colston K, Jiang WG, Sharma AK, Mokbel K: The relationship between the insulin-like growth factor-1 system and the oestrogen metabolising enzymes in breast cancer tissue and its adjacent non-cancerous tissue. Breast Cancer Res Treat; 2006 Oct;99(3):275-88
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: A series of 139 pairs of breast cancer tissue and ANCT were obtained and divided into ER positive and ER negative groups based on tumour ER alpha immunostaining.
  • All samples were processed for real-time quantitative-PCR to measure IGF-1, IGF-1R, ER alpha, STS and Cyp-19 mRNA levels.
  • In addition, ER positive MCF-7 and ER negative MDA-MB-231 cell lines were treated separately with IGF-1 and an IGF-1R inhibitor called Tyrphostin AG1024 to see the effects of stimulating and inhibiting the IGF-1R.
  • MCF-7 cell line was also treated with 4-hydroxytamoxifen.
  • The mRNA levels of IGF-1, IGF-1R, ER alpha, STS and Cyp-19 of treated cell lines were measured and compared to those of non-treated controls.
  • RESULTS: IGF-1R expression was higher in tumour tissue compared to ANCT (P = 0.038) while IGF-1 expression was marginally higher in ANCT compared to tumour tissue only in the ER positive samples (P = 0.098).
  • Using Spearman's Correlation test, IGF-1 positively correlated with STS, Cyp-19 and ER alpha in ER positive and negative groups (Coefficient = +0.497, +0.662 and +0.651 respectively, P = 0.000 in all).
  • IGF-1R correlated with IGF-1, STS, Cyp-19 and ER alpha only in the ER negative tumours (Coefficient = +0.620, +0.394, +0.692 and +0.662 respectively, P = 0.000, 0.012, 0.000 and 0.000 respectively).
  • In cell lines, IGF-1 treatment led to an increase in the mean expression of IGF-1, IGF-1R, STS and Cyp-19 in both cell lines while ER alpha expression increased only in MCF-7.
  • IGF-1R inhibition caused a decrease in expression of all five genes in MDA-MB-231 but not in the MCF-7 cell line.
  • CONCLUSIONS: IGF-1R is over-expressed in malignant tissue.
  • An IGF-1 paracrine relationship may exist between tumour and ANCT but for STS and Cyp-19, there may be an autocrine-paracrine relationship.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Estrogen Antagonists / pharmacology. Estrogen Receptor alpha / analysis. Estrogens / metabolism. Feedback, Physiological. Female. Humans. Immunohistochemistry. Middle Aged. RNA, Messenger / analysis. Receptor Cross-Talk. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Tamoxifen / analogs & derivatives. Tamoxifen / pharmacology. Tyrphostins / pharmacology

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16752221.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / Tyrphostins; 0 / tyrphostin AG 1024; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.14.1 / Aromatase; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.15 / steroid sulfotransferase
  •  go-up   go-down


27. Beckner ME, Chen X, An J, Day BW, Pollack IF: Proteomic characterization of harvested pseudopodia with differential gel electrophoresis and specific antibodies. Lab Invest; 2005 Mar;85(3):316-27
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant gliomas (astrocytomas) are lethal tumors that invade the brain.
  • Invasive cell migration is initiated by extension of pseudopodia into interstitial spaces.
  • Specific antibodies showed restricted immunoreactivity of the hepatocyte growth factor (HGF) alpha chain to pseudopodia, indicating localization of its active form.
  • Increased constituents of the pseudopodial proteome in glioma cells, identified in this study as actin, HGF, Met, and isoforms of AnxI, AnxII, and several glycolytic enzymes, represent therapeutic targets to consider for suppression of tumor invasion.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor. Brain Neoplasms / pathology. Proteome. Pseudopodia / metabolism
  • [MeSH-minor] Annexin A1 / metabolism. Annexin A2 / metabolism. Antibodies, Neoplasm / immunology. Electrophoresis, Gel, Two-Dimensional. Fructose-Bisphosphate Aldolase / metabolism. Hepatocyte Growth Factor / metabolism. Humans. Mitogens / metabolism. Neoplasm Invasiveness. Phosphopyruvate Hydratase / metabolism. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15654357.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A1; 0 / Annexin A2; 0 / Antibodies, Neoplasm; 0 / Biomarkers, Tumor; 0 / HGF protein, human; 0 / Mitogens; 0 / Proteome; 67256-21-7 / Hepatocyte Growth Factor; EC 4.1.2.13 / Fructose-Bisphosphate Aldolase; EC 4.2.1.11 / Phosphopyruvate Hydratase
  •  go-up   go-down


28. Kessler J, Hahnel A, Wichmann H, Rot S, Kappler M, Bache M, Vordermark D: HIF-1α inhibition by siRNA or chetomin in human malignant glioma cells: effects on hypoxic radioresistance and monitoring via CA9 expression. BMC Cancer; 2010;10:605
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF-1α inhibition by siRNA or chetomin in human malignant glioma cells: effects on hypoxic radioresistance and monitoring via CA9 expression.
  • BACKGROUND: Hypoxia induces activation of the HIF-1 pathway and is an essential characteristic of malignant gliomas.
  • Hypoxia has been linked to tumor progression, therapy resistance and poor prognosis.
  • However, little is known about the impact of HIF-1α inhibition on radioresistance of malignant glioma.
  • METHODS: In this study, we investigated the effects of the inhibition of HIF-1α on cell survival and radiosensitivity in U251MG and U343MG glioma cells, using two different strategies.
  • CA9 expression was investigated as a potential indicator of the efficacy of HIF-1 inhibition and the resulting radiosensitivity of malignant glioma cell lines was determined by clonogenic assay after irradiation under normoxic (2-10 Gy) or hypoxic (2-15 Gy) conditions.
  • RESULTS: Although siRNA and chetomin show distinct modes of action, both attenuated the hypoxia-induced radioresistance of malignant glioma cell lines U251MG (DMF10: 1.35 and 1.18) and U343MG (DMF10: 1.78 and 1.48).
  • CONCLUSIONS: Results from this in vitro study suggest that inhibition of HIF-1α is a promising strategy to sensitize human malignant gliomas to radiotherapy and that CA9 could serve as an indicator of effective HIF-1-related radiosensitization.
  • [MeSH-major] Anoxia. Antigens, Neoplasm / biosynthesis. Antineoplastic Agents / pharmacology. Carbonic Anhydrases / biosynthesis. Disulfides / pharmacology. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Indole Alkaloids / pharmacology. RNA, Small Interfering / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Survival. Disease Progression. Drug Resistance, Neoplasm. Humans. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Glioma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4316-24 [12154035.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Jul 15;56(4):1184-93 [12829158.001]
  • [Cites] Cell Mol Life Sci. 2003 Jul;60(7):1376-93 [12943226.001]
  • [Cites] Antioxid Redox Signal. 2003 Aug;5(4):467-73 [13678535.001]
  • [Cites] Strahlenther Onkol. 2003 Dec;179(12):801-11 [14652668.001]
  • [Cites] Mol Cancer Ther. 2004 May;3(5):647-54 [15141023.001]
  • [Cites] Neuropathol Appl Neurobiol. 2004 Jun;30(3):267-78 [15175080.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):33-43 [15261140.001]
  • [Cites] Int J Cancer. 2004 Nov 20;112(4):585-95 [15382039.001]
  • [Cites] Cancer. 1985 Sep 1;56(5):1106-11 [2990664.001]
  • [Cites] Brain Pathol. 1999 Jul;9(3):469-79 [10416987.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Mar 15;61(4):1197-207 [15752902.001]
  • [Cites] Radiother Oncol. 2005 Oct;77(1):18-24 [16098619.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):233-47 [16612574.001]
  • [Cites] Clin Cancer Res. 2006 Nov 1;12(21):6421-31 [17085655.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2007 Jan 1;67(1):1-5 [17084552.001]
  • [Cites] Int J Oncol. 2007 Apr;30(4):793-802 [17332917.001]
  • [Cites] Clin Cancer Res. 2007 Apr 15;13(8):2441-8 [17438103.001]
  • [Cites] Int J Cancer. 2007 Jul 15;121(2):276-83 [17372907.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Cancer Gene Ther. 2007 Dec;14(12):994-1001 [17885676.001]
  • [Cites] BMC Cancer. 2007;7:213 [17999771.001]
  • [Cites] Curr Med Chem. 2008;15(4):322-38 [18288988.001]
  • [Cites] Int J Cancer. 2008 Nov 15;123(10):2430-7 [18729192.001]
  • [Cites] Int J Oncol. 2009 Apr;34(4):1051-60 [19287962.001]
  • [Cites] Neurochem Res. 2009 May;34(5):984-90 [18937067.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):459-66 [19269895.001]
  • [Cites] J Biol Chem. 2009 Sep 25;284(39):26831-8 [19589782.001]
  • [Cites] Radiother Oncol. 1999 Nov;53(2):127-31 [10665789.001]
  • [Cites] Cancer. 2001 Jul 1;92(1):165-71 [11443623.001]
  • [Cites] Intern Med. 2002 Feb;41(2):79-83 [11868612.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Mar 15;55(4):1027-36 [12605983.001]
  • (PMID = 21050481.001).
  • [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 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Disulfides; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Indole Alkaloids; 0 / RNA, Small Interfering; 1403-36-7 / chetomin; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2992520
  •  go-up   go-down


29. Salonen J, Butzow R, Palvimo JJ, Heikinheimo M, Heikinheimo O: Oestrogen receptors and small nuclear ring finger protein 4 (RNF4) in malignant ovarian germ cell tumours. Mol Cell Endocrinol; 2009 Aug 13;307(1-2):205-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oestrogen receptors and small nuclear ring finger protein 4 (RNF4) in malignant ovarian germ cell tumours.
  • The peak incidence of malignant ovarian germ cell tumours occurs soon after puberty.
  • While ERbeta and SNURF are down-regulated in testicular germ cell tumours, their role in the ovarian germ cell tumours remains unknown.
  • We herein studied the different subtypes of malignant ovarian germ cell tumours, and found that they all express ERalpha, ERbeta, and SNURF.
  • Our results suggest that oestrogen signalling has a role in malignant ovarian germ cell tumours.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Neoplasms, Germ Cell and Embryonal / metabolism. Nuclear Proteins / metabolism. Ovarian Neoplasms / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Child. Estradiol / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Middle Aged. Oocytes / drug effects. Oocytes / metabolism. Ovary / cytology. RNA, Messenger / genetics. RNA, Messenger / metabolism

  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19524139.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / RNF4 protein, human; 0 / Transcription Factors; 4TI98Z838E / Estradiol
  •  go-up   go-down


30. Sumerauer D, Vicha A, Zuntova A, Stejskalova E, Krskova L, Kabickova E, Kodet R, Eckschlager T: Teratoma in an adolescent with malignant transformation into embryonal rhabdomyosarcoma: case report. J Pediatr Hematol Oncol; 2006 Oct;28(10):688-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Teratoma in an adolescent with malignant transformation into embryonal rhabdomyosarcoma: case report.
  • BACKGROUND: The somatic type tumors are occasionally found in nonseminomatous germ cell tumors in men.
  • These malignancies are presumed to arise from malignant transformation (MT) of teratoma or by differentiation of totipotential germ cell.
  • OBSERVATION: A case of MT of germ cell tumor in 17-year-old male into embryonal rhabdomyosarcoma is described.
  • The histopathologic diagnosis was that of embryonal rhabdomyosarcoma in which no germ cell elements were found.
  • The germ cell origin of transformed histology is supported by cytogenetic analysis (isochromosome 12p), and elevated alpha(1)-fetoprotein.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Lung Neoplasms / diagnosis. Mediastinal Neoplasms / diagnosis. Neoplasms, Second Primary / diagnosis. Rhabdomyosarcoma, Embryonal / diagnosis. Teratoma / diagnosis

  • Genetic Alliance. consumer health - Rhabdomyosarcoma embryonal.
  • Genetic Alliance. consumer health - Teratoma.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17023832.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


31. Giusti L, Iacconi P, Ciregia F, Giannaccini G, Donatini GL, Basolo F, Miccoli P, Pinchera A, Lucacchini A: Fine-needle aspiration of thyroid nodules: proteomic analysis to identify cancer biomarkers. J Proteome Res; 2008 Sep;7(9):4079-88
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At present, the clinical and pathological analysis used in the diagnosis of papillary thyroid cancer (PTC) are insufficient to discern tumor behavior, and new diagnostic and prognostic markers need to be identified.
  • In this study, we performed a comparative proteome analysis to examine the global changes of fine needle aspiration fluid (FNA) protein patterns of two variants of malignant PTC (classical variant PTC (cPTC) and tall cell variant PTC (TCV)) with respect to the controls.
  • These proteins included transthyretin precursor (TTR), ferritin light chain (FLC), proteasome activator complex subunit 1 and 2, alpha-1-antitrypsin precursor, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), lactate dehydrogenase chain B (LDH-B), apolipoprotein A1 precursor (Apo-A1), annexin A1, DJ-1 protein and cofilin-1.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Proteome. Thyroid Neoplasms / pathology


32. Schimmer AD, Thomas MP, Hurren R, Gronda M, Pellecchia M, Pond GR, Konopleva M, Gurfinkel D, Mawji IA, Brown E, Reed JC: Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors. Cancer Res; 2006 Feb 15;66(4):2367-75
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors.
  • Two major pathways for apoptosis have been identified, involving either mitochondria (intrinsic) or tumor necrosis factor (TNF)-family death receptors (extrinsic) as initiators of caspase protease activation and cell death.
  • Because tumor resistance to TNF-family death receptor ligands is a common problem, helping malignant cells evade host immune defenses, we sought to identify compounds that selectively sensitize resistant tumor cells to death receptor ligands.
  • We screened a 50,000-compound library for agents that enhanced anti-FAS antibody-mediated killing of FAS-resistant PPC-1 prostate cancer cell, then did additional analysis of the resulting hits to arrive at eight compounds that selectively sensitized PPC-1 cells to anti-FAS antibody (extrinsic pathway agonist) without altering sensitivity to staurosporine and etoposide (VP-16; intrinsic pathway agonists).
  • Of these, two reduced expression of c-FLIP, an intracellular antagonist of the extrinsic pathway.
  • Characterization of the effects of the eight compounds on a panel of 10 solid tumor cell lines revealed two structurally distinct compounds that frequently sensitize to extrinsic pathway agonists.
  • Altogether, these findings show the feasibility of identifying compounds that selectively enhance apoptosis via the extrinsic pathway, thus providing research tools for uncovering resistance mechanisms and a starting point for novel therapeutics aimed at restoring sensitivity of tumor cells to immune effector mechanisms.
  • [MeSH-major] Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Receptors, Tumor Necrosis Factor / physiology
  • [MeSH-minor] Antibodies / immunology. Antibodies / pharmacology. Antigens, CD95 / immunology. Apoptosis / drug effects. Apoptosis / physiology. Apoptosis Regulatory Proteins / pharmacology. Caspases / metabolism. Cell Line, Tumor. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor / methods. Etoposide / pharmacology. Humans. Ligands. Male. Membrane Glycoproteins / pharmacology. Staurosporine / pharmacology. TNF-Related Apoptosis-Inducing Ligand. Tumor Necrosis Factor-alpha / pharmacology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16489043.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD95; 0 / Apoptosis Regulatory Proteins; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspases; H88EPA0A3N / Staurosporine
  •  go-up   go-down


33. Messina C, Faraci M, de Fazio V, Dini G, Calò MP, Calore E, EBMT Paediatric Working Party: Prevention and treatment of acute GvHD. Bone Marrow Transplant; 2008 Jun;41 Suppl 2:S65-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Improving outcomes in stem cell transplant recipients requires additional therapeutic modalities for GvHD, especially for patients who fail to respond to initial therapy with steroids.
  • Moreover, while the absence of acute GvHD (aGvHD) is associated with a higher risk of relapse of the underlying malignant disease, severe aGvHD usually induces the occurrence of life-threatening complications such as severe infections.
  • [MeSH-minor] Child. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Steroids / therapeutic use. T-Lymphocytes, Regulatory. Tacrolimus / therapeutic use. Transplantation, Homologous. Tumor Necrosis Factor-alpha / antagonists & inhibitors

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18545247.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Steroids; 0 / Tumor Necrosis Factor-alpha; WM0HAQ4WNM / Tacrolimus
  • [Number-of-references] 59
  •  go-up   go-down


34. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


35. Karunakaran S, Umapathy NS, Thangaraju M, Hatanaka T, Itagaki S, Munn DH, Prasad PD, Ganapathy V: Interaction of tryptophan derivatives with SLC6A14 (ATB0,+) reveals the potential of the transporter as a drug target for cancer chemotherapy. Biochem J; 2008 Sep 15;414(3):343-55
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 1-Methyltryptophan is an inducer of immune surveillance against tumour cells through its ability to inhibit indoleamine dioxygenase.
  • In the present study, we investigated the role of ATB(0,+) in the uptake of 1-methyltryptophan as a potential mechanism for entry of this putative anticancer drug into tumour cells.
  • Evaluation of other derivatives of tryptophan has led to identification of alpha-methyltryptophan as a blocker, not a transportable substrate, for ATB(0,+).
  • ATB(0,+) can transport 18 of the 20 proteinogenic amino acids. alpha-Methyltryptophan blocks the transport function of ATB(0,+) with an IC(50) value of approximately 250 muM under conditions simulating normal plasma concentrations of all these 18 amino acids.
  • These results suggest that alpha-methyltryptophan may induce amino acid deprivation in cells which depend on the transporter for their amino acid nutrition.
  • Screening of several mammary epithelial cell lines shows that ATB(0,+) is expressed robustly in some cancer cell lines, but not in all; in contrast, non-malignant cell lines do not express the transporter.
  • Treatment of ATB(0,+)-positive tumour cells with alpha-methyltryptophan leads to suppression of their colony-forming ability, whereas ATB(0,+)-negative cell lines are not affected.
  • The blockade of ATB(0,+) in these cells with alpha-methyltryptophan is associated with cell cycle arrest.
  • [MeSH-minor] Amino Acid Transport Systems / metabolism. Animals. Biological Transport, Active / drug effects. Cell Line. Cell Line, Tumor. Humans. Large Neutral Amino Acid-Transporter 1 / genetics. Large Neutral Amino Acid-Transporter 1 / metabolism. Mice. Oocytes / metabolism. Plasma Membrane Neurotransmitter Transport Proteins / metabolism. Xenopus laevis

  • COS Scholar Universe. author profiles.
  • Guide to Pharmacology. gene/protein/disease-specific - Glycine transporter subfamily - overview and references .
  • Hazardous Substances Data Bank. (L)-Tryptophan .
  • The Lens. Cited by Patents in .
  • Xenbase. Xenbase .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18522536.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1-methyltryptophan; 0 / Amino Acid Transport Systems; 0 / Amino Acid Transport Systems, Neutral; 0 / Antineoplastic Agents; 0 / Large Neutral Amino Acid-Transporter 1; 0 / Plasma Membrane Neurotransmitter Transport Proteins; 0 / SLC6A14 protein, human; 0 / Slc6A14 protein, mouse; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan
  •  go-up   go-down


36. Benbrahim-Tallaa L, Webber MM, Waalkes MP: Acquisition of androgen independence by human prostate epithelial cells during arsenic-induced malignant transformation. Environ Health Perspect; 2005 Sep;113(9):1134-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquisition of androgen independence by human prostate epithelial cells during arsenic-induced malignant transformation.
  • Arsenic is a potential human prostate carcinogen that may affect tumor progression.
  • In this study, we used a prostate cancer cell model in which an immortalized, nontumorigenic human prostate epithelial cell line (RWPE-1) had been malignantly transformed by chronic low-level arsenic to help determine whether arsenic affects prostate tumor progression.
  • Although both control and CAsE-PE cells showed similar levels of androgen receptor (AR), androgens were less effective in stimulating cell proliferation and AR-related gene expression in CAsE-PE cells.
  • Thus, arsenic-induced malignant transformation is associated with acquired androgen independence in human prostate cells.
  • [MeSH-major] Androgens / metabolism. Arsenic / toxicity. Cell Transformation, Neoplastic / chemically induced. Epithelial Cells / drug effects. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Androgen Antagonists / pharmacology. Animals. Cell Line. Cell Proliferation / drug effects. Dihydrotestosterone / pharmacology. Epidermal Growth Factor. Estradiol / pharmacology. Estrogen Receptor alpha / genetics. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / genetics. Estrogen Receptor beta / metabolism. Flutamide / pharmacology. Gene Expression Regulation / drug effects. Humans. Male. Mice. Pituitary Gland / chemistry. Prostate / drug effects. Prostate / metabolism. Prostate / pathology. RNA, Messenger / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism

  • MedlinePlus Health Information. consumer health - Arsenic.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. ARSENIC, ELEMENTAL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocr Relat Cancer. 1999 Jun;6(2):131-7 [10731101.001]
  • [Cites] Prostate. 1999 Dec 1;41(4):263-74 [10544300.001]
  • [Cites] Rev Environ Contam Toxicol. 2001;169:165-214 [11330077.001]
  • [Cites] Am J Pathol. 2001 Jul;159(1):79-92 [11438457.001]
  • [Cites] J Natl Cancer Inst. 2001 Nov 21;93(22):1687-97 [11717329.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1008-13 [11861374.001]
  • [Cites] Prostate. 2002 Mar 1;50(4):222-35 [11870800.001]
  • [Cites] Endocrinology. 1988 Feb;122(2):552-62 [2828003.001]
  • [Cites] Cancer Res. 1990 Sep 1;50(17):5470-4 [2386951.001]
  • [Cites] Prostate. 1992;21(4):309-14 [1281323.001]
  • [Cites] Oncology. 1993 Jul-Aug;50(4):259-63 [7684519.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5474-8 [7522959.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):401-6 [7795646.001]
  • [Cites] J Steroid Biochem Mol Biol. 1995 Dec;55(3-4):375-83 [8541234.001]
  • [Cites] Cancer Lett. 1996 Apr 19;102(1-2):167-72 [8603365.001]
  • [Cites] J Natl Cancer Inst. 1996 Jul 3;88(13):908-17 [8656443.001]
  • [Cites] J Steroid Biochem Mol Biol. 1996 May;58(2):195-205 [8809201.001]
  • [Cites] Prostate. 1996 Oct;29(4):261-7 [8876709.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):314-9 [9000575.001]
  • [Cites] J Mol Endocrinol. 1997 Jun;18(3):203-11 [9195474.001]
  • [Cites] Carcinogenesis. 1997 Jun;18(6):1215-23 [9214605.001]
  • [Cites] Carcinogenesis. 1997 Jun;18(6):1225-31 [9214606.001]
  • [Cites] Cancer Detect Prev. 1998;22(5):476-84 [9727630.001]
  • [Cites] Clin Cancer Res. 1996 Feb;2(2):277-85 [9816170.001]
  • [Cites] Environ Health Perspect. 1999 May;107(5):359-65 [10210691.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5458-63 [10318905.001]
  • [Cites] Cancer Res. 1999 Jun 1;59(11):2511-5 [10363963.001]
  • [Cites] Endocrinology. 1999 Jul;140(7):3282-91 [10385425.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 Nov;92(4):297-305 [15663993.001]
  • [Cites] Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 [16039940.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1370-6 [11888907.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Endocr Relat Cancer. 2002 Mar;9(1):61-73 [11914183.001]
  • [Cites] Mol Cell Endocrinol. 2002 Jul 31;193(1-2):1-5 [12160995.001]
  • [Cites] J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483.001]
  • [Cites] Am J Pathol. 2003 Jan;162(1):233-41 [12507906.001]
  • [Cites] Prostate. 2003 May 15;55(3):180-6 [12692783.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1975-80 [12702591.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1981-9 [12702592.001]
  • [Cites] Endocr Relat Cancer. 2003 Jun;10(2):209-16 [12790784.001]
  • [Cites] J Urol. 2003 Nov;170(5):2019-25 [14532845.001]
  • [Cites] J Cell Biochem. 2004 Jan 1;91(1):13-25 [14689577.001]
  • [Cites] Carcinogenesis. 2004 Jan;25(1):133-41 [14514661.001]
  • [Cites] Urology. 2003 Dec 22;62(6 Suppl 1):3-12 [14706503.001]
  • [Cites] J Cell Biochem. 2004 Feb 15;91(3):483-90 [14755679.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 Jan;88(1):1-16 [15026079.001]
  • [Cites] Lancet Oncol. 2004 May;5(5):303-13 [15120667.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Aug 1;198(3):394-404 [15276419.001]
  • [Cites] Urology. 2004 Oct;64(4):814-20 [15491740.001]
  • [Cites] Clin Cancer Res. 1999 Oct;5(10):2891-8 [10537358.001]
  • [Cites] Prostate. 1999 Dec 1;41(4):224-32 [10544295.001]
  • [Cites] J Natl Cancer Inst Monogr. 2000;(27):39-66 [10963619.001]
  • (PMID = 16140617.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone; 4TI98Z838E / Estradiol; 62229-50-9 / Epidermal Growth Factor; 76W6J0943E / Flutamide; N712M78A8G / Arsenic
  • [Other-IDs] NLM/ PMC1280391
  •  go-up   go-down


37. Grosjean-Raillard J, Tailler M, Adès L, Perfettini JL, Fabre C, Braun T, De Botton S, Fenaux P, Kroemer G: ATM mediates constitutive NF-kappaB activation in high-risk myelodysplastic syndrome and acute myeloid leukemia. Oncogene; 2009 Feb 26;28(8):1099-109
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here, we show that an MDS/AML model cell line exhibits a constitutive interaction, within the nucleus, of activated, S1981-phosphorylated ataxia telangiectasia mutated (ATM) with NEMO.
  • Inhibition of ATM with two distinct pharmacological inhibitors suppressed the activating autophosphorylation of ATM, blocked the interaction of ATM and NEMO, delocalized NEMO as well as another putative NF-kappaB activator, PIDD, from the nucleus, abolished the activating phosphorylation of the catalytic proteins of the IKK complex (IKK1/2 on serines 176/180), enhanced the expression of I kappaB alpha and caused the relocalization of NF-kappaB from the nucleus to the cytoplasm, followed by apoptosis.
  • Pharmacological inhibition of ATM also induced the nucleocytoplasmic relocalization of p65 in malignant myeloblasts purified from patients with high-risk MDS or AML, correlating with the induction of apoptosis.
  • [MeSH-major] Apoptosis / physiology. Cell Cycle Proteins / metabolism. DNA-Binding Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. NF-kappa B / metabolism. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Adult. Aged. Aged, 80 and over. Ataxia Telangiectasia Mutated Proteins. Bone Marrow Cells. Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Nucleus / metabolism. Cytoplasm / metabolism. DNA Damage. Death Domain Receptor Signaling Adaptor Proteins. Electrophoretic Mobility Shift Assay. Fluorescent Antibody Technique. Humans. I-kappa B Kinase / genetics. I-kappa B Kinase / metabolism. Middle Aged. Phosphorylation. Protein Transport. Risk Factors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism. Tumor Cells, Cultured


38. Ide T, Kitajima Y, Miyoshi A, Ohtsuka T, Mitsuno M, Ohtaka K, Koga Y, Miyazaki K: Tumor-stromal cell interaction under hypoxia increases the invasiveness of pancreatic cancer cells through the hepatocyte growth factor/c-Met pathway. Int J Cancer; 2006 Dec 15;119(12):2750-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-stromal cell interaction under hypoxia increases the invasiveness of pancreatic cancer cells through the hepatocyte growth factor/c-Met pathway.
  • The hypoxic environment in tumor is reported to play an important role in pancreatic cancer progression.
  • The interaction between stromal and cancer cells also contributes to the malignant behavior of pancreatic cancer.
  • In the present study, we investigated whether hypoxic stimulation affects stromal as well as pancreatic cancer cells.
  • Our findings demonstrated that hypoxia remarkably elevated the HIF-1alpha expression in both pancreatic cancer (PK8) and fibroblast cells (MRC5).
  • Hypoxic stimulation also increased the hepatocyte growth factor (HGF) secretion from MRC5 cells, which led to an elevation of c-Met phosphorylation in PK8 cells.
  • In immunohistochemical study, the HIF-1alpha expression was observed in surrounding stromal as well as pancreatic cancer cells, thus indicating hypoxia exists in both of cancer and stromal cells.
  • These results indicate that the hypoxic environment within stromal as well as cancer cells activates the HGF/c-Met system, thereby contributing to the aggressive invasive features of pancreatic cancer.
  • [MeSH-major] Cell Communication / physiology. Hepatocyte Growth Factor / genetics. Proto-Oncogene Proteins c-met / genetics. Stromal Cells / metabolism
  • [MeSH-minor] Blotting, Western. Cell Hypoxia / physiology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Cell Proliferation / drug effects. Culture Media, Conditioned / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Fibroblasts / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinases / genetics. Matrix Metalloproteinases / metabolism. Neoplasm Invasiveness. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Signal Transduction / physiology. Time Factors. Tissue Inhibitor of Metalloproteinases / genetics. Tissue Inhibitor of Metalloproteinases / metabolism

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16998831.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinases; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2
  •  go-up   go-down


39. Hiraga T, Kizaka-Kondoh S, Hirota K, Hiraoka M, Yoneda T: Hypoxia and hypoxia-inducible factor-1 expression enhance osteolytic bone metastases of breast cancer. Cancer Res; 2007 May 1;67(9):4157-63
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypoxia is a common feature of solid tumors and is associated with their malignant phenotype.
  • The transcription factor hypoxia-inducible factor-1 (HIF-1) is a major regulator of adaptation to hypoxia and is implicated in the malignant progression of cancers.
  • TOP3 selectively induced apoptosis in hypoxic tumor cells in vitro and significantly reduced bone metastases in vivo.
  • Hypoxia and CA-HIF overexpression markedly inhibited osteoblastic differentiation, whereas hypoxia increased osteoclast-like cell formation.
  • In conclusion, these results suggest that tumor-associated hypoxia and HIF-1 expression promote the progression of bone metastases in breast cancer.
  • [MeSH-major] Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Cell Hypoxia / physiology. Cell Line, Tumor. Female. Humans. Indazoles / pharmacology. Mice. Mice, Inbred C3H. Mice, Nude. Recombinant Fusion Proteins / metabolism. Recombinant Fusion Proteins / pharmacology. Transfection

  • Genetic Alliance. consumer health - Bone Cancer.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17483326.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Indazoles; 0 / Recombinant Fusion Proteins; 0 / TOP3 fusion protein; 154453-18-6 / 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


40. Abdou AG, Aiad HA, Sultan SM: pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor status. APMIS; 2008 Nov;116(11):961-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor status.
  • It is also considered to be one of the major estrogen-regulated proteins and an indicator of estrogen receptor (ER) functionality. pS2 has previously been investigated in benign and malignant prostate lesions with little information about its relationship to steroid receptor status.
  • Our purpose was to correlate pS2 expression with steroid receptor status (ER alpha and progesterone receptor (PR)) and other pathologic variables in prostate carcinoma.
  • 15 benign prostate hyperplasia (BPH) and 47 prostate carcinoma cases were investigated by means of immunohistochemistry for pS2, ER and PR expression.
  • 80% of BPH showed pS2 cytoplasmic immunoreactivity in hyperplastic acini and about half of these cases also exhibited nuclear staining decorating basal or both basal and luminal nuclei. pS2 was highly expressed in prostate carcinoma (91.4%) with both cytoplasmic and nuclear patterns of staining.
  • The latter pattern was significantly associated with carcinoma having a low Gleason score (p=0.02).
  • The diagnostic value of pS2 expression in prostate carcinoma validated 74.19% accuracy, 91.48% sensitivity and 78.18% positive predictive value.
  • The high sensitivity of pS2 expression in prostate carcinoma could make it a suitable marker for diagnosis of prostate carcinoma, especially in metastatic cases of unknown origin.
  • The absence of correlation and dissimilarity in immunolocalization between pS2 and ER alpha leads to the assumption that ER alpha could not be the regulatory protein for pS2 and may raise questions about the functionality of ER alpha in prostate.
  • The nuclear pattern of pS2 immunoreactivity either in benign or malignant prostatic lesions is similar to the published data on ER beta distribution and could also identify a subset of carcinoma patients with a favorable prognosis.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Carcinoma / pathology. Estrogen Receptor alpha / metabolism. Presenilin-2 / biosynthesis. Prostate / pathology. Prostatic Neoplasms / pathology. Receptors, Progesterone / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cytoplasm / metabolism. Estrogens / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19132993.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / PSEN2 protein, human; 0 / Presenilin-2; 0 / Receptors, Progesterone
  •  go-up   go-down


41. Li SH, Ryu JH, Park SE, Cho YS, Park JW, Lee WJ, Chun YS: Vitamin C supplementation prevents testosterone-induced hyperplasia of rat prostate by down-regulating HIF-1alpha. J Nutr Biochem; 2010 Sep;21(9):801-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To alleviate BPH symptoms or to find a cure for this disease, key molecules should be identified that control prostate cell proliferation.
  • Recently, HIF-1alpha has attracted attention in this context, because it is highly expressed in hyperplasic prostates and prevents prostate cell death.
  • Thus, given that vitamin C inhibits HIF-1alpha expression in several malignant tumors, we examined its therapeutic potential in BPH.
  • Moreover, vitamin C treatment abolished cell proliferation induced by testosterone treatment to the control level.
  • [MeSH-major] Ascorbic Acid / therapeutic use. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Prostatic Hyperplasia / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Down-Regulation. Humans. Male. Prostate / drug effects. Prostate / metabolism. Rats. Rats, Sprague-Dawley. Testosterone / antagonists & inhibitors. Testosterone / pharmacology. Vascular Endothelial Growth Factor A / biosynthesis

  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • MedlinePlus Health Information. consumer health - Vitamin C.
  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19716283.001).
  • [ISSN] 1873-4847
  • [Journal-full-title] The Journal of nutritional biochemistry
  • [ISO-abbreviation] J. Nutr. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 3XMK78S47O / Testosterone; PQ6CK8PD0R / Ascorbic Acid
  •  go-up   go-down


42. Esheba GE, Pate LL, Longacre TA: Oncofetal protein glypican-3 distinguishes yolk sac tumor from clear cell carcinoma of the ovary. Am J Surg Pathol; 2008 Apr;32(4):600-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncofetal protein glypican-3 distinguishes yolk sac tumor from clear cell carcinoma of the ovary.
  • Clear cell carcinoma (CCC) of the ovary is the surface epithelial neoplasm most often confused with primitive germ cell tumors, particularly yolk sac tumor (YST) and dysgerminoma.
  • Recent studies suggest that glypican-3 (GPC3), an oncofetal protein expressed in fetal liver and malignant tumors of hepatocytic lineage, is also expressed in germ cell tumors, particularly YST.
  • To investigate whether GPC3 is useful in distinguishing YST from ovarian CCC, we studied the expression of GPC3 in a large series of ovarian neoplasms and compared it to the expression profiles of CK7 and alpha-fetoprotein.
  • Tissue microarrays containing over 400 benign and malignant ovarian neoplasms, including 34 CCCs were stained with monoclonal GPC3 (clone 1G12, Biomosaics, Burlington, VT).
  • These arrays contained a wide assortment of ovarian surface epithelial neoplasms and sex cord stromal neoplasms, as well as germ cell tumors.
  • All but one YST (97%), including those associated with mixed germ cell tumor were positive for GPC3, whereas all teratomas and embryonal carcinomas were negative.
  • The syncytiotrophoblastic cells in the germ cell tumors and placental villi included in the arrays were also positive for GPC3.
  • Because GPC3 may be associated with alpha-fetoprotein expression, further studies are required to determine the utility of GPC3 in differentiating YST from CCC with hepatoid differentiation.
  • [MeSH-major] Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Carcinoma / chemistry. Endodermal Sinus Tumor / chemistry. Glypicans / analysis. Ovarian Neoplasms / chemistry
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Immunohistochemistry. Keratin-7 / analysis. Predictive Value of Tests. Sensitivity and Specificity. Tissue Array Analysis. alpha-Fetoproteins / analysis

  • Genetic Alliance. consumer health - Yolk sac tumor.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18277882.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / GPC3 protein, human; 0 / Glypicans; 0 / KRT7 protein, human; 0 / Keratin-7; 0 / alpha-Fetoproteins; 0 / oncofetal antigens
  •  go-up   go-down


43. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Glucagonoma.
  • Hazardous Substances Data Bank. GLUCAGON .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


44. Schnater JM, Bruder E, Bertschin S, Woodtli T, de Theije C, Pietsch T, Aronson DC, von Schweinitz D, Lamers WH, Köhler ES: Subcutaneous and intrahepatic growth of human hepatoblastoma in immunodeficient mice. J Hepatol; 2006 Sep;45(3):377-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND/AIMS: Hepatoblastoma is the most frequent malignant pediatric liver tumor.
  • METHODS: The alpha-fetoprotein-expressing hepatoblastoma-cell lines HepT1, HuH6 and the childhood hepatocellular carcinoma-cell line HepG2 were injected subcutaneously and intrasplenically into NMRI nu/nu mice.
  • Tumor growth was monitored by measuring tumor size for subcutaneous and serum human alpha-fetoprotein levels for intra-abdominal tumors.
  • RESULTS: Subcutaneous tumor growth occurred in 70% (7/10) of mice injected with HuH6 and 50% (5/10) of mice injected with HepG2.
  • Accumulation of serum alpha-fetoprotein reflected tumor growth.
  • Growth pattern and alpha-fetoprotein production were similar at the subcutaneous and intra-abdominal location.
  • CONCLUSIONS: We established an intrahepatic mouse model for human hepatoblastoma, in which tumor growth could be monitored by serum alpha-fetoprotein levels.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Hepatoblastoma / pathology. Liver Neoplasms / pathology. Neoplasm Invasiveness / pathology. Neoplasm Transplantation / pathology
  • [MeSH-minor] Animals. Biomarkers, Tumor / blood. Carcinoma, Hepatocellular / blood. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Humans. Mice. Mice, Nude. Neoplasm Metastasis / pathology. Neoplasms, Experimental / pathology. Splenic Neoplasms / pathology. alpha-Fetoproteins / analysis

  • Genetic Alliance. consumer health - Hepatoblastoma.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16780998.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
  •  go-up   go-down


45. Zhang Y, Zhang Y: Growth inhibition of insulin-like growth factor I receptor monoclonal antibody to human colorectal cancer cells. Cancer Invest; 2008 Apr-May;26(3):230-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: Insulin-like growth factors (IGFs) and their receptors play a critical role in the growth and regulation of many type of malignant cells.
  • The purpose of this study was to clarify the expression of Insulin-like growth factor I receptor (IGF-IR) in a human colorectal cancer cell line HT-29 and investigate the effects of 2 IGF-IR monoclonal antibodies (Mab) on the biological behavior of HT-29 cell line.
  • METHODS: Immunohistochemistry was used to test the expression of IGF-IR in HT-29 cell line, MTT assay was used to determine the antiproliferation effects of 2 kinds of IGF-IR monoclonal antibody on HT-29 cells.
  • The effects of apoptosis rate and cell cycle of HT-29 cells were estimated by flow cytometry (FCM).
  • RESULTS: IGF-IR was expressed in the membranes of HT-29 cell line; MTT results show that each IGF-IR (alpha-Subunit)Ab-3 Mab group has remarkable difference (p < 0.01) as compared with control group, each IGF-IRalpha(1H7)L Mab group has no remarkable difference (p > 0.05) as compared with control group, each IGF-IRalpha(1H7)L Mab group has light antiproliferation effect on the HT-29 cells.
  • IGF-IR(alpha-Subunit)Ab-3 has stronger antiproliferation effect on the HT-29 cells and dose-depended growth inhibition effects were observed when concentration is less than 1.5 ug/ml;The 2 kinds of IGF-IR monoclonal antibody can arrest the cell cycle at any phase of HT-29 cells and induce apoptosis.
  • Under the incubating conditions of containing 5 percent fetal bovine serum (FCS) and no FCS, the apoptosis percentage of IGF-IR(alpha-Subunit)Ab-3 group and IGF-IRalpha(1H7)L group have obviously increased (p < 0.01).
  • After the number of cells was increased 30 times, the apoptosis percentage of IGF-IR(alpha-Subunit)Ab-3 group and IGF-IRalpha(1H7)L group have no remarkable differences as compared with control group (p > 0.05).
  • CONCLUSIONS: Blockade of the IGF-IR with IGF-IR Mab inhibiting proliferation, arresting cell cycle and inducing apoptosis of HT-29 cells may represent a valid approach to inhibit tumor growth.
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Flow Cytometry. HT29 Cells. Humans. Immunohistochemistry

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18317963.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.1 / Receptor, IGF Type 1
  •  go-up   go-down


46. Boggess JF, Zhou C, Bae-Jump VL, Gehrig PA, Whang YE: Estrogen-receptor-dependent regulation of telomerase activity in human endometrial cancer cell lines. Gynecol Oncol; 2006 Nov;103(2):417-24
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estrogen-receptor-dependent regulation of telomerase activity in human endometrial cancer cell lines.
  • METHODS: ER-positive and ER-negative endometrial cancer cell lines were used.
  • ER alpha expression was reconstituted in ER-negative cell lines by transient transfection.
  • RESULTS: E2 induced both hTERT gene transcription and telomerase activity in the ER-positive cell lines, but not in the ER-negative cell lines.
  • Transfection of ER alpha into ER-negative cell lines restored E2-induced hTERT gene transcription and telomerase activity.
  • Gel shift assays revealed two EREs in the hTERT promoter that specifically bind to ER alpha.
  • Luciferase assays demonstrated that at least the proximal ERE is responsible for transcriptional activation by ligand-stimulated ER alpha.
  • CONCLUSIONS: Telomerase activity and hTERT mRNA were increased in response to estrogen in an ER alpha-dependent fashion in endometrial cancer cells.
  • Binding of complexed estrogen with ER alpha to the EREs found within the hTERT promoter suggests a possible mechanism for telomerase induction that may facilitate the malignant transformation of hormone-dependent endometrial cells.
  • [MeSH-major] Endometrial Neoplasms / enzymology. Estrogen Receptor alpha / physiology. Telomerase / metabolism
  • [MeSH-minor] Cell Line, Tumor. Estradiol / pharmacology. Female. Humans. Promoter Regions, Genetic. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Response Elements. Transcription, Genetic. Transfection

  • Genetic Alliance. consumer health - Endometrial cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16690106.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5K08CA085772
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / RNA, Messenger; 4TI98Z838E / Estradiol; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  •  go-up   go-down


47. Han CY, Lim SC, Choi HS, Kang KW: Induction of ErbB2 by ultraviolet A irradiation: potential role in malignant transformation of keratinocytes. Cancer Sci; 2008 Mar;99(3):502-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of ErbB2 by ultraviolet A irradiation: potential role in malignant transformation of keratinocytes.
  • Exposure of keratinocytes to UVA has previously been reported to lead to the activation of a variety of epidermal growth factor receptors (EGFR), including ErbB2, and ErbB2 activation is involved in skin tumor development.
  • UVA irradiation also selectively increased the levels of activator protein (AP)-2 alpha, but not AP-2 beta and AP-2 gamma.
  • Inhibition of cAMP-dependent protein kinase caused complete blockage of ErbB2 induction and AP-2 alpha activation by UVA irradiation.
  • These results support the hypothesis that UVA enhances the expression of ErbB2 via cAMP- and protein kinase-dependent AP-2 alpha activation in keratinocytes, which may serve as a key mechanistic basis for the malignant transformation of keratinocytes exposed to UVA irradiation.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Keratinocytes / metabolism. Keratinocytes / radiation effects. Receptor, ErbB-2 / metabolism. Ultraviolet Rays
  • [MeSH-minor] Animals. Cyclic AMP-Dependent Protein Kinases / metabolism. Humans. Immunohistochemistry. Mice. Mice, Hairless. Signal Transduction. Skin Neoplasms / metabolism. Transcription Factor AP-2 / metabolism. Tumor Cells, Cultured

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18177484.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transcription Factor AP-2; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  •  go-up   go-down


48. Meager A: Measurement of cytokines by bioassays: theory and application. Methods; 2006 Apr;38(4):237-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A large number of cytokines have been characterized, of which several have proved successful in the clinic as biotherapeutic agents for malignant, infectious or autoimmune diseases.
  • Since cytokines exert various biological activities in vitro, cultured cell line-based bioassay methods have mainly been developed to quantify potency.
  • Thus, measurement of potency of a particular cytokine must be made relative to a common, stable, reference preparation of the same cytokine to permit valid inter-assay and inter-laboratory comparisons.
  • More extensive details for the potency determinations of tumor necrosis factor-alpha (TNF-alpha), related cytokines, and biotherapeutic anti-TNF-alpha products are provided.
  • [MeSH-minor] Animals. Calibration. Humans. Quality Control. Reference Standards. Reproducibility of Results. Tumor Necrosis Factor-alpha / metabolism

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16481200.001).
  • [ISSN] 1046-2023
  • [Journal-full-title] Methods (San Diego, Calif.)
  • [ISO-abbreviation] Methods
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 117
  •  go-up   go-down


49. Yasuda M, Matsubara J, Yamasaki H, Fujita Y, Konishi H, Koinuma S, Taketani S, Horiuchi Y, Utsumi H, Yasuda Y: Death-resistant and nonresistant malignant human cell lines under anoxia in vitro. Int J Clin Oncol; 2007 Dec;12(6):455-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Death-resistant and nonresistant malignant human cell lines under anoxia in vitro.
  • We previously demonstrated that 24 malignant human cell lines expressed erythropoietin and its receptor and that erythropoietin secretion was enhanced under anoxia.
  • In this study, we examined the viability of 22 of these cell lines excluding two leukemia cell lines under anoxia.
  • METHODS: Twenty-two cancer cell lines of various origins were cultured under anoxia or normoxia for 4 days, and their viability was examined at 1-day intervals.
  • RESULTS: Eleven of the 22 cancer cell lines examined showed 80% to 100% cell viability after 4 days under anoxia; 2 cell lines showed similar viability for 3 days, 3 cell lines showed similar viability for 2 days, and 6 cell lines showed similar viability for 1 day or less.
  • These 11 death-resistant cell lines, which secrete various amounts of erythropoietin under anoxia, produced significantly more lactate during 2 days under anoxia than under normoxia, with ATP levels about 60% of those before anoxia.
  • However, the nonresistant cell lines responded to anoxia by yielding significantly more lactate without a reduction of the ATP level.
  • CONCLUSION: The majority of the cancer cell lines examined survived under anoxia in vitro, through the Pasteur effect, in a dormant state without direct support of erythropoietin.
  • [MeSH-major] Cell Line, Tumor. Hypoxia / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • [MeSH-minor] Blotting, Western. Cell Survival / physiology. Erythropoietin / physiology. Gene Expression. Gene Expression Regulation, Neoplastic / physiology. Genes, bcl-2 / genetics. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Physiol Rev. 1996 Jul;76(3):839-85 [8757790.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2002 Nov;283(5):L922-31 [12376345.001]
  • [Cites] Trends Cell Biol. 2000 Sep;10(9):369-77 [10932094.001]
  • [Cites] Nat Med. 1997 Feb;3(2):177-82 [9018236.001]
  • [Cites] J Lab Clin Med. 1998 Mar;131(3):207-14 [9523843.001]
  • [Cites] J Biol Chem. 1991 Aug 25;266(24):15563-6 [1874713.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Jan;2(1):63-7 [11413467.001]
  • [Cites] Nature. 1996 Jan 4;379(6560):88-91 [8538748.001]
  • [Cites] Curr Opin Genet Dev. 1995 Feb;5(1):97-104 [7749333.001]
  • [Cites] Am J Physiol. 1996 Oct;271(4 Pt 1):C1172-80 [8897823.001]
  • [Cites] J Biol Chem. 1996 Dec 13;271(50):32253-9 [8943284.001]
  • [Cites] J Cell Biol. 1994 Jan;124(1-2):1-6 [8294493.001]
  • [Cites] J Biol Chem. 1997 Apr 25;272(17 ):11205-14 [9111021.001]
  • [Cites] Cell. 1993 Sep 10;74(5):777-9 [8104100.001]
  • [Cites] Carcinogenesis. 2003 Jun;24(6):1021-9 [12807756.001]
  • [Cites] Genes Dev. 1998 Jan 15;12(2):149-62 [9436976.001]
  • [Cites] Mol Cell. 2000 Jul;6(1):53-63 [10949027.001]
  • [Cites] Cell Mol Biol Res. 1994;40(1):35-9 [7528597.001]
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4010-5 [10945599.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8104-9 [9223322.001]
  • [Cites] Trends Biochem Sci. 1999 Feb;24(2):68-72 [10098401.001]
  • [Cites] J Biol Chem. 1997 Sep 5;272(36):22642-7 [9278421.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5680-4 [2062846.001]
  • [Cites] EMBO J. 2006 Mar 8;25(5):1114-25 [16467844.001]
  • [Cites] Cell. 1993 Aug 27;74(4):609-19 [8358790.001]
  • [Cites] Exp Cell Res. 1958 Aug;15(1):112-7 [13574164.001]
  • [Cites] Mol Cell Biol. 2001 May;21(10):3436-44 [11313469.001]
  • [Cites] Nature. 1998 Jul 30;394(6692):485-90 [9697772.001]
  • (PMID = 18071865.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 11096-26-7 / Erythropoietin
  •  go-up   go-down


50. Katsoulidis E, Mavrommatis E, Woodard J, Shields MA, Sassano A, Carayol N, Sawicki KT, Munshi HG, Platanias LC: Role of interferon {alpha} (IFN{alpha})-inducible Schlafen-5 in regulation of anchorage-independent growth and invasion of malignant melanoma cells. J Biol Chem; 2010 Dec 17;285(51):40333-41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of interferon {alpha} (IFN{alpha})-inducible Schlafen-5 in regulation of anchorage-independent growth and invasion of malignant melanoma cells.
  • IFNα exerts potent inhibitory activities against malignant melanoma cells in vitro and in vivo, but the mechanisms by which it generates its antitumor effects remain unknown.
  • We examined the effects of interferon α (IFNα) on the expression of human members of the Schlafen (SLFN) family of genes, a group of cell cycle regulators that mediate growth-inhibitory responses.
  • Using quantitative RT-real time PCR, we found detectable basal expression of all the different human SLFN genes examined (SLFN5, SLFN11, SLFN12, SLFN13, and SLFN14), in malignant melanoma cells and primary normal human melanocytes, but SLFN5 basal expression was suppressed in all analyzed melanoma cell lines.
  • Treatment of melanoma cells with IFNα resulted in induction of expression of SLFN5 in malignant cells, suggesting a potential involvement of this gene in the antitumor effects of IFNα.
  • Importantly, stable knockdown of SLFN5 in malignant melanoma cells resulted in increased anchorage-independent growth, as evidenced by enhanced colony formation in soft agar assays.
  • Altogether, our findings suggest an important role for the SLFN family of proteins in the generation of the anti-melanoma effects of IFNα and for the first time directly implicate a member of the human SLFN family in the regulation of cell invasion.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Gene Expression Regulation, Neoplastic / drug effects. Immunologic Factors / pharmacology. Interferon-alpha / pharmacology. Melanocytes / metabolism. Melanoma / metabolism
  • [MeSH-minor] Cell Line, Tumor. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Humans. Neoplasm Invasiveness

  • MedlinePlus Health Information. consumer health - Melanoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Interferon Cytokine Res. 2005 Dec;25(12):749-56 [16375603.001]
  • [Cites] J Biol Chem. 1999 Oct 15;274(42):30127-31 [10514501.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6763-71 [16818652.001]
  • [Cites] N Engl J Med. 2006 Jul 6;355(1):51-65 [16822996.001]
  • [Cites] J Biol Chem. 2006 Aug 11;281(32):22446-52 [16762916.001]
  • [Cites] Immunity. 2006 Sep;25(3):361-72 [16979568.001]
  • [Cites] J Biol Chem. 2007 Jan 19;282(3):1757-68 [17114181.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1373-80 [17062732.001]
  • [Cites] Mol Immunol. 2007 Jul;44(13):3273-82 [17434208.001]
  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):5010-9 [17785551.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 25;105(12):4808-13 [18339807.001]
  • [Cites] Biochem Biophys Res Commun. 2008 May 23;370(1):62-6 [18355440.001]
  • [Cites] Biochem J. 2008 Jul 15;413(2):239-50 [18373498.001]
  • [Cites] J Cell Biol. 2009 Feb 9;184(3):399-408 [19188491.001]
  • [Cites] Nat Rev Cancer. 2009 Apr;9(4):253-64 [19242414.001]
  • [Cites] J Biol Chem. 2009 Apr 17;284(16):10301-14 [19211565.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12097-102 [19574459.001]
  • [Cites] Gene. 2009 Nov 1;447(1):1-11 [19619625.001]
  • [Cites] J Biol Chem. 2009 Sep 11;284(37):25051-64 [19592487.001]
  • [Cites] Biochem Biophys Res Commun. 2009 Oct 30;388(4):752-6 [19703412.001]
  • [Cites] Nat Immunol. 2010 Apr;11(4):335-43 [20190759.001]
  • [Cites] Nat Immunol. 2010 Apr;11(4):281-2 [20300134.001]
  • [Cites] J Clin Oncol. 1996 Jan;14(1):7-17 [8558223.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2390-7 [9036989.001]
  • [Cites] J Biol Chem. 1997 Nov 7;272(45):28779-85 [9353349.001]
  • [Cites] Annu Rev Biochem. 1998;67:227-64 [9759489.001]
  • [Cites] Immunity. 1998 Nov;9(5):657-68 [9846487.001]
  • [Cites] J Biol Chem. 2000 Sep 8;275(36):27634-40 [10878008.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2370-80 [11331315.001]
  • [Cites] Br J Cancer. 2001 Jul 6;85(1):107-14 [11437411.001]
  • [Cites] J Biol Chem. 2001 Jul 27;276(30):28570-7 [11353767.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):7726-35 [11773065.001]
  • [Cites] J Biol Chem. 2002 Apr 26;277(17):14408-16 [11839738.001]
  • [Cites] Nat Rev Immunol. 2002 Sep;2(9):675-87 [12209136.001]
  • [Cites] Genes Dev. 2003 Feb 15;17(4):455-60 [12600939.001]
  • [Cites] J Biol Chem. 2003 May 9;278(19):16608-13 [12582176.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):267-73 [12817007.001]
  • [Cites] J Biol Chem. 2003 Jul 25;278(30):27772-80 [12759354.001]
  • [Cites] Curr Opin Oncol. 2003 Nov;15(6):431-9 [14624225.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14742-7 [14645718.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):53-61 [14665609.001]
  • [Cites] Exp Cell Res. 2004 Apr 15;295(1):173-82 [15051500.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):24152-62 [15056668.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 29;101(26):9578-83 [15210966.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):30358-68 [15123634.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):29911-20 [15150272.001]
  • [Cites] Int Immunol. 2004 Oct;16(10):1535-48 [15351786.001]
  • [Cites] J Biol Chem. 2004 Sep 24;279(39):40362-7 [15194680.001]
  • [Cites] Science. 1977 Jul 29;197(4302):461-3 [560061.001]
  • [Cites] Annu Rev Biochem. 1987;56:727-77 [2441659.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11455-9 [1837150.001]
  • [Cites] Science. 1994 Jun 3;264(5164):1415-21 [8197455.001]
  • [Cites] J Immunol. 1995 Mar 1;154(5):2248-56 [7532663.001]
  • [Cites] J Clin Oncol. 2000 Jun;18(12):2444-58 [10856105.001]
  • [Cites] Science. 1995 Sep 22;269(5231):1721-3 [7569900.001]
  • [Cites] Nat Med. 2004 Dec;10(12):1374-8 [15531891.001]
  • [Cites] Exp Hematol. 2005 May;33(5):550-7 [15850832.001]
  • [Cites] Nat Rev Immunol. 2005 May;5(5):375-86 [15864272.001]
  • [Cites] J Biol Chem. 2005 Sep 2;280(35):30723-34 [15946944.001]
  • [Cites] Genetics. 2006 Jan;172(1):411-23 [16172501.001]
  • (PMID = 20956525.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA121192; United States / NCI NIH HHS / CA / R01 CA077816; United States / PHS HHS / / C100579; United States / NCI NIH HHS / CA / R01 CA126888-03; United States / NCI NIH HHS / CA / CA77816; United States / NCI NIH HHS / CA / R01 CA126888; United States / NCI NIH HHS / CA / P30 CA060553; United States / NCI NIH HHS / CA / CA126888; United States / NCI NIH HHS / CA / CA121192
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / schlafen-5 protein, human
  • [Other-IDs] NLM/ PMC3001013
  •  go-up   go-down


51. Yaskiv O, Cao D, Humphrey PA: Microcystic adenocarcinoma of the prostate: a variant of pseudohyperplastic and atrophic patterns. Am J Surg Pathol; 2010 Apr;34(4):556-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Limited data exist on the pathologic attributes of microcystic change in malignant prostatic glands.
  • This alteration was defined as cystic dilatation and rounded expansion of the malignant gland profile, with a flat luminal cell lining layer.
  • The greatest diameter of the dilated cancer glands was 0.4 to 0.9 mm, with a mean diameter 10-fold greater than adjacent small malignant glands.
  • Gleason grade 3 was the predominant grade of the adjacent nonmicrocystic malignant glands.
  • Ninety-six percent of the microcystic cases showed alpha-methylacyl CoA racemase overexpression and all cases showed complete basal cell loss (using 34betaE12 and p63 antibodies) in immunohistochemistry.
  • Detection of intraluminal crystalloids or wispy blue mucin at low magnification, immunostains for alpha-methylacyl CoA racemase, and basal cells, and a search for adjacent usual small acinar adenocarcinoma are helpful diagnostic aids.
  • Diagnostic awareness of this growth pattern of prostatic carcinoma is important to avoid underdiagnosis of adenocarcinoma of the prostate.
  • [MeSH-minor] Atrophy. Biomarkers, Tumor / metabolism. Cysts / enzymology. Cysts / pathology. Humans. Male. Prostatectomy. Racemases and Epimerases / metabolism

  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20216381.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  •  go-up   go-down


52. Yin D, Ogawa S, Kawamata N, Tunici P, Finocchiaro G, Eoli M, Ruckert C, Huynh T, Liu G, Kato M, Sanada M, Jauch A, Dugas M, Black KL, Koeffler HP: High-resolution genomic copy number profiling of glioblastoma multiforme by single nucleotide polymorphism DNA microarray. Mol Cancer Res; 2009 May;7(5):665-77
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Glioblastoma multiforme (GBM) is an extremely malignant brain tumor.
  • To identify new genomic alterations in GBM, genomic DNA of tumor tissue/explants from 55 individuals and 6 GBM cell lines were examined using single nucleotide polymorphism DNA microarray (SNP-Chip).
  • The phosphoinositide 3-kinase pathway was altered in 71% (39 of 55) GBMs either by deletion of PTEN or amplification of epidermal growth factor receptor and/or vascular endothelial growth factor receptor/platelet-derived growth factor receptor alpha.
  • Notably, three samples had homozygous deletion encompassing this site.
  • Also, a novel internal deletion of a putative tumor suppressor gene, LRP1B, was discovered causing an aberrant protein.
  • AUPDs occurred in 58% (32 of 55) of the GBM samples and five of six GBM cell lines.
  • A common AUPD was found at chromosome 17p13.3-12 (included p53 gene) in 13 of 61 samples and cell lines.
  • [MeSH-minor] Adolescent. Adult. Aged. Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Female. Gene Amplification. Humans. Loss of Heterozygosity. Male. Middle Aged. Models, Biological. Molecular Sequence Data. Polymorphism, Single-Stranded Conformational. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Sequence Deletion. Signal Transduction / genetics. Signal Transduction / physiology. Uniparental Disomy. Young Adult


53. Kristiansen G: [Immunohistochemical algorithms in prostate diagnostics: what's new?]. Pathologe; 2009 Dec;30 Suppl 2:146-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In particular the use of basal cell markers can be useful to differentiate benign and malignant lesions as a lack of basal cells is considered a hallmark of malignancy.
  • Basal cell cytokeratins and p63 have therefore a long standing place in the diagnostic portfolio of most genito-urinary pathologists.
  • The most widely used positive marker is alpha-methylacyl-CoA racemase (AMACR), which is strongly upregulated in prostate cancer and which can even be combined with p63 in a single immunostaining.
  • [MeSH-major] Algorithms. Biomarkers, Tumor / analysis. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hematol Oncol Clin North Am. 2006 Aug;20(4):845-55 [16861118.001]
  • [Cites] Prostate. 2008 Dec 1;68(16):1806-15 [18767028.001]
  • [Cites] Hum Pathol. 2006 Apr;37(4):401-9 [16564913.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1677-82 [10749139.001]
  • [Cites] Am J Surg Pathol. 2008 Mar;32(3):461-7 [18300803.001]
  • [Cites] Urol Oncol. 2007 Nov-Dec;25(6):505-9 [18047961.001]
  • [Cites] Neoplasia. 2008 Nov;10(11):1285-94 [18953438.001]
  • [Cites] Cancer Res. 1985 Aug;45(8):3663-7 [2410099.001]
  • [Cites] Br J Cancer. 2008 Sep 16;99(6):939-48 [18781151.001]
  • [Cites] Am J Surg Pathol. 1989 May;13(5):389-96 [2469333.001]
  • [Cites] Hum Pathol. 2006 Mar;37(3):292-7 [16613324.001]
  • [Cites] Mod Pathol. 2004 Mar;17(3):307-15 [14739905.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Cancer Biol Ther. 2007 Aug;6(8):1263-8 [17786030.001]
  • [Cites] Hum Pathol. 2004 Oct;35(10):1272-8 [15492996.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):24561-8 [15150260.001]
  • [Cites] J Natl Cancer Inst. 2009 Apr 1;101(7):519-32 [19318631.001]
  • [Cites] J Cell Biochem. 2004 Jan 1;91(1):47-53 [14689581.001]
  • [Cites] BJU Int. 2007 Dec;100(6):1259-63 [17850375.001]
  • [Cites] Hum Pathol. 1996 Sep;27(9):917-21 [8816886.001]
  • [Cites] Eur Urol. 2009 Jun;55(6):1321-30 [19286302.001]
  • [Cites] Histopathology. 2004 Sep;45(3):218-25 [15330799.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1302-8 [12481011.001]
  • [Cites] Urology. 1995 Jan;45(1):81-6 [7817483.001]
  • [Cites] Cancer Res. 2002 Apr 15;62(8):2220-6 [11956072.001]
  • [Cites] J Pathol. 2005 Feb;205(3):359-76 [15532095.001]
  • [Cites] Nature. 2001 Aug 23;412(6849):822-6 [11518967.001]
  • [Cites] Am J Surg Pathol. 2008 Jun;32(6):851-7 [18408595.001]
  • [Cites] Mol Cancer Res. 2003 Aug;1(10):707-15 [12939396.001]
  • [Cites] Clin Cancer Res. 2008 Mar 15;14(6):1734-43 [18347174.001]
  • [Cites] Am J Surg Pathol. 2008 Dec;32(12):1890-5 [18813120.001]
  • [Cites] Am J Pathol. 2000 Dec;157(6):1769-75 [11106548.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Dec;4(12):692-8 [18037873.001]
  • [Cites] BMC Urol. 2008 Jun 17;8:9 [18559088.001]
  • [Cites] Int J Cancer. 2002 Mar 1;98(1):19-22 [11857379.001]
  • [Cites] JAMA. 2002 Apr 3;287(13):1662-70 [11926890.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 15;97(17):9437-42 [10931945.001]
  • [Cites] Histopathology. 2007 Jan;50(2):243-51 [17222253.001]
  • [Cites] Prostate. 2008 Sep 15;68(13):1387-95 [18543251.001]
  • [Cites] World J Surg. 2006 Apr;30(4):628-36 [16555021.001]
  • [Cites] Am J Surg Pathol. 2004 Feb;28(2):239-43 [15043314.001]
  • [Cites] J Cell Biochem. 2008 Apr 1;103(5):1354-68 [17879953.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5477-85 [14654526.001]
  • (PMID = 19795124.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CK-34 beta E12; 0 / CKAP4 protein, human; 0 / GOLM1 protein, human; 0 / Keratin-5; 0 / Keratin-6; 0 / Membrane Proteins; 68238-35-7 / Keratins; EC 2.3.1.85 / FASN protein, human; EC 2.3.1.85 / Fatty Acid Synthase, Type I; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  • [Number-of-references] 43
  •  go-up   go-down


54. Smith-Beckerman DM, Fung KW, Williams KE, Auersperg N, Godwin AK, Burlingame AL: Proteome changes in ovarian epithelial cells derived from women with BRCA1 mutations and family histories of cancer. Mol Cell Proteomics; 2005 Feb;4(2):156-68
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant transformation of the ovarian surface epithelium (OSE) accounts for most ovarian carcinoma.
  • We identified OSE proteins with altered expression derived from women with a family history (FH) of ovarian and/or breast cancer and mutations in the BRCA1 tumor suppressor gene.
  • Proteins from SV-40-transformed FH-OSE cell lines and control OSE lines derived from women without such histories (non-family history) were separated by two-dimensional PAGE.
  • In contrast, proteins suppressed in FH lines include the 27-kDa heat shock protein, translationally controlled tumor protein, and several proteins associated with actin modification such as actin prepeptide, F-actin capping protein alpha subunit, and cofilin.
  • Identification of these and other OSE proteins may be useful in detecting changes suggestive of increased risk of developing preneoplastic disease and defining the possible role(s) of the BRCA1 gene in regulation of OSE cell function.
  • [MeSH-minor] Actin Depolymerizing Factors. Actins / chemistry. Algorithms. Amino Acid Sequence. Blotting, Western. Cell Line, Tumor. Cell Transformation, Neoplastic. Down-Regulation. Electrophoresis, Gel, Two-Dimensional. Family Health. Female. Humans. Immunoblotting. Isoelectric Focusing. Lactoylglutathione Lyase / biosynthesis. Mass Spectrometry. Microfilament Proteins / chemistry. Molecular Sequence Data. Neoplasms / metabolism. Peptides / chemistry. Phosphorylation. Protein Processing, Post-Translational. Silver Staining. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Time Factors. Trypsin / pharmacology. Ubiquitin / chemistry. Up-Regulation


55. Mendoza J, Zamora R, Gallardo JC, Ceballos G, Aldana A, Espinosa M, Maldonado V, Melendez-Zajgla J: NF-kappaB does not influence the induction of apoptosis by Ukrain. Cancer Biol Ther; 2006 Jul;5(7):788-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has immunoregulatory effects on T lymphocyte subsets and cytotoxic and cytostatic effects on various malignant cells.
  • Although Ukrain has been reported to induce alterations in the cell cycle and tubulin polymerization, the specific cellular target has not been described.
  • Ukrain induced apoptosis in a panel of cancer cell lines by activating the intrinsic cell death pathway, as demonstrated by the cleavage of caspase 9 and the upregulation and cleavage of caspase 3.
  • Nevertheless, this activation was not required for, and did not modulate, the Ukrain effect: neither blockage of activation by a dominant negative version of Ikappa-B alpha or a Bcl-3 siRNA, nor activation of the pathway by overexpression of IKK2, changed the response to the drug.
  • [MeSH-minor] Caspase 3 / analysis. Caspase 3 / metabolism. Caspase 9 / analysis. Caspase 9 / metabolism. Cell Line, Tumor. Gene Expression. Genes, Reporter. Humans. I-kappa B Kinase / antagonists & inhibitors. I-kappa B Kinase / genetics. I-kappa B Kinase / metabolism. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. RNA, Small Interfering / genetics. RNA, Small Interfering / pharmacology. Transcription Factors / antagonists & inhibitors. Transcription Factors / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16721042.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Berberine Alkaloids; 0 / NF-kappa B; 0 / Phenanthridines; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3; 6251Q9UK1S / ukrain; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
  •  go-up   go-down


56. Diakos C, Krapf G, Gerner C, Inthal A, Lemberger C, Ban J, Dohnal AM, Panzer-Grümayer ER: RNAi-mediated silencing of TEL/AML1 reveals a heat-shock protein- and survivin-dependent mechanism for survival. Blood; 2007 Mar 15;109(6):2607-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We therefore silenced TEL/AML1 expression in leukemic REH cells by RNA inhibition, which eventually led to programmed cell death.
  • Our data suggest that TEL/AML1 not only contributes to leukemogenesis by affecting an antiapoptotic network but also seems to be indispensable for maintaining the malignant phenotype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. Heat-Shock Proteins / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. RNA Interference
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. Cell Survival. Gene Expression Regulation, Neoplastic. Humans. Inhibitor of Apoptosis Proteins

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Blood. 2009 Feb 12;113(7):1613. Panzer-Gruemayer, E Renate [corrected to Panzer-Grümayer, E Renate]
  • [Cites] Blood. 2003 May 1;101(9):3635-40 [12506024.001]
  • [Cites] Oncogene. 2003 Dec 8;22(56):9041-7 [14663482.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8443-8 [15155899.001]
  • [Cites] FEBS Lett. 2005 Oct 31;579(26):5996-6007 [16115631.001]
  • [Cites] Leukemia. 2005 May;19(5):710-2 [15759036.001]
  • [Cites] Mol Cell Proteomics. 2002 Jul;1(7):528-37 [12239281.001]
  • [Cites] Blood. 2001 Aug 1;98(3):558-64 [11468150.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):502-13 [12094236.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):761-72 [16175177.001]
  • [Cites] Nature. 2001 May 24;411(6836):494-8 [11373684.001]
  • [Cites] Blood. 2004 May 15;103(10):3890-6 [14726384.001]
  • [Cites] Oncogene. 2005 Nov 17;24(51):7579-91 [16044150.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4275-83 [15156184.001]
  • [Cites] Blood. 2005 Aug 1;106(3):787-94 [15827131.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):13791-6 [14614132.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1566-9 [12393533.001]
  • [Cites] Oncogene. 2002 Aug 22;21(37):5716-24 [12173041.001]
  • [Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):213-7 [12676580.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4584-8 [9539781.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3559-66 [16046533.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Nat Rev Cancer. 2003 Jan;3(1):46-54 [12509766.001]
  • (PMID = 17095626.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 17551
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Heat-Shock Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ EMS32870; NLM/ PMC4194423
  •  go-up   go-down


57. Morla D, Alazemi S, Lichtstein D: Stauffer's syndrome variant with cholestatic jaundice: a case report. J Gen Intern Med; 2006 Jul;21(7):C11-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cholestasis is a common feature of several malignant diseases, including pancreatic, hepatic, gallbladder, and ampullary carcinomas.
  • Stauffer's syndrome is a rare paraneoplastic manifestation of renal cell carcinoma (RCC) that is characterized by elevated alkaline phosphatase, erythrocyte sedimentation rate, alpha-2-globulin, and gamma-glutamyl transferase, thrombocytosis, prolongation of prothrombin time, and hepatosplenomegaly, in the absence of hepatic metastasis and jaundice.
  • Jaundice and liver dysfunction resolved completely after surgical resection of the tumor.
  • This case illustrates the protean manifestations of RCC, and the importance of considering Stauffer's syndrome and its variant in the differential diagnosis of anicteric and icteric cholestasis, which may allow early recognition and treatment of an underlying malignancy.
  • [MeSH-major] Carcinoma, Renal Cell / diagnosis. Jaundice, Obstructive / etiology. Kidney Neoplasms / diagnosis. Paraneoplastic Syndromes / etiology

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastroenterology. 1992 Jul;103(1):330-2 [1612341.001]
  • [Cites] Semin Urol Oncol. 1996 Nov;14(4):216-22 [8946620.001]
  • [Cites] Eur J Gastroenterol Hepatol. 1997 Mar;9(3):311-4 [9096437.001]
  • [Cites] Int J Cancer. 1997 Jul 29;72(3):424-30 [9247285.001]
  • [Cites] Cancer. 1971 Nov;28(5):1165-77 [5125665.001]
  • [Cites] Ann Med Interne (Paris). 2003 May;154(3):171-5 [12910044.001]
  • [Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]
  • [Cites] Clin Gastroenterol Hepatol. 2003 Nov;1(6):480-3 [15017648.001]
  • [Cites] Int J Urol. 2005 Aug;12(8):757-9 [16174051.001]
  • (PMID = 16808761.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1924715
  •  go-up   go-down


58. Ragel BT, Couldwell WT, Gillespie DL, Jensen RL: Identification of hypoxia-induced genes in a malignant glioma cell line (U-251) by cDNA microarray analysis. Neurosurg Rev; 2007 Jul;30(3):181-7; discussion 187
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of hypoxia-induced genes in a malignant glioma cell line (U-251) by cDNA microarray analysis.
  • We compared the gene expression profiles of the U-251 malignant glioma cell line under normoxic and hypoxic conditions to discover future research targets.
  • Identified genes were divided into cell cycle control, stress response, and "newly connected" genes.
  • Hybridization identified 11 hypoxia-induced genes: 1 involved with cell cycle control (CCNG2), 6 in stress response (IGFBP3, SLC2A3, GSTT2, FOS, DDIT3, AKR1C3), and 2 newly connected genes (Depp, AKAP4).
  • Possible functions of the highly expressed gene Depp include tumor vascularization.
  • [MeSH-minor] Cell Hypoxia / genetics. Cell Hypoxia / physiology. Cell Line, Tumor. Cell Proliferation. Cytokines / biosynthesis. Cytokines / genetics. DNA Damage. Glucose Transporter Type 1 / biosynthesis. Glucose Transporter Type 1 / genetics. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Intercellular Signaling Peptides and Proteins / biosynthesis. Intercellular Signaling Peptides and Proteins / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. Stress, Physiological / genetics. Up-Regulation / genetics. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurosurg Focus. 2006 Apr 15;20(4):E24 [16709030.001]
  • [Cites] J Biochem. 1998 Nov;124(5):940-6 [9792917.001]
  • [Cites] Mutat Res. 2000 Oct;463(3):247-83 [11018744.001]
  • [Cites] Microsc Res Tech. 2003 May 1;61(1):103-15 [12672126.001]
  • [Cites] EMBO J. 2005 Oct 5;24(19):3470-81 [16148948.001]
  • [Cites] Mol Cell Neurosci. 2006 Jul;32(3):217-29 [16769221.001]
  • [Cites] Am J Surg Pathol. 1998 Jul;22(7):816-26 [9669344.001]
  • [Cites] Neurology. 1988 Feb;38(2):289-93 [3340296.001]
  • [Cites] Mol Pharmacol. 1995 Oct;48(4):639-47 [7476889.001]
  • [Cites] Oncogene. 2002 Sep 5;21(39):6017-31 [12203114.001]
  • [Cites] Endocrinology. 2001 Apr;142(4):1652-8 [11250947.001]
  • [Cites] Cancer Res. 1992 Jul 15;52(14):3972-9 [1617673.001]
  • [Cites] Genes Dev. 2004 Dec 15;18(24):3066-77 [15601821.001]
  • [Cites] Brain Res Bull. 2001 Sep 1;56(1):43-8 [11604247.001]
  • [Cites] J Biol Chem. 1995 Aug 25;270(34):20162-8 [7650035.001]
  • [Cites] Mol Hum Reprod. 2005 Jul;11(7):471-6 [16123073.001]
  • [Cites] FEBS Lett. 2006 Jun 12;580(14):3462-8 [16716308.001]
  • [Cites] Curr Opin Genet Dev. 2006 Feb;16(1):65-70 [16377173.001]
  • [Cites] Eur J Neurosci. 2000 Apr;12(4):1155-64 [10762347.001]
  • [Cites] J Biol Chem. 2004 Sep 24;279(39):40462-9 [15265861.001]
  • [Cites] Horm Res. 1999;51(2):53-67 [10352394.001]
  • [Cites] J Neurochem. 1993 Dec;61(6):2048-53 [8245960.001]
  • [Cites] J Neurosurg. 1989 Jun;70(6):910-5 [2541227.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):403-15 [14752508.001]
  • [Cites] Brain Res Mol Brain Res. 1994 Nov;27(1):51-7 [7877454.001]
  • [Cites] Nature. 1992 Oct 29;359(6398):843-5 [1279431.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):5325-31 [12414909.001]
  • [Cites] J Clin Invest. 1993 Jan;91(1):153-9 [8380810.001]
  • [Cites] Mol Cell Biol. 2004 Mar;24(5):2181-9 [14966295.001]
  • [Cites] Endocr Relat Cancer. 2006 Mar;13(1):169-80 [16601286.001]
  • [Cites] J Neurosci. 2004 Apr 7;24(14):3627-36 [15071111.001]
  • [Cites] Dev Dyn. 2005 Aug;233(4):1589-604 [15977181.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):233-47 [16612574.001]
  • [Cites] J Biol Chem. 1999 Oct 15;274(42):30280-7 [10514522.001]
  • [Cites] Biochem J. 2000 Oct 1;351(Pt 1):67-77 [10998348.001]
  • [Cites] Neuro Oncol. 2005 Apr;7(2):134-53 [15831232.001]
  • [Cites] Eur J Cancer. 2005 Jul;41(11):1515-27 [15979304.001]
  • [Cites] Oncogene. 1996 Sep 5;13(5):1103-9 [8806701.001]
  • [Cites] Am J Kidney Dis. 1999 Jul;34(1):189-202 [10401038.001]
  • [Cites] Cell Tissue Res. 2002 Dec;310(3):331-8 [12457232.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Mar;86(3):1274-80 [11238520.001]
  • (PMID = 17486380.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Glucose Transporter Type 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Neoplasm; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


59. Wyler E, Kaminska M, Coïc YM, Baleux F, Véron M, Agou F: Inhibition of NF-kappaB activation with designed ankyrin-repeat proteins targeting the ubiquitin-binding/oligomerization domain of NEMO. Protein Sci; 2007 Sep;16(9):2013-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Inhibiting this pathway is therefore a promising approach in the treatment of certain cancers through a pro-apoptotic effect in malignant cells.
  • When expressed in human cells, some of the selected molecules, despite their partial degradation, inhibited TNF-alpha-mediated NF-kappaB activation while having no effect on the basal activity.
  • [MeSH-minor] Cell Line. DNA, Complementary. Escherichia coli / genetics. Genes, Reporter. Green Fluorescent Proteins / metabolism. Humans. Kidney / cytology. Luciferases / analysis. Luciferases / metabolism. Models, Molecular. Plasmids. Protein Structure, Tertiary. Recombinant Fusion Proteins / antagonists & inhibitors. Recombinant Fusion Proteins / chemistry. Recombinant Fusion Proteins / metabolism. Transfection. Tumor Necrosis Factor-alpha / pharmacology. beta-Galactosidase / analysis. beta-Galactosidase / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mol Biol. 2003 Sep 12;332(2):489-503 [12948497.001]
  • [Cites] Nature. 2006 May 25;441(7092):431-6 [16724054.001]
  • [Cites] Nat Biotechnol. 2004 May;22(5):575-82 [15097997.001]
  • [Cites] Trends Immunol. 2004 Jun;25(6):280-8 [15145317.001]
  • [Cites] J Biol Chem. 2004 Jul 2;279(27):27861-9 [15107419.001]
  • [Cites] Genes Dev. 2004 Sep 15;18(18):2195-224 [15371334.001]
  • [Cites] Cell. 1998 Jun 26;93(7):1231-40 [9657155.001]
  • [Cites] J Exp Med. 2006 Jul 10;203(7):1745-59 [16818673.001]
  • [Cites] Proteins. 2006 Nov 1;65(2):280-4 [16493627.001]
  • [Cites] Sci STKE. 2006 Oct 17;2006(357):re13 [17047224.001]
  • [Cites] Mol Cell Biol. 2006 Dec;26(24):9209-19 [17000764.001]
  • [Cites] FEBS J. 2007 May;274(10):2540-51 [17419723.001]
  • [Cites] Oncogene. 2007 Apr 5;26(16):2299-307 [17043643.001]
  • [Cites] Nat Methods. 2007 Mar;4(3):269-79 [17327848.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Trends Cell Biol. 2000 Apr;10(4):129-33 [10740266.001]
  • [Cites] J Biol Chem. 2000 Dec 1;275(48):37966-77 [10980203.001]
  • [Cites] J Biol Chem. 2002 May 17;277(20):17464-75 [11877453.001]
  • [Cites] Nat Immunol. 2002 Oct;3(10):958-65 [12352969.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):2029-41 [12612076.001]
  • [Cites] Nature. 1998 Sep 17;395(6699):297-300 [9751060.001]
  • [Cites] Trends Biochem Sci. 1999 Aug;24(8):311-6 [10431175.001]
  • [Cites] J Biol Chem. 2004 Dec 24;279(52):54248-57 [15466857.001]
  • [Cites] Nat Rev Cancer. 2005 Nov;5(11):886-97 [16239905.001]
  • [Cites] Protein Sci. 2006 Jan;15(1):14-27 [16373474.001]
  • [Cites] Nat Cell Biol. 2006 Apr;8(4):398-406 [16547522.001]
  • [Cites] Cell Death Differ. 2006 May;13(5):738-47 [16485028.001]
  • [Cites] Mol Cell. 2006 Apr 21;22(2):245-57 [16603398.001]
  • [Cites] Cell. 2003 Nov 26;115(5):565-76 [14651848.001]
  • (PMID = 17766391.001).
  • [ISSN] 0961-8368
  • [Journal-full-title] Protein science : a publication of the Protein Society
  • [ISO-abbreviation] Protein Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / IKBKG protein, human; 0 / NF-kappa B; 0 / Recombinant Fusion Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / Ubiquitin; 147336-22-9 / Green Fluorescent Proteins; EC 1.13.12.- / Luciferases; EC 2.7.11.10 / I-kappa B Kinase; EC 3.2.1.23 / beta-Galactosidase
  • [Other-IDs] NLM/ PMC2206981
  •  go-up   go-down


60. Hassan I, Barth P, Celik I, Hoffmann S, Langer P, Ramaswamy A, Wagner HJ, Rothmund M, Zielke A: An authentic malignant epithelioid hemangioendothelioma of the thyroid: a case report and review of the literature. Thyroid; 2005 Dec;15(12):1377-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An authentic malignant epithelioid hemangioendothelioma of the thyroid: a case report and review of the literature.
  • We report the second case of an epithelioid hemangioendothelioma (EHE) of the thyroid gland and the first clinical case with malignant behavior.
  • Histologically the lesion had characteristic epithelioid and spindle cell proliferation in a background of chondromyxoid stroma.
  • Tumor cells were positive for factor VIII-related antigen, MNF116, PAN-ceratin, CD 34, and CD 31 and negative for cytokeratin allowing the diagnosis of EHE.
  • Nine months after the primary resection the tumor locally recurred.
  • A palliative resection was performed in a second operation followed by interferon-alpha therapy.
  • The patient rapidly developed a second local relapse and died 13 months after the diagnosis of an EHE had been made.
  • An improvement of the very poor prognosis of this rare tumor may depend on early tumor diagnosis and surgery combined with a multimodal treatment.

  • Genetic Alliance. consumer health - Hemangioendothelioma.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16405412.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


61. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Glucagonoma.
  • Genetic Alliance. consumer health - Glucagonoma Syndrome.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


62. Dagvadorj A, Collins S, Jomain JB, Abdulghani J, Karras J, Zellweger T, Li H, Nurmi M, Alanen K, Mirtti T, Visakorpi T, Bubendorf L, Goffin V, Nevalainen MT: Autocrine prolactin promotes prostate cancer cell growth via Janus kinase-2-signal transducer and activator of transcription-5a/b signaling pathway. Endocrinology; 2007 Jul;148(7):3089-101
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autocrine prolactin promotes prostate cancer cell growth via Janus kinase-2-signal transducer and activator of transcription-5a/b signaling pathway.
  • Prolactin (Prl) is a local growth factor produced in high-grade prostate cancer, and exogenously added Prl in tissue or explant cultures of normal and malignant prostate is a strong mitogen and survival factor for prostate epithelium.
  • Using a specific Prl receptor antagonist (Delta1-9G129R-hPRL), we demonstrate here for the first time that autocrine Prl in androgen-independent human prostate cancer cells promotes cell viability via Stat5 signaling pathway.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoblotting. Male. Mice. Mice, Nude. Neoplasm Metastasis. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. Oligodeoxyribonucleotides, Antisense / genetics. Phosphorylation / drug effects. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / drug effects. Transplantation, Heterologous. Tumor Suppressor Proteins. Tyrphostins / pharmacology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17412813.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA113580-01A1; United States / NCI NIH HHS / CA / CA56036-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligodeoxyribonucleotides, Antisense; 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / Tumor Suppressor Proteins; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 9002-62-4 / Prolactin; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


63. Pilloni L, Bianco P, Manieli C, Senes G, Coni P, Atzori L, Aste N, Faa G: Immunoreactivity for alpha-smooth muscle actin characterizes a potentially aggressive subgroup of little basal cell carcinomas. Eur J Histochem; 2009 Apr-Jun;53(2):113-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoreactivity for alpha-smooth muscle actin characterizes a potentially aggressive subgroup of little basal cell carcinomas.
  • Basal cell carcinoma (BCC) is a very common malignant skin tumor that rarely metastatizes, but is often locally aggressive.
  • An immunohistochemical profile, characterized by reactivity of tumor cells for p53, Ki67 and alpha-SMA has been associated with a more aggressive behaviour in large BCCs.
  • The aim of this study was to verify if also little (<3 cm) basal cell carcinomas can express immunohistochemical markers typical for an aggressive behaviour.
  • [MeSH-major] Actins / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Basal Cell / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Invasiveness. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Suppressor Protein p53 / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19683985.001).
  • [ISSN] 1121-760X
  • [Journal-full-title] European journal of histochemistry : EJH
  • [ISO-abbreviation] Eur J Histochem
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ACTA2 protein, human; 0 / Actins; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


64. Binai NA, Damert A, Carra G, Steckelbroeck S, Löwer J, Löwer R, Wessler S: Expression of estrogen receptor alpha increases leptin-induced STAT3 activity in breast cancer cells. Int J Cancer; 2010 Jul 1;127(1):55-66
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of estrogen receptor alpha increases leptin-induced STAT3 activity in breast cancer cells.
  • Adipositas correlates with an enhanced risk of developing malignant diseases such as breast cancer, endometrial tumor or prostate carcinoma, but the molecular basis for this is not well understood.
  • Here, we investigated cross-talk between ERalpha (estrogen receptor alpha) and leptin-induced activation of signal transducer and activator of transcription 3 (STAT3), a transactivator of important oncogenes.
  • We also detected ERalpha binding to STAT3 and JAK2 (Janus kinase 2), resulting in enhanced JAK2 activity upstream of STAT3 in response to leptin that might lead to an increased ERalpha-dependent cell viability.
  • Altogether, our results indicate that leptin-induced STAT3 activation acts as a key event in ERalpha-dependent development of malignant diseases.
  • [MeSH-major] Breast Neoplasms / metabolism. Estrogen Receptor alpha / metabolism. Leptin / physiology. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Female. Humans. Polymerase Chain Reaction. Transfection

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19876927.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Estrogen Receptor alpha; 0 / Leptin; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human
  •  go-up   go-down


65. Tsunematsu T, Kudo Y, Iizuka S, Ogawa I, Fujita T, Kurihara H, Abiko Y, Takata T: RUNX3 has an oncogenic role in head and neck cancer. PLoS One; 2009;4(6):e5892
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Runt-related transcription factor 3 (RUNX3) is a tumor suppressor of cancer and appears to be an important component of the transforming growth factor-beta (TGF-ss)-induced tumor suppression pathway.
  • Surprisingly, we found that RUNX3 expression level in head and neck squamous cell carcinoma (HNSCC) tissues, which is one of the most common types of human cancer, was higher than that in normal tissues by a previously published microarray dataset in our preliminary study.
  • PRINCIPAL FINDINGS: Frequent RUNX3 expression and its correlation with malignant behavior were observed in HNSCC.
  • Ectopic RUNX3 overexpression promoted cell growth and inhibited serum starvation-induced apoptosis and chemotherapeutic drug induced apoptosis in HNSCC cells.
  • CONCLUSIONS/SIGNIFICANCE: Our findings suggest that i) RUNX3 has an oncogenic role in HNSCC, ii) RUNX3 expression observed in HNSCC may be caused in part by demethylation during cancer development, and iii) RUNX3 expression can be a useful marker for predicting malignant behavior and the effect of chemotherapeutic drugs in HNSCC.
  • [MeSH-major] Core Binding Factor Alpha 3 Subunit / biosynthesis. Core Binding Factor Alpha 3 Subunit / physiology. Gene Expression Regulation, Neoplastic. Head and Neck Neoplasms / metabolism
  • [MeSH-minor] Apoptosis. Biomarkers, Tumor. Carcinoma, Squamous Cell. Cell Line, Tumor. DNA Methylation. Epithelial Cells / metabolism. Genes, Tumor Suppressor. Humans. Mouth Neoplasms / metabolism. Neoplasms / metabolism. RNA, Small Interfering / metabolism. Transforming Growth Factor beta / metabolism

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1994 Aug 1;74(3):893-9 [8039116.001]
  • [Cites] Oncogene. 1992 Feb;7(2):269-75 [1549348.001]
  • [Cites] Hum Mol Genet. 1995;4 Spec No:1751-5 [8541875.001]
  • [Cites] Mech Dev. 1998 Jul;75(1-2):3-28 [9739099.001]
  • [Cites] Am J Pathol. 2004 Dec;165(6):2147-55 [15579456.001]
  • [Cites] Liver Int. 2005 Apr;25(2):380-8 [15780064.001]
  • [Cites] Oncogene. 2005 Jun 30;24(28):4477-85 [15856017.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7743-50 [16140942.001]
  • [Cites] Oncol Rep. 2005 Oct;14(4):817-22 [16142337.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9347-54 [16230397.001]
  • [Cites] Cancer Sci. 2006 Jan;97(1):51-6 [16367921.001]
  • [Cites] Int J Cancer. 2006 Feb 15;118(4):924-31 [16108009.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6512-20 [16818622.001]
  • [Cites] Anat Rec A Discov Mol Cell Evol Biol. 2006 Jul;288(7):695-9 [16761282.001]
  • [Cites] Cancer Sci. 2006 Nov;97(11):1211-6 [16965393.001]
  • [Cites] Oncogene. 2006 Dec 7;25(58):7646-9 [16767156.001]
  • [Cites] Cancer Lett. 2008 Feb 8;259(2):209-17 [18054154.001]
  • [Cites] Blood. 2008 Oct 15;112(8):3391-402 [18663147.001]
  • [Cites] Nature. 2001 May 24;411(6836):494-8 [11373684.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8601-10 [11751371.001]
  • [Cites] Mol Cell Biol. 2002 Jan;22(2):547-54 [11756550.001]
  • [Cites] Cell. 2002 Apr 5;109(1):113-24 [11955451.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3775-81 [12824416.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):55-63 [14729608.001]
  • [Cites] Lab Invest. 2004 Apr;84(4):479-84 [14968123.001]
  • [Cites] Pathobiology. 2004;71(3):137-43 [15051926.001]
  • [Cites] Cancer Cell. 2004 Apr;5(4):311-6 [15093538.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4198-208 [15156173.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4308-14 [15156187.001]
  • [Cites] Oncogene. 2004 Sep 2;23(40):6736-42 [15273736.001]
  • [Cites] Acta Radiol Ther Phys Biol. 1973 Feb;12(1):1-8 [4725642.001]
  • [Cites] Science. 1980 Nov 7;210(4470):604-10 [6254144.001]
  • [Cites] Biochem Biophys Res Commun. 1983 Feb 28;111(1):47-54 [6187346.001]
  • [Cites] Nucleic Acids Res. 1983 Oct 11;11(19):6883-94 [6314264.001]
  • [Cites] J Natl Cancer Inst. 1984 Nov;73(5):1057-65 [6092764.001]
  • [Cites] Blood. 1988 Dec;72(6):2042-4 [2904292.001]
  • [Cites] Cancer Res. 1990 Oct 1;50(19):6130-8 [1698118.001]
  • [Cites] Gene. 1995 Jul 4;159(2):245-8 [7622058.001]
  • (PMID = 19521519.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 3 Subunit; 0 / RNA, Small Interfering; 0 / Runx3 protein, human; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2690822
  •  go-up   go-down


66. Mancuso M, Gallo D, Leonardi S, Pierdomenico M, Pasquali E, De Stefano I, Rebessi S, Tanori M, Scambia G, Di Majo V, Covelli V, Pazzaglia S, Saran A: Modulation of basal and squamous cell carcinoma by endogenous estrogen in mouse models of skin cancer. Carcinogenesis; 2009 Feb;30(2):340-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of basal and squamous cell carcinoma by endogenous estrogen in mouse models of skin cancer.
  • Patched1 heterozygous mice (Ptch1(+/-)) are useful for basal cell carcinoma (BCC) studies, being remarkably susceptible to BCC induction by ultraviolet or ionizing radiation.
  • Analogously, skin carcinogenesis-susceptible (Car-S) mice are elective for studies of papilloma and squamous cell carcinoma (SCC) induction.
  • We previously reported a striking effect of gender on BCC induction in Ptch1(+/-) mice, with total resistance of females; likewise, Car-S females show increased skin tumor resistance relative to males.
  • Remarkably, progression of initially benign papillomas to malignant SCC occurred only in ovariectomized Car-S females.
  • We explored the mechanisms underlying tumor progression and report overexpression of estrogen receptor (ER)-alpha, downregulation of ERbeta and upregulation of cyclin D1 in papillomas from ovariectomized Car-S relative to papillomas from CN females.
  • [MeSH-major] Carcinoma, Basal Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Estrogens / physiology. Skin Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Cyclin D1 / metabolism. Disease Models, Animal. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Female. Male. Mice. Neoplasms, Radiation-Induced / metabolism. Neoplasms, Radiation-Induced / pathology. Ovariectomy. Papilloma / metabolism. Papilloma / pathology. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Ultraviolet Rays


67. Li B, Vincent A, Cates J, Brantley-Sieders DM, Polk DB, Young PP: Low levels of tumor necrosis factor alpha increase tumor growth by inducing an endothelial phenotype of monocytes recruited to the tumor site. Cancer Res; 2009 Jan 1;69(1):338-48
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low levels of tumor necrosis factor alpha increase tumor growth by inducing an endothelial phenotype of monocytes recruited to the tumor site.
  • Microenvironmental cues instruct infiltrating tumor-associated myeloid cells to drive malignant progression.
  • A subpopulation of tumor-associated myeloid cells coexpressing endothelial and myeloid markers, although rare in peripheral blood, are primarily associated with tumors where they enhance tumor growth and angiogenesis.
  • These biphenotypic vascular leukocytes result from the endothelial differentiation of myeloid progenitors, a process regulated by tumor necrosis factor (TNF)alpha in vitro.
  • An in vivo increase in tumor-derived TNFalpha expression promoted tumor growth and vascularity of mouse melanoma, lung cancer, and mammary tumors.
  • Notably, tumor growth was accompanied by a significant increase in myeloid/endothelial biphenotypic populations.
  • TNFalpha-associated tumor growth, vascularity, and generation of tumor vascular leukocytes in mouse melanoma tumors were dependent on intact host TNFalpha receptors.
  • Our studies suggest that TNFalpha constitutes a tumor microenvironment signal that biases recruited monocytes toward a proangiogenic/provasculogenic myeloid/endothelial phenotype.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2006 Jan 15;66(2):605-12 [16423985.001]
  • [Cites] J Neuroimmunol. 2006 Feb;171(1-2):45-56 [16288810.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2006 Apr;26(4):744-50 [16439712.001]
  • [Cites] Eur J Cancer. 2006 Apr;42(6):745-50 [16517151.001]
  • [Cites] Am J Pathol. 2006 May;168(5):1710-21 [16651636.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 29;103(35):13156-61 [16920790.001]
  • [Cites] J Leukoc Biol. 2006 Dec;80(6):1183-96 [16997855.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):585-92 [17234767.001]
  • [Cites] Circulation. 2007 Feb 13;115(6):752-62 [17261656.001]
  • [Cites] Cancer Lett. 2007 May 18;250(1):1-8 [17049723.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5276-85 [17327411.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8429-32 [17875679.001]
  • [Cites] J Clin Invest. 2008 Jan;118(1):64-78 [18079969.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3422-7 [10725398.001]
  • [Cites] Cardiovasc Res. 2001 Feb 16;49(3):671-80 [11166280.001]
  • [Cites] Trends Cell Biol. 2001 Sep;11(9):372-7 [11514191.001]
  • [Cites] J Immunol. 2001 Oct 1;167(7):3944-52 [11564813.001]
  • [Cites] Oncogene. 2002 Jul 18;21(31):4728-38 [12101411.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6682-7 [12438267.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] Circulation. 2003 Mar 4;107(8):1164-9 [12615796.001]
  • [Cites] Int Immunol. 2003 Apr;15(4):515-24 [12663681.001]
  • [Cites] Mol Cancer Ther. 2003 May;2(5):445-51 [12748306.001]
  • [Cites] Nat Med. 2003 Jun;9(6):789-95 [12740570.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):71-8 [14708027.001]
  • [Cites] Oncogene. 2004 Mar 11;23(10):1902-10 [14661063.001]
  • [Cites] Nat Med. 2004 Sep;10(9):950-8 [15334073.001]
  • [Cites] Cancer Cell. 2004 Oct;6(4):409-21 [15488763.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2752-60 [15226175.001]
  • [Cites] Nature. 1987 Oct 15-21;329(6140):630-2 [2443857.001]
  • [Cites] J Clin Invest. 1988 Feb;81(2):455-60 [2828427.001]
  • [Cites] Nature. 1995 Jul 6;376(6535):62-6 [7596435.001]
  • [Cites] Endocr Rev. 1997 Feb;18(1):4-25 [9034784.001]
  • [Cites] Circ Res. 1999 Aug 6;85(3):221-8 [10436164.001]
  • [Cites] Blood. 2005 Jan 15;105(2):679-81 [15358628.001]
  • [Cites] Transfusion. 2005 Jan;45(1):21-5 [15647014.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):211-7 [15766659.001]
  • [Cites] J Leukoc Biol. 2005 Aug;78(2):352-8 [15894588.001]
  • [Cites] Circ Res. 2005 Aug 19;97(4):314-22 [16020753.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):211-26 [16169466.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9113-6 [16230363.001]
  • [Cites] Cancer Immun. 2006;6:6 [16551058.001]
  • (PMID = 19118019.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL088424-01A1; United States / NHLBI NIH HHS / HL / R01 HL088424-01A1; United States / NIDDK NIH HHS / DK / DK056008-10; United States / NIDDK NIH HHS / DK / R01 DK056008-10; United States / NHLBI NIH HHS / HL / R01 HL088424; United States / NHLBI NIH HHS / HL / HL 088424; United States / NIDDK NIH HHS / DK / DK 56008; United States / NIDDK NIH HHS / DK / R01 DK056008; United States / NIDDK NIH HHS / DK / Z01 DK056008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS86128; NLM/ PMC2651676
  •  go-up   go-down


68. Chan AL, Juarez M, Allen R, Volz W, Albertson T: Pharmacokinetics and clinical effects of mono-L-aspartyl chlorin e6 (NPe6) photodynamic therapy in adult patients with primary or secondary cancer of the skin and mucosal surfaces. Photodermatol Photoimmunol Photomed; 2005 Apr;21(2):72-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A single intravenous dose of Npe6 was administered to 14 cancer patients with superficial malignancies (basal cell carcinoma = 22 lesions, squamous cell cancer = 13 lesions, papillary carcinoma = 14 lesions).
  • The total light dose (range 25-200 J/cm2) depended on the tumor shape and size.
  • RESULTS: Four weeks post-PDT, 20 of 22 basal cell carcinoma tumors (91%) showed a complete response.
  • Eighteen of 27 other malignant cutaneous tumors showed a complete (n = 15/27, 56%) or partial (n = 3/27, 11%) response.
  • The mean alpha, beta, and terminal half-lives were 8.63+/-2.92, 105.90+/-37.59 and 168.11+/-53.40 h (+/-1 SD), respectively.
  • [MeSH-minor] Aged. Aged, 80 and over. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / pathology. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Female. Humans. Male. Middle Aged. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15752124.001).
  • [ISSN] 0905-4383
  • [Journal-full-title] Photodermatology, photoimmunology & photomedicine
  • [ISO-abbreviation] Photodermatol Photoimmunol Photomed
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Porphyrins; P4ROX5ELT2 / Talaporfin
  •  go-up   go-down


69. Yoneda K, Morii T, Nieda M, Tsukaguchi N, Amano I, Tanaka H, Yagi H, Narita N, Kimura H: The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy. Leuk Res; 2005 Feb;29(2):147-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy.
  • Valpha24TCR+ CD161+ NKT (Valpha24+ NKT) cells are activated by alpha-galactosylceramide and can exert anti-tumor activity against a variety of tumor cells.
  • In this study, we assessed the Valpha24+ NKT cell numbers in peripheral blood (PB) from 30 healthy donors and 70 patients with haematopoietic malignancy including chronic myelogenous leukemia (CML), malignant lymphoma (ML), acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).
  • Here, we demonstrated that PB Valpha24+ NKT cell numbers were significantly decreased in all the patients with haematopoietic malignancy in comparison with that in healthy donors (P < 0.005).
  • In particular CD4- CD8- Valpha24+ NKT cell numbers were more significantly decreased in the patients with haematopoietic malignancy (P < 0.0001).
  • [MeSH-major] Hematologic Neoplasms / blood. Killer Cells, Natural / cytology. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15607362.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Receptors, Antigen, T-Cell, alpha-beta
  •  go-up   go-down


70. Muehling BM, Toelkes S, Schelzig H, Barth TF, Sunder-Plassmann L: Tyrosine kinase expression in pulmonary metastases and paired primary tumors. Interact Cardiovasc Thorac Surg; 2010 Feb;10(2):228-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tissue specimen from 35 lung metastases of 33 patients with renal cell carcinoma (n=8), sarcoma (n=10), colorectal carcinoma (n=6), otolaryngologic carcinoma (OLC, n=4), testicular and endometrial cancer (n=1 each), malignant melanoma (n=1), adrenal cancer (n=2), malignant fibrous histiocytoma and malignant peripheral nerve sheath tumor (n=1 each) have been immunohistochemically tested for the expression of PDGFR alpha/beta, VEGFR and EGFR.
  • Our investigation of a pilot character represents a 'biomarker-based' analysis of pulmonary metastases of different primary tumors; we conclude that an immediate 'tumor profiling' at initial diagnosis should be considered in order to guide tumor therapy individually.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lung Neoplasms / enzymology. Lung Neoplasms / secondary. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Angiogenesis Inhibitors / therapeutic use. Female. Humans. Immunohistochemistry. Male. Middle Aged. Protein Kinase Inhibitors / therapeutic use. Receptor, Epidermal Growth Factor / analysis. Receptor, Platelet-Derived Growth Factor alpha / analysis. Receptor, Platelet-Derived Growth Factor beta / analysis. Receptors, Vascular Endothelial Growth Factor / analysis. Young Adult

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19948538.001).
  • [ISSN] 1569-9285
  • [Journal-full-title] Interactive cardiovascular and thoracic surgery
  • [ISO-abbreviation] Interact Cardiovasc Thorac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  •  go-up   go-down


71. Taura M, Fukuda R, Suico MA, Eguma A, Koga T, Shuto T, Sato T, Morino-Koga S, Kai H: TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis. Cancer Sci; 2010 Jul;101(7):1610-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis.
  • Toll-like receptor 3 (TLR3) has gained recognition as a novel molecular target for cancer therapy because TLR3 activation by its synthetic ligand poly I:C directly causes tumor cell death.
  • Recently, we reported that tumor suppressor p53 increases the expression of TLR3 in several tumor cell lines.
  • Another study also showed that interferon-alpha (IFN-alpha) up-regulates TLR3 expression.
  • We thus hypothesized that various anticancer drugs such as p53-activating reagents and IFNs may potentiate poly I:C-induced tumor cell death through the up-regulation of TLR3 expression.
  • Here, we screened several anticancer drugs that, together with poly I:C, effectively cause tumor cell death in colon carcinoma HCT116 cells.
  • On the other hand, IFN-alpha increased poly I:C-induced apoptosis and the TLR3 mRNA level in HCT116 p53(+/+) and p53(-/-) cell lines.
  • Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.
  • Considering that the p53 status in malignant cells is heterogeneous, this combination approach may provide a highly effective tumor therapy.
  • [MeSH-minor] Adenocarcinoma / genetics. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line. Cell Line, Tumor. Colorectal Neoplasms / genetics. DNA Damage / drug effects. Fluorouracil / pharmacology. Humans. Interferon-alpha / pharmacology. Interferon-beta / pharmacology. Kidney. Lung Neoplasms / genetics. Mice

  • Hazardous Substances Data Bank. FLUOROURACIL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20367642.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta; U3P01618RT / Fluorouracil
  •  go-up   go-down


72. Zhou J, Li NY, Zhou XJ, Zhou HB, Wu B, Jiang SJ, Ma HH, Zhang RS: [Clinicopathologic study of von Hippel-Lindau syndrome-related and sporadic hemangioblastomas of central nervous system]. Zhonghua Bing Li Xue Za Zhi; 2010 Mar;39(3):145-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To study clinicopathologic features, diagnosis, treatment and prognosis of von Hippel-Lindau (VHL) syndrome-related and sporadic hemangioblastomas of the central nervous system (CNS-HB).
  • There were 10 patients presenting other lesions related to VHL, including 6 retinal HBs, 4 pancreatic tumors (endocrine tumor and microcystic cystadenoma), 1 clear renal cell carcinoma, 4 renal cysts and 1 endolymphatic sac tumor.
  • Tumor cells of HB stained positive for vimentin, EGFR, Inhibin alpha and D2-40, but negative for CD34 and CD68.
  • CONCLUSIONS: VHL syndrome is a multisystem disorder with a poor prognosis and a high rate of missed diagnosis.
  • The syndrome is characterized by development of various benign and malignant tumors.
  • The most common tumor is CNS-HB, which occurs predominantly in the cerebellum.
  • [MeSH-minor] Adolescent. Adult. Carcinoma, Renal Cell / metabolism. Carcinoma, Renal Cell / pathology. Carcinoma, Renal Cell / surgery. Child. Female. Follow-Up Studies. Glial Fibrillary Acidic Protein / metabolism. Humans. Inhibins / metabolism. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Recurrence, Local. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Receptor, Epidermal Growth Factor / metabolism. Retinal Neoplasms / metabolism. Retinal Neoplasms / pathology. Retinal Neoplasms / surgery. Survival Analysis. Vimentin / metabolism. Young Adult

  • Genetic Alliance. consumer health - Von Hippel-Lindau syndrome.
  • MedlinePlus Health Information. consumer health - Von Hippel-Lindau Disease.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20450758.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Vimentin; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


73. Castor A, Nilsson L, Astrand-Grundström I, Buitenhuis M, Ramirez C, Anderson K, Strömbeck B, Garwicz S, Békássy AN, Schmiegelow K, Lausen B, Hokland P, Lehmann S, Juliusson G, Johansson B, Jacobsen SE: Distinct patterns of hematopoietic stem cell involvement in acute lymphoblastic leukemia. Nat Med; 2005 Jun;11(6):630-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct patterns of hematopoietic stem cell involvement in acute lymphoblastic leukemia.
  • The cellular targets of primary mutations and malignant transformation remain elusive in most cancers.
  • Primary ETV6-RUNX1 (also known as TEL-AML1) fusions and subsequent leukemic transformations were targeted to committed B-cell progenitors.
  • Major breakpoint BCR-ABL1 fusions (encoding P210 BCR-ABL1) originated in hematopoietic stem cells (HSCs), whereas minor BCR-ABL1 fusions (encoding P190 BCR-ABL1) had a B-cell progenitor origin, suggesting that P190 and P210 BCR-ABL1 ALLs represent largely distinct tumor biological and clinical entities.
  • In all patients, normal and leukemic repopulating stem cells could successfully be separated prospectively, and notably, the size of the normal HSC compartment in ETV6-RUNX1 and P190 BCR-ABL1 ALLs was found to be unaffected by the expansive leukemic stem cell population.
  • [MeSH-major] Fusion Proteins, bcr-abl / physiology. Hematopoietic Stem Cells / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification
  • [MeSH-minor] ADP-ribosyl Cyclase. Adult. Antigens, CD. Antigens, CD19. Antigens, CD34. Antigens, CD38. Child. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit. DNA-Binding Proteins / physiology. Flow Cytometry. Humans. Membrane Glycoproteins. Mutation. Nuclear Proteins / physiology. Oncogene Proteins, Fusion / physiology. Phenotype. Proto-Oncogene Proteins c-ets. Repressor Proteins / physiology. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15908956.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD34; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Membrane Glycoproteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
  •  go-up   go-down


74. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


75. Shiu SY, Pang B, Tam CW, Yao KM: Signal transduction of receptor-mediated antiproliferative action of melatonin on human prostate epithelial cells involves dual activation of Gα(s) and Gα(q) proteins. J Pineal Res; 2010 Oct;49(3):301-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Melatonin has been shown to inhibit the proliferation of malignant and transformed human prostate epithelial cells by transcriptional up-regulation of p27(Kip1) expression via MTNR1A receptor-mediated activation of protein kinase A (PKA) and protein kinase C (PKC) in parallel.
  • In 22Rv1 and RWPE-1 cells, knockdown of either Gα(s) or Gα(q) , but not Gα(i2) expression by RNA interference, abrogated the effects of melatonin on p27(Kip1) and cell proliferation.
  • Conversely, cellular overexpression of activated mutants of Gα(s) and Gα(q) in 22Rv1 and RWPE-1 cells mimicked the effects of melatonin on prostate epithelial cell antiproliferation by increasing p27(Kip1) expression through downstream activation of PKA and PKC in parallel.
  • [MeSH-major] Antioxidants / pharmacology. Cell Proliferation / drug effects. GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism. GTP-Binding Protein alpha Subunits, Gs / metabolism. Melatonin / pharmacology. Signal Transduction
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p27 / genetics. GTP-Binding Protein alpha Subunit, Gi2 / genetics. GTP-Binding Protein alpha Subunit, Gi2 / metabolism. Human papillomavirus 18 / genetics. Humans. RNA Interference. Radioimmunoassay. Receptors, Melatonin / antagonists & inhibitors. Reverse Transcriptase Polymerase Chain Reaction. Tetrahydronaphthalenes / pharmacology. Tryptamines / pharmacology

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MELATONIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 The Authors. Journal of Pineal Research © 2010 John Wiley & Sons A/S.
  • (PMID = 20695976.001).
  • [ISSN] 1600-079X
  • [Journal-full-title] Journal of pineal research
  • [ISO-abbreviation] J. Pineal Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-phenyl-2-propionamidotetraline; 0 / Antioxidants; 0 / Receptors, Melatonin; 0 / Tetrahydronaphthalenes; 0 / Tryptamines; 117946-91-5 / luzindole; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 3.6.5.1 / GTP-Binding Protein alpha Subunit, Gi2; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; JL5DK93RCL / Melatonin
  •  go-up   go-down


76. Bernardi RJ, Lowery AR, Thompson PA, Blaney SM, West JL: Immunonanoshells for targeted photothermal ablation in medulloblastoma and glioma: an in vitro evaluation using human cell lines. J Neurooncol; 2008 Jan;86(2):165-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunonanoshells for targeted photothermal ablation in medulloblastoma and glioma: an in vitro evaluation using human cell lines.
  • We are developing a novel approach to specifically target malignant brain tumor cells for photothermal ablation using antibody-tagged, near infrared-absorbing gold-silica nanoshells, referred to as immunonanoshells.
  • Once localized to tumor cells, these nanoshells are extremely efficient at absorbing near-infrared light and can generate sufficient heat to kill cancer cells upon exposure to laser light.
  • In this study, we evaluated the efficacy of immunonanoshells in vitro against both medulloblastoma and high-grade glioma cell lines.
  • We show that treatment with HER2-targeted nanoshells, but not non-targeted nanoshells, followed by exposure to laser light, can induce cell death in the HER2-overexpressing medulloblastoma cell line Daoy.2, as well as the parental Daoy cell line, which expresses HER2 at a moderate level, but not in dermal fibroblasts that do not express HER2.
  • In an analogous set of experiments, we conjugated gold-silica nanoshells to an antibody against interleukin-13 receptor-alpha 2 (IL13Ralpha2), an antigen that is frequently overexpressed in gliomas.
  • We demonstrate that these immunonanoshells are capable of inducing cell death in two high-grade glioma cell lines that express IL13Ralpha2, U373 and U87, but not in A431 epidermoid carcinoma cells that do not express significant levels of IL13Ralpha2.
  • [MeSH-minor] Combined Modality Therapy. Drug Delivery Systems / methods. Humans. Hyperthermia, Induced / methods. Infrared Rays. Interleukin-13 Receptor alpha2 Subunit / immunology. Interleukin-13 Receptor alpha2 Subunit / metabolism. Lasers. Radiation-Sensitizing Agents / therapeutic use. Receptor, ErbB-2 / immunology. Receptor, ErbB-2 / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioma.
  • Genetic Alliance. consumer health - Medulloblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Lasers Surg Med. 2006 Jun;38(5):384-9 [16788926.001]
  • [Cites] Br J Cancer. 2001 Sep 1;85(5):705-12 [11531256.001]
  • [Cites] Cancer Invest. 2006 Feb;24(1):77-81 [16466996.001]
  • [Cites] Clin Cancer Res. 2004 Nov 15;10(22):7613-20 [15569993.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5883-91 [16740728.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):140-8 [12517790.001]
  • [Cites] Cancer Lett. 2004 Jun 25;209(2):171-6 [15159019.001]
  • [Cites] Oncogene. 1990 Jul;5(7):953-62 [1973830.001]
  • [Cites] Curr Probl Cancer. 2003 Jul-Aug;27(4):177-97 [12855950.001]
  • [Cites] Int J Nanomedicine. 2006;1(2):149-54 [17722530.001]
  • [Cites] Nat Biotechnol. 2001 Apr;19(4):316-7 [11283581.001]
  • [Cites] J Natl Cancer Inst. 2002 Dec 4;94(23):1740-2 [12464643.001]
  • [Cites] J Neurosurg. 2005 Jan;102(1 Suppl):44-52 [16206733.001]
  • [Cites] Technol Cancer Res Treat. 2006 Jun;5(3):239-50 [16700620.001]
  • [Cites] Int Immunopharmacol. 2003 Mar;3(3):319-28 [12639809.001]
  • [Cites] Neoplasia. 2002 Sep-Oct;4(5):388-99 [12192597.001]
  • [Cites] Technol Cancer Res Treat. 2003 Aug;2(4):303-9 [12892512.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13549-54 [14597719.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5508-13 [16554374.001]
  • [Cites] Anticancer Drugs. 2006 Oct;17(9):1003-16 [17001172.001]
  • [Cites] J Clin Oncol. 2006 Mar 10;24(8):1273-80 [16525182.001]
  • [Cites] Ann Biomed Eng. 2006 Jan;34(1):15-22 [16528617.001]
  • [Cites] Cancer. 2004 Sep 1;101(5):1036-42 [15329913.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):984-93 [14970185.001]
  • (PMID = 17805488.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / 3U10 HD 037242-08S1; United States / NIDDK NIH HHS / DK / 5T90 DK 070121-02; United States / NCI NIH HHS / CA / R21 CA 118788
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / Radiation-Sensitizing Agents; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


77. Meyuhas R, Pikarsky E, Tavor E, Klar A, Abramovitch R, Hochman J, Lago TG, Honigman A: A Key role for cyclic AMP-responsive element binding protein in hypoxia-mediated activation of the angiogenesis factor CCN1 (CYR61) in Tumor cells. Mol Cancer Res; 2008 Sep;6(9):1397-409
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A Key role for cyclic AMP-responsive element binding protein in hypoxia-mediated activation of the angiogenesis factor CCN1 (CYR61) in Tumor cells.
  • Hypoxia is a prominent feature of solid tumors known to contribute to malignant progression and therapeutic resistance.
  • Induction of new blood vessel formation via the secretion of proangiogenic factors is one of the main adaptive responses engaged by tumor cells under hypoxic conditions.
  • In this work, we show that the expression of the angiogenesis-related, immediate early gene CCN1 (formerly known as CYR61), considered to be involved in tumor growth and invasiveness, is enhanced upon hypoxia stress primarily in a protein kinase A and cyclic AMP-responsive element binding protein (CREB) and CRE-dependent manner in various cell lines.
  • [MeSH-major] Cell Hypoxia. Cyclic AMP Response Element-Binding Protein / physiology. Gene Expression Regulation / physiology. Immediate-Early Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Response Elements
  • [MeSH-minor] Animals. Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Blotting, Western. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cells, Cultured. Cyclic AMP / pharmacology. Cyclic AMP-Dependent Protein Kinases / physiology. Cysteine-Rich Protein 61. Dinoprostone / pharmacology. Electrophoretic Mobility Shift Assay. Fibroblasts / metabolism. Fibroblasts / pathology. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. In Situ Hybridization. Liver Neoplasms, Experimental / genetics. Liver Neoplasms, Experimental / metabolism. Liver Neoplasms, Experimental / pathology. Luciferases / metabolism. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Lymphoma, T-Cell / pathology. Mice. Mice, Inbred BALB C. NIH 3T3 Cells. Promoter Regions, Genetic. RNA Probes. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription, Genetic. Transfection

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18819928.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CYR61 protein, human; 0 / Creb1 protein, mouse; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Cyr61 protein, mouse; 0 / Cysteine-Rich Protein 61; 0 / HIF1A protein, human; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA Probes; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / endothelial PAS domain-containing protein 1; E0399OZS9N / Cyclic AMP; EC 1.13.12.- / Luciferases; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K7Q1JQR04M / Dinoprostone
  •  go-up   go-down


78. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


79. Sampson JH, Akabani G, Archer GE, Berger MS, Coleman RE, Friedman AH, Friedman HS, Greer K, Herndon JE 2nd, Kunwar S, McLendon RE, Paolino A, Petry NA, Provenzale JM, Reardon DA, Wong TZ, Zalutsky MR, Pastan I, Bigner DD: Intracerebral infusion of an EGFR-targeted toxin in recurrent malignant brain tumors. Neuro Oncol; 2008 Jun;10(3):320-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intracerebral infusion of an EGFR-targeted toxin in recurrent malignant brain tumors.
  • The purpose of this study is to determine the maximum tolerated dose (MTD), dose-limiting toxicity (DLT), and intracerebral distribution of a recombinant toxin (TP-38) targeting the epidermal growth factor receptor in patients with recurrent malignant brain tumors using the intracerebral infusion technique of convection-enhanced delivery (CED).
  • Twenty patients were enrolled and stratified for dose escalation by the presence of residual tumor from 25 to 100 ng/ml in a 40-ml infusion volume.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Med. 2003 May;9(5):589-95 [12669033.001]
  • [Cites] Cancer Metastasis Rev. 1987;6(4):559-93 [3327633.001]
  • [Cites] Acta Neurochir Suppl. 2003;88:93-103 [14531567.001]
  • [Cites] Acta Neurochir Suppl. 2003;88:105-11 [14531568.001]
  • [Cites] J Neurosurg. 2003 Nov;99(5):893-8 [14609170.001]
  • [Cites] J Neurooncol. 2003 Oct;65(1):27-35 [14649883.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5514-20 [14654531.001]
  • [Cites] J Neurooncol. 2004 Jan;66(1-2):197-201 [15015787.001]
  • [Cites] J Neurosurg. 2004 Mar;100(3):472-9 [15035283.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2572-9 [15059914.001]
  • [Cites] J Neurooncol. 2004 May;68(1):1-9 [15174514.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6858-62 [15466173.001]
  • [Cites] Cancer Res. 1989 May 15;49(10):2807-13 [2469537.001]
  • [Cites] Cancer Res. 1990 Feb 1;50(3 Suppl):814s-819s [2404582.001]
  • [Cites] Front Radiat Ther Oncol. 1990;24:32-46; discussion 64-8 [2187763.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Ann Neurol. 1990 Dec;28(6):818-22 [2178330.001]
  • [Cites] Cancer Metastasis Rev. 1990 Nov;9(3):253-66 [2292138.001]
  • [Cites] Cancer Immunol Immunother. 1991;33(1):61-4 [2021959.001]
  • [Cites] Science. 1991 Nov 22;254(5035):1173-7 [1683495.001]
  • [Cites] APMIS. 1992 Aug;100(8):713-9 [1520484.001]
  • [Cites] Am J Physiol. 1994 Jan;266(1 Pt 2):R292-305 [8304553.001]
  • [Cites] Cancer Res. 1994 Feb 15;54(4):1008-15 [8313355.001]
  • [Cites] J Neurosurg. 1994 Mar;80(3):520-6 [8113865.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2076-80 [8134351.001]
  • [Cites] J Neurosurg. 1995 Jun;82(6):1021-9 [7539062.001]
  • [Cites] Cancer Res. 1996 Dec 15;56(24):5631-7 [8971168.001]
  • [Cites] J Neurosurg. 1997 Oct;87(4):586-94 [9322847.001]
  • [Cites] Biochim Biophys Acta. 1997 Oct 24;1333(2):C1-6 [9395287.001]
  • [Cites] Nat Med. 1997 Dec;3(12):1362-8 [9396606.001]
  • [Cites] Curr Top Microbiol Immunol. 1998;234:97-114 [9670615.001]
  • [Cites] J Neurosurg. 1999 Feb;90(2):321-31 [9950504.001]
  • [Cites] Am J Physiol. 1999 Oct;277(4 Pt 2):R1218-29 [10516265.001]
  • [Cites] J Neurosurg. 2004 Dec;101(6):1004-11 [15597761.001]
  • [Cites] Ann Neurol. 2005 Feb;57(2):298-302 [15668979.001]
  • [Cites] Neuro Oncol. 2005 Jan;7(1):90-6 [15701286.001]
  • [Cites] J Neurosurg. 2005 Feb;102(2):267-75 [15739554.001]
  • [Cites] Clin Cancer Res. 2000 Feb;6(2):326-34 [10690507.001]
  • [Cites] Leukemia. 2000 Apr;14(4):576-85 [10764142.001]
  • [Cites] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2157-65 [10873064.001]
  • [Cites] Clin Cancer Res. 2000 Oct;6(10):4148-53 [11051269.001]
  • [Cites] Cell Transplant. 2000 Sep-Oct;9(5):585-94 [11144956.001]
  • [Cites] Exp Neurol. 2001 Mar;168(1):155-61 [11170730.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):376-88 [11208829.001]
  • [Cites] Neuro Oncol. 2000 Jan;2(1):45-59 [11302254.001]
  • [Cites] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661.001]
  • [Cites] Neurosurgery. 2005 Jun;56(6):1243-52; discussion 1252-3 [15918940.001]
  • [Cites] Nat Med. 2005 Jul;11(7):703-4 [16015352.001]
  • [Cites] Exp Neurol. 2005 Aug;194(2):476-83 [16022872.001]
  • [Cites] J Neurosurg. 2005 Nov;103(5):923-9 [16304999.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3145-51 [16707614.001]
  • [Cites] Neuro Oncol. 2007 Jul;9(3):343-53 [17435179.001]
  • [Cites] Cancer Res. 1984 Feb;44(2):753-60 [6318976.001]
  • [Cites] Cancer Res. 1987 Jun 15;47(12):3039-51 [3555767.001]
  • [Cites] J Neurooncol. 2003 Aug-Sep;64(1-2):125-37 [12952293.001]
  • (PMID = 18403491.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NCRR NIH HHS / RR / K23 RR016065; United States / NCRR NIH HHS / RR / K23 RR16065; United States / NCRR NIH HHS / RR / S10 RR15697; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / CA11898; United States / NCI NIH HHS / CA / R01 CA097611; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NCI NIH HHS / CA / P50-CA097257; United States / NINDS NIH HHS / NS / 2P50-NS20023; United States / NCI NIH HHS / CA / R37 CA011898
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Exotoxins; 0 / Immunotoxins; 0 / Transforming Growth Factor alpha; 0 / transforming growth factor(alpha)-Pseudomonas aeruginosa exotoxin (38); EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2563054
  •  go-up   go-down


80. Maxwell PJ, Gallagher R, Seaton A, Wilson C, Scullin P, Pettigrew J, Stratford IJ, Williams KJ, Johnston PG, Waugh DJ: HIF-1 and NF-kappaB-mediated upregulation of CXCR1 and CXCR2 expression promotes cell survival in hypoxic prostate cancer cells. Oncogene; 2007 Nov 15;26(52):7333-45
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF-1 and NF-kappaB-mediated upregulation of CXCR1 and CXCR2 expression promotes cell survival in hypoxic prostate cancer cells.
  • Hypoxic cancer cells are resistant to treatment, leading to the selection of cells with a more malignant phenotype.
  • Finally, inhibition of IL-8 signaling potentiated etoposide-induced cell death in hypoxic PC3 cells.
  • These results suggest that IL-8 signaling confers a survival advantage to hypoxic prostate cancer cells, and therefore, strategies to inhibit IL-8 signaling may sensitize hypoxic tumor cells to conventional treatments.
  • [MeSH-major] Hypoxia. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. NF-kappa B / metabolism. Prostatic Neoplasms / metabolism. Receptors, Interleukin-8A / genetics. Receptors, Interleukin-8B / genetics
  • [MeSH-minor] Cell Survival. Chromatin Immunoprecipitation. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoblotting. Immunoprecipitation. Interleukin-8 / metabolism. Male. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription, Genetic. Up-Regulation

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17533374.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500366; United Kingdom / Wellcome Trust / / 067104/Z/02/Z
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Receptors, Interleukin-8A; 0 / Receptors, Interleukin-8B
  •  go-up   go-down


81. Karmakar S, Banik NL, Ray SK: Combination of all-trans retinoic acid and paclitaxel-induced differentiation and apoptosis in human glioblastoma U87MG xenografts in nude mice. Cancer; 2008 Feb 1;112(3):596-607
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Glioblastoma, which is the most malignant brain tumor, remains incurable and almost always causes death.
  • The efficacy of treatments in controlling tumor growth was assessed by histologic examination, Western blot analysis, and immunofluorescent labelings.
  • Combination therapy activated the receptor-mediated pathway of apoptosis with induction of TNF-alpha, activation of caspase-8, and cleavage of Bid to tBid.
  • In addition, combination therapy promoted phosphorylation of Bcl-2 for its inactivation and down-regulated NF-kappaB and BIRC proteins, indicating suppression of several cell survival factors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Differentiation / drug effects. Central Nervous System Neoplasms / pathology. Glioblastoma / pathology. Paclitaxel / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cysteine Endopeptidases / metabolism. Glial Fibrillary Acidic Protein / metabolism. Humans. Inhibitor of Apoptosis Proteins / metabolism. Mice. Mice, Nude. Mitogen-Activated Protein Kinase Kinases / metabolism. NF-kappa B / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Telomerase / metabolism. Ubiquitin-Protein Ligases. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / metabolism

  • Genetic Alliance. consumer health - Glioblastoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. TAXOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18098270.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / C06 RR15455; United States / NCI NIH HHS / CA / CA-91460; United States / NINDS NIH HHS / NS / NS-57811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC2 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Inhibitor of Apoptosis Proteins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 5688UTC01R / Tretinoin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Cysteine Endopeptidases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


82. Netto CD, da Silva AJ, Salustiano EJ, Bacelar TS, Riça IG, Cavalcante MC, Rumjanek VM, Costa PR: New pterocarpanquinones: synthesis, antineoplasic activity on cultured human malignant cell lines and TNF-alpha modulation in human PBMC cells. Bioorg Med Chem; 2010 Feb 15;18(4):1610-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New pterocarpanquinones: synthesis, antineoplasic activity on cultured human malignant cell lines and TNF-alpha modulation in human PBMC cells.
  • These compounds showed to be active against human leukemic cell lines and human lung cancer cell lines.
  • Even multidrug resistant cells were sensitive to 5a, which presented low toxicity toward peripheral blood mononuclear cells (PBMC) cells and decreased the production of TNF-alpha by these cells.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Antineoplastic Agents / pharmacology. Monocytes / drug effects. Pterocarpans / chemical synthesis. Pterocarpans / pharmacology. Quinones / chemical synthesis. Quinones / pharmacology. Tumor Necrosis Factor-alpha / drug effects
  • [MeSH-minor] Cell Line, Tumor. Humans. Magnetic Resonance Spectroscopy. Spectrometry, Mass, Electrospray Ionization

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20117936.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pterocarpans; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


83. Watanabe A, Mabuchi T, Satoh E, Furuya K, Zhang L, Maeda S, Naganuma H: Expression of syndecans, a heparan sulfate proteoglycan, in malignant gliomas: participation of nuclear factor-kappaB in upregulation of syndecan-1 expression. J Neurooncol; 2006 Mar;77(1):25-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of syndecans, a heparan sulfate proteoglycan, in malignant gliomas: participation of nuclear factor-kappaB in upregulation of syndecan-1 expression.
  • Invasion of tumor cells into the surrounding normal brain tissues is a prominent feature of malignant gliomas.
  • Malignant glioma cells secrete thrombospondin-1 which participates in the motility of glioma cells and binds cell surface heparan sulfate proteoglycan.
  • To clarify the invasion mechanism of tumor cells, expression of the syndecans (syndecan-1, -2, -3, and -4), a major cell surface heparan sulfate proteoglycan family, was analyzed in malignant gliomas.
  • Using reverse transcription-PCR, the authors analyzed the expression of syndecan-1, -2, -3, and -4 in 10 malignant glioma cell lines, 2 glioblastoma specimens, and 2 normal brain specimens.
  • All malignant glioma cell lines and glioblastoma specimens expressed all types of syndecan mRNA, except in one glioma cell line that lacked syndecan-3 expression.
  • Syndecan-1 protein was localized in the cell surface of all malignant glioma cell lines by flow cytometry.
  • Various levels of active nuclear factor-kappa B (NF-kappaB) was detected in all malignant glioma cell lines using immunoblotting.
  • The expression of active NF-kappaB and syndecan-1 increased in U251 glioma cells after tumor necrosis factor-alpha or interleukin-1beta treatment, which can activate NF-kappaB.
  • The amplification of active NF-kappaB and syndecan-1 by tumor necrosis factor-alpha or interleukin-1beta was suppressed by an inhibitor of NF-kappaB activation (emodin).
  • These results indicate that malignant glioma cells express all types of syndecans and suggest that NF-kappaB participates in the upregulation of the syndecan-1 expression at the transcriptional level, and increased expression of syndecan-1 could associate with extracellular matrices including thrombospondin-1.
  • [MeSH-minor] Cell Line, Tumor. Cerebral Cortex / metabolism. Extracellular Matrix Proteins / genetics. Extracellular Matrix Proteins / metabolism. Fibroblast Growth Factor 2 / physiology. Gene Expression Regulation, Neoplastic. Humans. Lymphotoxin-alpha / physiology. Proteoglycans / classification. Proteoglycans / genetics. Proteoglycans / metabolism. RNA, Messenger / analysis. Syndecan-1. Syndecan-2. Syndecan-3. Syndecan-4. Syndecans. Thrombospondin 1 / metabolism