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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
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  • 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.

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  • (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
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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
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  • 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

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  • (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
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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
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  • [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

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  • (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
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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
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  • [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

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  • (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
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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
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  • 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

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  • (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
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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
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  • 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
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  • [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

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  • (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
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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
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  • [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.

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  • (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
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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
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  • [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
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  • [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

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  • (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
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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
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  • [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

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  • (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
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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
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  • 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

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  • (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
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13. 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
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  • [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

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  • (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
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14. 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
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  • [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

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  • (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
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15. 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
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  • [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

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  • (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
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16. Greco S, Elia MG, Muscella A, Romano S, Storelli C, Marsigliante S: Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. J Endocrinol; 2005 Aug;186(2):291-301
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  • [Title] Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture.
  • We here investigated the mitogenic effects and the signalling pathways of BK in primary cultured human epithelial breast cells obtained from a tumour and from the histologically proven non-malignant tissue adjacent to the tumour.
  • BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2).
  • In conclusion, the mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression.
  • [MeSH-minor] Analysis of Variance. Calcium / analysis. Cell Proliferation / drug effects. Enzyme Activation. Female. Humans. Immunoblotting / methods. Intracellular Fluid / chemistry. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / metabolism. Receptors, Bradykinin / metabolism. Tumor Cells, Cultured

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  • (PMID = 16079255.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mitogens; 0 / Receptors, Bradykinin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
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17. 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
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  • [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.

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  • (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
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18. 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
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  • [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.

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  • (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
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19. 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
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  • [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

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  • [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
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20. 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
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  • [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

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  • (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
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26. 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
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  • 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

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  • (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
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27. 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
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  • [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

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  • (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
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28. 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
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  • [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

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  • (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
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29. 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
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  • [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

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  • (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
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30. 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
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  • 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


31. 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
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  • [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

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  • (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
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32. 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
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  • 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

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

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  • (PMID = 18522536.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1-methyltryptophan; 0 / Amino Acid Transport Systems; 0 / Amino Acid Transport Systems, Neutral; 0 / Antineoplastic Agents; 0 / Large Neutral Amino Acid-Transporter 1; 0 / Plasma Membrane Neurotransmitter Transport Proteins; 0 / SLC6A14 protein, human; 0 / Slc6A14 protein, mouse; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan
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34. 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
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  • [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

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  • (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
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35. 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
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  • 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


36. 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
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  • [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

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  • [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
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37. Abdou AG, Aiad HA, Sultan SM: pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor status. APMIS; 2008 Nov;116(11):961-71
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  • [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

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  • (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
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38. 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
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  • 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

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  • [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
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39. 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
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  • [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

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  • (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
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40. Appetecchia M, Ferretti E, Carducci M, Izzo F, Carpanese L, Marandino F, Terzoli E: Malignant glucagonoma. New options of treatment. J Exp Clin Cancer Res; 2006 Mar;25(1):135-9
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  • [Title] Malignant glucagonoma. New options of treatment.
  • Few cases of malignant glucagonomas have been described in the literature.
  • In this paper we present a case of a 77-year-old woman with necrolytic migratory erythema and high plasma glucagon and chromogranin A levels caused by a neuroendocrine tumour.
  • An abdominal CT scan suggested a pancreatic lesion and two liver metastases.
  • The patient underwent pancreatic debulking and liver metastasectomy.
  • Histological and immunohistochemical investigations revealed a well differentiated neuroendocrine tumour with vascular invasion and scattered immunopositivity for somatostatin receptors.
  • The patient was treated with octreotide (30 mg i.m. every 28 days) and interferon-alpha (6 MU s.cc 3 times per week) plus three cycles of hepatic chemoembolisation.
  • The patient is now asymptomatic with persistent hepatic disease and normal serum glucagon levels forty months after primary treatment.
  • So far, only few immunohistochemical studies are reported on malignant glucagonoma and combined treatment schedules.
  • We demonstrated, for the first time, a scattered immunopositivity for somatostatin receptors in a malignant glucagonoma.
  • A combined antiproliferative medical treatment and the hepatic chemoembolization have been able to control tumor growth and disease symptoms for a long time after surgery.
  • [MeSH-major] Glucagonoma / therapy
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Female. Glucagon / blood. Humans. Immunohistochemistry. Interferon-alpha / metabolism. Neuroendocrine Tumors / blood. Octreotide / pharmacology. Proglucagon / metabolism. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16761630.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Interferon-alpha; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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41. 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
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  • 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

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  • (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
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42. 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
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  • [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

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  • (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
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43. 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
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  • [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

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  • (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
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44. 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
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  • [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

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  • (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
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45. 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
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  • [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

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  • (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
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46. 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
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  • 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

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  • (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
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47. 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
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  • 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


48. Kristiansen G: [Immunohistochemical algorithms in prostate diagnostics: what's new?]. Pathologe; 2009 Dec;30 Suppl 2:146-53
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  • 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

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  • (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
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49. 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
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  • 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


50. 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
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  • 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

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  • (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
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51. 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
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  • 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

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  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
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  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1924715
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52. 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
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  • [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

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  • (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
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53. 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
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  • 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

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  • (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
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54. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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55. 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
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  • [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

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  • (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
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56. 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
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  • [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

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  • (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
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57. 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
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  • [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

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  • (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
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58. 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
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  • 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

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  • (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
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59. 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
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  • [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


60. 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
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  • [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.

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  • (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
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61. 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
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  • 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

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  • (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
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62. 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
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  • [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

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  • (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
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63. 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
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  • 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

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  • (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
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64. 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
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  • [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

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  • (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
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65. 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
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  • 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

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  • (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
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66. 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
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  • [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

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  • (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
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67. Przybyło M, Lityńska A, Pocheć E: Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation. Biochimie; 2005 Feb;87(2):133-42
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  • [Title] Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation.
  • In tumour cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • This study used cell lines having very different behaviour in vivo: HCV29 non-malignant transitional epithelium and T24 bladder transitional cell carcinoma.
  • The functional role of carbohydrates was studied by treating these cells with swainsonine, an inhibitor of Golgi alpha-mannosidase II, and in vitro adhesion and migration assays.
  • Swainsonine treatment reduced the rate of T24 cell migration by 20%.
  • We concluded that beta1-6 branched tri- and tetraantennary complex-type glycans have an important function in adhesion and migration in the studied cell lines.
  • [MeSH-major] Cell Movement. Epithelial Cells / metabolism. Polysaccharides / biosynthesis. Ureter / metabolism. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Glycosylation / drug effects. Humans. Male. Species Specificity. Swainsonine / pharmacology

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  • (PMID = 15760705.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Polysaccharides; RSY4RK37KQ / Swainsonine
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68. 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
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  • 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

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  • [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
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69. 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
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  • [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

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

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  • (PMID = 16079290.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alpha2beta1; 0 / Protease Inhibitors; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; 9007-34-5 / Collagen; EC 3.4.- / Metalloproteases
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76. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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77. Mathieu J, Besançon F: Clinically tolerable concentrations of arsenic trioxide induce p53-independent cell death and repress NF-kappa B activation in Ewing sarcoma cells. Int J Cancer; 2006 Oct 1;119(7):1723-7
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  • [Title] Clinically tolerable concentrations of arsenic trioxide induce p53-independent cell death and repress NF-kappa B activation in Ewing sarcoma cells.
  • Ewing sarcoma (ES), a highly malignant pediatric tumor, is consistently associated with translocations that fuse the EWS gene with a member of the ETS family gene, most commonly FLI-1.
  • It is therefore necessary to explore novel agents for possible treatment of this tumor.
  • Here the authors investigated the sensitivity of ES cells to clinically tolerable concentrations of arsenic trioxide (As2O3), a compound known to induce differentiation and apoptosis of other types of malignant cells.
  • The authors report that As2O3 uniformly induced death of 6 ES-derived cell lines irrespective of their p53 status.
  • These effects, combined with its antiangiogenic action, define As2O3 as a good candidate for future protocols to improve treatments of Ewing sarcomas, irrespective of the p53 status of the tumor.
  • [MeSH-minor] Caspases / metabolism. Cell Line, Tumor. Enzyme Activation / drug effects. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Mitochondria / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Protein p53 / metabolism

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16646077.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / NF-kappa B; 0 / Oxides; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
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78. Marsee DK, Vadysirisack DD, Morrison CD, Prasad ML, Eng C, Duh QY, Rauen KA, Kloos RT, Jhiang SM: Variable expression of coxsackie-adenovirus receptor in thyroid tumors: implications for adenoviral gene therapy. Thyroid; 2005 Sep;15(9):977-87
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  • Moreover, preincubation with alpha-CAR antibody decreased infectivity in FTC 238 cells, a human thyroid tumor line.
  • Immunohistochemical analysis revealed that CAR is expressed at the cell surface in the majority of malignant thyroid tumors.
  • [MeSH-minor] Animals. Cell Line, Tumor. Flow Cytometry. Immunohistochemistry. Integrin alphaVbeta3 / genetics. Integrins / genetics. Plasmids / genetics. Polylysine / metabolism. Rats. Receptors, Vitronectin / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16187905.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA60074; United States / NIDCR NIH HHS / DE / T32DE14320
  • [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 / Integrin alphaVbeta3; 0 / Integrins; 0 / Receptors, Virus; 0 / Receptors, Vitronectin; 0 / integrin alphaVbeta5; 25104-18-1 / Polylysine
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79. Kashiwagi K, Virgona N, Harada K, Kido W, Yano Y, Ando A, Hagiwara K, Yano T: A redox-silent analogue of tocotrienol acts as a potential cytotoxic agent against human mesothelioma cells. Life Sci; 2009 May 8;84(19-20):650-6
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  • AIMS: Malignant mesothelioma is an aggressive cancer with no effective treatment options.
  • A redox-silent analogue of alpha-tocotrienol, 6-O-carboxypropyl-alpha-tocotrienol (T3E) is a new potential anti-carcinogenic agent with less toxic effect on non-tumorigenic cells.
  • Here, we evaluated the effect of T3E on killing of chemoresistant mesothelioma cell (H28).
  • MAIN METHODS: The cytotoxic effect of T3E was evaluated by a WST-1 assay, and cell cycle and apoptosis analysis were done by FACS.
  • KEY FINDINGS: T3E effectively inhibited H28 cell growth at practical pharmacological concentrations (10-20 muM) without any effect on non-tumorigenic mesothelial cell (Met-5A).
  • Inhibition of H28 cell growth by T3E mediated through G2/M arrest in cell cycle and induction of apoptosis.
  • However, the blockade of the EGFR signaling was not associated with the T3E-dependent H28 cell growth control.
  • These results suggest that T3E suppresses H28 cell growth via the inhibition of Src activation and Src-independent Stat3 activation.
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Drug Resistance, Neoplasm. Enzyme Activation. Humans. Oxidation-Reduction. Protein Array Analysis. STAT3 Transcription Factor / metabolism. src-Family Kinases / metabolism


80. Kamata S, Kishimoto T, Kobayashi S, Miyazaki M, Ishikura H: Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells. Cancer Biol Ther; 2007 Jul;6(7):1036-43
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  • [Title] Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells.
  • AFP-producing gastric carcinoma (AFPGC) is a highly malignant variant of gastric cancer.
  • Survival signals activated by intracellular kinase networks could be involved in chemoresistance in malignant tumors.
  • We investigated the role of a pivotal kinase pathway, the mammalian target of rapamycin complex 1 (mTORC1) pathway, in the effectiveness of chemotherapeutic agents in three AFPGC cell lines (GCIY, FU97 and Takigawa) as well as in four cell lines of conventional-type gastric carcinoma (CGC).
  • Downstream targets of mTORC1, including p70S6K and 4EBP1, were phosphorylated in all cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cisplatin / pharmacology. Protein Kinases / physiology. Signal Transduction / physiology. Stomach Neoplasms / drug therapy. alpha-Fetoproteins / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. Male. Mice. Mice, Inbred BALB C. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Transcription Factors / physiology. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / analysis

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  • (PMID = 17568186.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CRTC1 protein, human; 0 / Transcription Factors; 0 / alpha-Fetoproteins; 0 / bcl-2-Associated X Protein; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
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81. Rainov NG, Söling A: Clinical studies with targeted toxins in malignant glioma. Rev Recent Clin Trials; 2006 May;1(2):119-31
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  • [Title] Clinical studies with targeted toxins in malignant glioma.
  • Targeted toxins represent a new class of agents with high specificity for tumor cells.
  • Toxins in current clinical use for the treatment of brain tumors are mostly recombinant polypeptides consisting of a tumor-selective ligand coupled to a peptide toxin of bacterial origin.
  • Targeted toxins are highly potent - one single molecule of toxin is enough to cause cell death.
  • Toxins are able to kill tumor cells independent of any malignancy-associated genetic alterations and/or mutations.
  • The blood-brain barrier has been a major obstacle for using targeted toxins for treatment of malignant glioma.
  • Convection-enhanced delivery (CED), a method for delivery of large molecules to brain tissue via continuous interstitial microinfusion, has permitted direct administration of toxins to brain tumors or to surrounding brain tissue infiltrated by tumor cells.
  • Four targeted toxins advanced to at least phase II clinical trials and are being used for treatment of adult or pediatric patients with recurrent or progressive malignant glioma.
  • These are IL4-P. aeruginosa exotoxin (IL4-PE, NBI-3001), tumor growth factor (TGF)alpha-P. aeruginosa exotoxin (TP-38), IL13-P. aeruginosa exotoxin (IL13-PE38), and transferrin-C. diphtheriae toxin (TransMID(trade mark), Tf-CRM107).
  • All of these toxins have shown an acceptable profile of toxicity and safety in phase I and II clinical studies and have demonstrated some evidence for tumor response.
  • Current phase I and II clinical protocols are exploring several parameters, such as placement of catheters for CED either intratumorally or in the brain tissue surrounding a tumor, surgical resection of tumor before or after toxin infusion, and single vs. repeated infusion.
  • This review summarizes the study protocols and key findings of all previously completed and currently ongoing clinical studies with targeted toxins for malignant glioma.
  • [MeSH-major] Brain Neoplasms / therapy. Clinical Trials as Topic. Exotoxins / therapeutic use. Glioma / therapy. Immunologic Factors / therapeutic use. Immunotoxins / therapeutic use. Transforming Growth Factor alpha / therapeutic use

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  • (PMID = 18473963.001).
  • [ISSN] 1574-8871
  • [Journal-full-title] Reviews on recent clinical trials
  • [ISO-abbreviation] Rev Recent Clin Trials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Exotoxins; 0 / IL13-PE38; 0 / Immunologic Factors; 0 / Immunotoxins; 0 / Interleukin-13; 0 / Recombinant Fusion Proteins; 0 / Tf-CRM107; 0 / Transferrin; 0 / Transforming Growth Factor alpha; 0 / interleukin-4-Pseudomonas exotoxin; 0 / transforming growth factor(alpha)-Pseudomonas aeruginosa exotoxin (38); 207137-56-2 / Interleukin-4
  • [Number-of-references] 85
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82. Diaz Z, Mann KK, Marcoux S, Kourelis M, Colombo M, Komarnitsky PB, Miller WH Jr: A novel arsenical has antitumor activity toward As2O3-resistant and MRP1/ABCC1-overexpressing cell lines. Leukemia; 2008 Oct;22(10):1853-63
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  • [Title] A novel arsenical has antitumor activity toward As2O3-resistant and MRP1/ABCC1-overexpressing cell lines.
  • Darinaparsin is significantly more potent than As(2)O(3) at mediating apoptosis in various malignant cell lines and is highly active against APL cells derived for As(2)O(3) resistance.
  • However, darinaparsin does not induce promyelocytic leukemia/retinoic acid receptor alpha (PML/RAR alpha) degradation or rearrange PML nuclear bodies in APL cells, nor is its toxicity increased by glutathione depletion.
  • Our studies indicate that darinaparsin efficiently kills tumor cells with increased antioxidant capacity and drug exporters and suggest that darinaparsin may have a broader therapeutic spectrum than As(2)O(3).
  • [MeSH-minor] Animals. Anthracenes / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. MAP Kinase Kinase 4 / physiology. Mice. Oncogene Proteins, Fusion / metabolism. Oxidative Stress / drug effects

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  • [ErratumIn] Leukemia. 2009 Feb;23(2):431
  • (PMID = 18633430.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracenes; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Multidrug Resistance-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; 0 / multidrug resistance-associated protein 1; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 9XX54M675G / darinaparsin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; GAN16C9B8O / Glutathione; S7V92P67HO / arsenic trioxide
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83. Fan QW, Knight ZA, Goldenberg DD, Yu W, Mostov KE, Stokoe D, Shokat KM, Weiss WA: A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. Cancer Cell; 2006 May;9(5):341-9
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  • The PI3 kinase family of lipid kinases promotes cell growth and survival by generating the second messenger phosphatidylinositol-3,4,5-trisphosphate.
  • The unique cellular activity of PI-103 was traced directly to its ability to inhibit both PI3 kinase alpha and mTOR.
  • These data demonstrate an emergent efficacy due to combinatorial inhibition of mTOR and PI3 kinase alpha in malignant glioma.

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  • (PMID = 16697955.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097257-04; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / P50 CA097257-05; United States / NCI NIH HHS / CA / P50 CA097257-04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 0 / Protein Isoforms; 0 / Tumor Suppressor Protein p53; 0 / platinum 103; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.1.137 / PIK3CB protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ NIHMS225839; NLM/ PMC2925230
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84. Mon NN, Kokuryo T, Hamaguchi M: Inflammation and tumor progression: a lesson from TNF-alpha-dependent FAK signaling in cholangiocarcinoma. Methods Mol Biol; 2009;512:279-93
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  • [Title] Inflammation and tumor progression: a lesson from TNF-alpha-dependent FAK signaling in cholangiocarcinoma.
  • We have shown that FAK plays a critical role in MMP-9 production and subsequent invasion of the cholangiocarcinoma activated by an inflammatory cytokine, TNF-alpha.
  • Immunoprecipitation and western blot analysis together with site specific phosphorylated FAK antibodies showed aberrant FAK activity in inflammation-mediated tumor cells.
  • Confocal immunofluorescence staining could confirm not only localization but also phosphotyrosine contents of phosphorylated FAK by TNF-alpha stimulation.
  • Destruction or penetration of the basement membrane is thought to be an essential step in successful metastasis by tumor cells, we used a matrix of basement membrane which was reconstituted on to a filter in the Boyden Chamber and assayed the ability of cancer cells to penetrate through matrigel-coated filter.
  • We demonstrated the effectiveness of FAK siRNA treatment to prevent tumor invasion.
  • Our observations suggested the importance of FAK as a therapeutic target for malignant neoplasm.
  • [MeSH-major] Bile Duct Neoplasms / metabolism. Bile Ducts, Intrahepatic / metabolism. Cholangiocarcinoma / metabolism. Focal Adhesion Protein-Tyrosine Kinases / metabolism. Inflammation / metabolism. Signal Transduction. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Blotting, Western. Cell Movement. Fluorescent Antibody Technique. Humans. Immunoprecipitation. Phosphorylation. Tumor Cells, Cultured

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  • (PMID = 19347283.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
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85. Qi Y, Chiu JF, Wang L, Kwong DL, He QY: Comparative proteomic analysis of esophageal squamous cell carcinoma. Proteomics; 2005 Jul;5(11):2960-71
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  • [Title] Comparative proteomic analysis of esophageal squamous cell carcinoma.
  • Ranking as the fourth commonest cancer, esophageal squamous cell carcinoma (ESCC) represents one of the leading causes of cancer death in China.
  • A better understanding of the malignant mechanism and early diagnosis are important for fighting ESCC.
  • Compared to those in adjacent normal epitheliums, the expression of 15 proteins including enolase, elongation factor Tu, isocitrate dehydrogenase, tubulin alpha-1 chain, tubulin beta-5 chain, actin (cytoplasmic 1), glyceraldehyde-3 phosphate dehydrogenase, tropomyosin isoform 4 (TPM4), prohibitin, peroxiredoxin 1 (PRX1), manganese-containing superoxide dismutase (MnSOD), neuronal protein, and transgelin was up-regulated; and the expression of five proteins including TPM1, squamous cell carcinoma antigen 1 (SCCA1), stratifin, peroxiredoxin 2 isoform a, and alpha B crystalline was down-regulated in cancer tissues with a statistical significance (p < 0.05).
  • These data may suggest that these proteins contribute to the multistage process of carcinogenesis, tumor progression, and invasiveness of ESCC.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Neoplasm Proteins / isolation & purification


86. Adegboyega PA, Rodriguez S, McLarty J: Stromal expression of actin is a marker of aggressiveness in basal cell carcinoma. Hum Pathol; 2010 Aug;41(8):1128-37
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  • [Title] Stromal expression of actin is a marker of aggressiveness in basal cell carcinoma.
  • Basal cell carcinoma is a very common malignant skin tumor that rarely metastasizes but is often locally aggressive.
  • In a number of studies conducted by different investigators, Bcl2, beta-catenin, cyclin D1, hMSH2, and alpha-smooth muscle actin have been reported to have potential for predicting basal cell carcinoma aggressiveness.
  • We therefore studied the expression and topographic locations (tumor versus stroma) of all these gene products in a group of clinically proven aggressive basal cell carcinomas (n = 30) and randomly selected control cases of nonaggressive basal cell carcinomas (n = 33).
  • Alpha-smooth muscle actin was expressed by tumor cells in both study groups, but stromal expression of alpha-smooth muscle actin was restricted to the aggressive tumors and highly predictive of aggressive behavior (P < .001; accuracy, 87%).
  • Logistic regression combining the expression of alpha-smooth muscle actin and hMSH2 yielded a predictive model with 97% accuracy (P < .001).
  • These data show conclusively that aggressive basal cell carcinomas express alpha-smooth muscle actin in the stroma, whereas nonaggressive basal cell carcinomas express alpha-smooth muscle actin in the tumor cells, and that stromal expression of alpha-smooth muscle actin is an accurate, reliable, and easy to use marker of aggressiveness in basal cell carcinomas and can be used in clinical practice for surgical therapeutic decisions.
  • [MeSH-major] Actins / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Basal Cell / pathology. Neoplasm Recurrence, Local / pathology. Skin Neoplasms / pathology. Stromal Cells / metabolism

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20381122.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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87. Perseghin P, D'Amico G, Dander E, Gaipa G, Dassi M, Biagi E, Biondi A: Isolation of monocytes from leukapheretic products for large-scale GMP-grade generation of cytomegalovirus-specific T-cell lines by means of an automated elutriation device. Transfusion; 2008 Aug;48(8):1644-9
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  • [Title] Isolation of monocytes from leukapheretic products for large-scale GMP-grade generation of cytomegalovirus-specific T-cell lines by means of an automated elutriation device.
  • BACKGROUND: Dendritic cells (DC) act as antigen-presenting cells in immune response-mediated mechanisms against malignant cells and/or viral or fungal pathogens.
  • Here the effectiveness of a commercially available cell separation system (Elutra, Gambro BCT) in the separation of monocytes and the large-scale production of cytomegalovirus (CMV)-specific T-cell lines were investigated.
  • STUDY DESIGN AND METHODS: Six mononuclear cell (MNC) collections were processed with the Elutra system.
  • After 6 days of culture, DCs were matured in the presence of interferon (IFN)-gamma, IFN-alpha, IL-1beta, tumor necrosis factor-alpha, and poly(I:C) and pulsed with a pool of 48 MHC Class I and II-binding CMV peptides.
  • CONCLUSION: Our findings might be helpful for an appropriate MNC collection, to maximize the efficiency of the elutriation system and subsequently obtain an optimal monocyte-enriched yield for further DC generation and T-cell stimulation.
  • [MeSH-minor] Antigen Presentation. Antigens, Viral / immunology. Cell Culture Techniques. Cell Line. Dendritic Cells / cytology. Epitopes. Humans

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  • (PMID = 18513258.001).
  • [ISSN] 0041-1132
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Epitopes
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88. Patel RV, Clark LN, Lebwohl M, Weinberg JM: Treatments for psoriasis and the risk of malignancy. J Am Acad Dermatol; 2009 Jun;60(6):1001-17
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  • RESULTS: PUVA, when given long term, is associated with increased risks of cutaneous squamous cell carcinoma and malignant melanoma.
  • However, the majority of studies examining this carcinogenic risk suggest that tumor necrosis factor-alpha inhibitors may cause a slightly increased risk of cancer, including nonmelanoma skin cancer and hematologic malignancies.

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  • [ErratumIn] J Am Acad Dermatol. 2009 Dec;61(6):1059
  • (PMID = 19344980.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biological Products; 0 / Dermatologic Agents; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 131
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89. Bialer G, Horovitz-Fried M, Ya'acobi S, Morgan RA, Cohen CJ: Selected murine residues endow human TCR with enhanced tumor recognition. J Immunol; 2010 Jun 1;184(11):6232-41
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  • [Title] Selected murine residues endow human TCR with enhanced tumor recognition.
  • TCR-gene transfer can mediate tumor regression in terminally ill melanoma patients.
  • We constructed murine/human chimeras of alpha- and beta-chains and assessed for their surface expression and function.
  • This information led us to design improved and minimally murinized human TCR C regions that mediate increased tumor recognition.
  • Overall, these findings could have implications for the treatment of malignant diseases using TCR-gene transfer.
  • [MeSH-major] Genes, T-Cell Receptor alpha / genetics. Genes, T-Cell Receptor beta / genetics. Melanoma / immunology. Receptors, Antigen, T-Cell / genetics. Receptors, Antigen, T-Cell / immunology
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. Cell Separation. Flow Cytometry. Gene Transfer Techniques. Genetic Therapy. Humans. Mice. Molecular Sequence Data. Sequence Homology, Amino Acid

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  • (PMID = 20427762.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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90. Garrison JB, Kyprianou N: Doxazosin induces apoptosis of benign and malignant prostate cells via a death receptor-mediated pathway. Cancer Res; 2006 Jan 1;66(1):464-72
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  • [Title] Doxazosin induces apoptosis of benign and malignant prostate cells via a death receptor-mediated pathway.
  • These results show that doxazosin exerts its apoptotic effects against benign and malignant prostate cells via a death receptor-mediated mechanism with a potential integrin contribution towards cell survival outcomes.

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  • (PMID = 16397262.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107575; United States / NCI NIH HHS / CA / R01 CA107575-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adrenergic alpha-Antagonists; 0 / Antigens, CD95; 0 / FADD protein, human; 0 / Fas-Associated Death Domain Protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
  • [Other-IDs] NLM/ NIHMS19062; NLM/ PMC1850148
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91. Henze AT, Acker T: Feedback regulators of hypoxia-inducible factors and their role in cancer biology. Cell Cycle; 2010 Jul 15;9(14):2749-63
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  • Malignant tumors are characterized by regions of low oxygen concentration (hypoxia).
  • The hypoxic tumor microenvironment contributes to tumor progression by activating a set of adaptive responses via the key transcriptional regulators HIF-1alpha and HIF-2alpha.
  • These factors have been traditionally linked to an aggressive tumor phenotype by promoting processes essential for tumor growth, such as angiogenesis, glycolysis, metastasis and invasion, as well as differentiation and self renewal.
  • Notably, the complex HIF pathway also initiates anti-tumorigenic mechanisms that lead to cell cycle arrest or cell death, indicating the need for a stringent control of the extent and the direction of the hypoxia response.
  • The importance of this control for tumor cell survival is illustrated by the intricate regulation of HIF activity at the mRNA, protein and epigenetic level by a complex network of positive and negative feedback regulators.
  • We propose that these feedback regulators help to flexibly adjust and adapt HIF activated responses to the fluctuating oxygen concentrations within tumors during acute and chronic hypoxia and to curtail the tumor-suppressing components of the HIF pathway.
  • Moreover, feedback regulation of HIF induces a switch from HIF-1alpha to HIF-2alpha driven responses under chronic hypoxia which may have essential functions in the regulation of tumor cell differentiation and tumor stem cell maintenance.
  • Given their central role in cancer biology, HIF feedback regulators may represent an attractive and novel anti-tumor therapy target to overcome cell death resistance in tumors.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression Regulation, Neoplastic. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • [MeSH-minor] Carcinoma, Renal Cell / metabolism. Cell Hypoxia. Humans. Kidney Neoplasms / metabolism. MicroRNAs / metabolism. Nitric Oxide Synthase Type II / metabolism. Repressor Proteins / metabolism. Trans-Activators / metabolism. Transcription Factors / metabolism

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  • (PMID = 20603601.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [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 / CITED2 protein, human; 0 / DDIT4 protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / MicroRNAs; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / endothelial PAS domain-containing protein 1; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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92. Kreizenbeck GM, Berger AJ, Subtil A, Rimm DL, Gould Rothberg BE: Prognostic significance of cadherin-based adhesion molecules in cutaneous malignant melanoma. Cancer Epidemiol Biomarkers Prev; 2008 Apr;17(4):949-58
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  • [Title] Prognostic significance of cadherin-based adhesion molecules in cutaneous malignant melanoma.
  • BACKGROUND: The need for novel molecular prognostic markers that can supplement validated clinicopathologic correlates for cutaneous malignant melanoma is well recognized.
  • Proteins that mediate the epithelial-mesenchymal transition, the process by which a cancer cell disengages from its parent tumor, are important candidates.
  • METHODS: The prognostic relevance of E-cadherin, N-cadherin, and P-cadherin, calcium-dependent transmembrane glycoproteins that regulate cell-cell adhesion, and their adaptors, alpha-catenin, beta-catenin, and p120-catenin, was evaluated on a cohort of 201 primary and 274 metastatic melanoma tumors using fluorescence-based immunohistochemical methods and Automated Quantitative Analysis of protein expression on digitally captured photomicrographs.
  • Cluster 4, expressing high E-cadherin and N-cadherin levels, possessed the most favorable outcome and cluster 2, featuring low E-cadherin and alpha-catenin but modest N-cadherin, showed least favorable outcomes.
  • In contrast, for neural crest-derived cutaneous malignant melanoma, N-cadherin overexpression can be associated with either a successful epithelial-mesenchymal transition or a favorably differentiated tumor.

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  • (PMID = 18398036.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114277; United States / NCI NIH HHS / CA / R01 CA114277-01A1; United States / NCI NIH HHS / CA / R01 CA 114277
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Cell Adhesion Molecules
  • [Other-IDs] NLM/ NIHMS356518; NLM/ PMC3312613
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93. Indra AK, Castaneda E, Antal MC, Jiang M, Messaddeq N, Meng X, Loehr CV, Gariglio P, Kato S, Wahli W, Desvergne B, Metzger D, Chambon P: Malignant transformation of DMBA/TPA-induced papillomas and nevi in the skin of mice selectively lacking retinoid-X-receptor alpha in epidermal keratinocytes. J Invest Dermatol; 2007 May;127(5):1250-60
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  • [Title] Malignant transformation of DMBA/TPA-induced papillomas and nevi in the skin of mice selectively lacking retinoid-X-receptor alpha in epidermal keratinocytes.
  • Retinoid-X-receptor alpha (RXRalpha), a member of the nuclear receptor (NR) superfamily, is a ligand-dependent transcriptional regulatory factor.
  • We investigated the role of RXRalpha and its partners on mouse skin tumor formation and malignant progression upon topical DMBA/TPA treatment.
  • As keratinocyte-selective peroxisome proliferator-activated receptor gamma (PPARgamma) ablation had similar effects, RXRalpha/PPARgamma heterodimers most probably mediate epidermal tumor suppression.
  • Distinct RXRalpha-mediated molecular events appear therefore to be involved, in keratinocytes, in cell-autonomous suppression of epidermal tumorigenesis and malignant progression, and in non-cell-autonomous suppression of nevi formation and progression.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Epidermis / metabolism. Keratinocytes / metabolism. Nevus, Pigmented / pathology. Papilloma / pathology. Retinoid X Receptor alpha / metabolism. Skin Neoplasms / pathology


94. Yang Y, Ge JP, Zhou ZT: Effects of thalidomide on DMBA-induced oral carcinogenesis in hamster with respect to angiogenesis. J Oral Pathol Med; 2009 May;38(5):455-62
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  • However, the effects of thalidomide on oral pre-malignant lesions and oral carcinogenesis remain unexplored.
  • RESULTS: Thalidomide significantly decreased the squamous cell carcinoma (SCC) incidence from 57.9 to 11.8%; angiogenesis was inhibited in dysplasia and SCC.
  • The gene expression of vascular endothelium growth factor and tumor necrosis factor (TNF)-alpha was downregulated.
  • CONCLUSIONS: Thalidomide has inhibitory effect against the malignant transformation of oral pre-cancerous lesion and angiogenesis during oral carcinogenesis.
  • Such inhibition is related to its modulation of TNF-alpha.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Carcinoma, Squamous Cell / prevention & control. Mouth Mucosa / drug effects. Mouth Neoplasms / prevention & control. Neoplasms, Experimental / prevention & control. Thalidomide / therapeutic use
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Animals. Anticarcinogenic Agents / therapeutic use. Carcinogens. Cell Transformation, Neoplastic / chemically induced. Cell Transformation, Neoplastic / drug effects. Chemoprevention / methods. Cricetinae. Male. Mesocricetus. Neovascularization, Pathologic / prevention & control. Precancerous Conditions / chemically induced. Precancerous Conditions / drug therapy. RNA, Messenger / analysis. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19141066.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anticarcinogenic Agents; 0 / Carcinogens; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 4Z8R6ORS6L / Thalidomide; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
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95. Epping MT, Wang L, Plumb JA, Lieb M, Gronemeyer H, Brown R, Bernards R: A functional genetic screen identifies retinoic acid signaling as a target of histone deacetylase inhibitors. Proc Natl Acad Sci U S A; 2007 Nov 6;104(45):17777-82
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  • Inhibitors of histone deacetylases (HDACI) selectively inhibit proliferation of malignant cells and are used for the treatment of cancer, but their cancer selectivity is understood poorly.
  • We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling.
  • Finally, a combination of RA and HDACI acted synergistically to activate RA signaling and inhibit tumor growth.
  • [MeSH-minor] Animals. Cell Division / drug effects. Colony-Forming Units Assay. Embryo, Mammalian. Enzyme Inhibitors / pharmacology. Fibroblasts / physiology. Humans. Mice. Neoplasm Transplantation. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / physiology. Transplantation, Heterologous