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1. van Tilborg GA, Mulder WJ, van der Schaft DW, Reutelingsperger CP, Griffioen AW, Strijkers GJ, Nicolay K: Improved magnetic resonance molecular imaging of tumor angiogenesis by avidin-induced clearance of nonbound bimodal liposomes. Neoplasia; 2008 Dec;10(12):1459-69
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  • [Title] Improved magnetic resonance molecular imaging of tumor angiogenesis by avidin-induced clearance of nonbound bimodal liposomes.
  • Angiogenic, that is, newly formed, blood vessels play an important role in tumor growth and metastasis and are a potential target for tumor treatment.
  • In previous studies, the alpha(v)beta(3) integrin, which is strongly expressed in angiogenic vessels, has been used as a target for Arg-Gly-Asp (RGD)-functionalized nanoparticulate contrast agents for magnetic resonance imaging-based visualization of angiogenesis.
  • This was accomplished by the use of a so-called avidin chase, which allowed rapid clearance of non-bound paramagnetic RGD-biotin-liposomes from the blood circulation.
  • Postcontrast images showed similar percentages of contrast-enhanced pixels in the tumors of mice that received RGD-biotin-liposomes and biotin-liposomes.
  • Ex vivo fluorescence microscopy confirmed association of the RGD-biotin-liposomes to tumor endothelial cells both with and without avidin infusion, whereas biotin-liposomes were predominantly found within the vessel lumen.
  • The clearance methodology presented in this study successfully enhanced the specificity of molecular magnetic resonance imaging and opens exciting possibilities for studying detection limits and targeting kinetics of site-directed contrast agents in vivo.
  • [MeSH-minor] Animals. Cell Line, Tumor. Endothelium, Vascular / pathology. Humans. Integrin alphaVbeta3 / metabolism. Melanoma / metabolism. Mice. Mice, Inbred C57BL. Microscopy, Fluorescence / methods. Nanoparticles / chemistry. Oligopeptides / chemistry

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  • (PMID = 19048124.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 0 / Liposomes; 0 / Oligopeptides; 1405-69-2 / Avidin; 99896-85-2 / arginyl-glycyl-aspartic acid
  • [Other-IDs] NLM/ PMC2586696
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2. Sato H, Kuwashima N, Sakaida T, Hatano M, Dusak JE, Fellows-Mayle WK, Papworth GD, Watkins SC, Gambotto A, Pollack IF, Okada H: Epidermal growth factor receptor-transfected bone marrow stromal cells exhibit enhanced migratory response and therapeutic potential against murine brain tumors. Cancer Gene Ther; 2005 Sep;12(9):757-68
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  • [Title] Epidermal growth factor receptor-transfected bone marrow stromal cells exhibit enhanced migratory response and therapeutic potential against murine brain tumors.
  • We have created a novel cellular vehicle for gene therapy of malignant gliomas by transfection of murine bone marrow stroma cells (MSCs) with a cDNA encoding epidermal growth factor receptor (EGFR).
  • These cells (EGFR-MSCs) demonstrate enhanced migratory responses toward glioma-conditioned media in comparison to primary MSCs in vitro.
  • Unlike primary MSCs, EGFR-MSCs were resistant to FasL-mediated cytotoxicity and were capable of stimulating allogeneic mixed lymphocyte reaction, suggesting EGFR-MSCs possess suitable characteristics as vehicles for brain tumor immuno-gene therapy.
  • Finally, intratumoral injection with EGFR-MSC adenovirally engineered to secrete interferon-alpha to intracranial GL261 resulted in significantly prolonged survival in comparison to controls.
  • [MeSH-major] Bone Marrow Cells / physiology. Brain Neoplasms / therapy. Cell Movement. Genetic Therapy / methods. Glioma / therapy. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Actins / metabolism. Animals. Cell Line. Epidermal Growth Factor / metabolism. Mice. Phosphatidylinositol 3-Kinases / metabolism. Protein Kinase C / metabolism. Stromal Cells / physiology. Transfection

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  • (PMID = 15832173.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / P01 NS40923
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 62229-50-9 / Epidermal Growth Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.13 / Protein Kinase C
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3. Nevo J, Mai A, Tuomi S, Pellinen T, Pentikäinen OT, Heikkilä P, Lundin J, Joensuu H, Bono P, Ivaska J: Mammary-derived growth inhibitor (MDGI) interacts with integrin α-subunits and suppresses integrin activity and invasion. Oncogene; 2010 Dec 9;29(49):6452-63
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  • The majority of mortality associated with cancer is due to formation of metastases from the primary tumor.
  • Adhesion mediated by different integrin heterodimers has an important role during cell migration and invasion.
  • In breast cancer cell lines, MDGI expression correlates with suppression of the active conformation of integrins.
  • This results in reduced integrin adhesion to type I collagen and fibronectin and inhibition of cell migration and invasion.
  • In tissue microarray of 1331 breast cancer patients, patients with MDGI-positive tumors had more favorable 10-year distant disease-free survival compared with patients with MDGI-negative tumors.
  • Our data indicate that MDGI is a novel interacting partner for integrin α-subunits, and its expression modulates integrin activity and suppresses cell invasion in breast cancer patients.
  • [MeSH-major] Breast Neoplasms / metabolism. Breast Neoplasms / mortality. Fatty Acid-Binding Proteins / metabolism. Integrin alpha Chains / metabolism
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Cell Movement. Collagen Type I / metabolism. Disease-Free Survival. Extracellular Matrix / chemistry. Female. Fibronectins / metabolism. Humans. Middle Aged. Molecular Sequence Data. Neoplasm Invasiveness. Protein Interaction Domains and Motifs


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4. Suen AW, Galoforo S, Marples B, McGonagle M, Downing L, Martinez AA, Robertson JM, Wilson GD: Sorafenib and radiation: a promising combination in colorectal cancer. Int J Radiat Oncol Biol Phys; 2010 Sep 1;78(1):213-20
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  • PURPOSE: To examine the combination of radiation and the multikinase inhibitor sorafenib in human colorectal cancer cell lines and xenografts.
  • METHODS AND MATERIALS: HT29 and SW48 colorectal cancer cells were studied in vitro using MTT assays to establish the optimal timing of radiation and sorafenib.
  • Xenografts were established, and the effect of a 3-week schedule of daily radiation and sorafenib was studied by growth delay.
  • RESULTS: Sorafenib predominantly had minimal effects on cell growth or radiation response in MTT growth assays, though growth inhibition was significantly enhanced in HT29 cells when sorafenib was administered after radiation.
  • The highest dose of sorafenib altered the alpha component of the cell survival curve in clonogenic assays.
  • The combination of radiation and sorafenib was synergistic in SW48 xenografts, with a mean time to threshold tumor size of 11.4 +/- 1.0 days, 37.0 +/- 9.5 days, 15.5 +/- 3.2 days, and 98.0 +/- 11.7 days in the control, radiation, sorafenib, and combined treatment group, respectively.
  • The effect on HT29 tumors was additive, with mean time to threshold volume of 12.6 +/- 1.1 days, 61.0 +/- 4.3 days, 42.6 +/- 11.7 days, and 100.2 +/- 12.4 days.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Animals. Cell Division / drug effects. Cell Division / radiation effects. Combined Modality Therapy / methods. HT29 Cells. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Niacinamide / analogs & derivatives. Phenylurea Compounds. Protein Kinase Inhibitors / administration & dosage. Radiotherapy Dosage. Random Allocation. Time Factors. Tumor Cells, Cultured. Tumor Stem Cell Assay / methods

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20708486.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
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5. Guillory B, Sakwe AM, Saria M, Thompson P, Adhiambo C, Koumangoye R, Ballard B, Binhazim A, Cone C, Jahanen-Dechent W, Ochieng J: Lack of fetuin-A (alpha2-HS-glycoprotein) reduces mammary tumor incidence and prolongs tumor latency via the transforming growth factor-beta signaling pathway in a mouse model of breast cancer. Am J Pathol; 2010 Nov;177(5):2635-44
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  • [Title] Lack of fetuin-A (alpha2-HS-glycoprotein) reduces mammary tumor incidence and prolongs tumor latency via the transforming growth factor-beta signaling pathway in a mouse model of breast cancer.
  • Whereas the control group (PyMT/Fet+/+) formed mammary tumors 90 days after birth, tumor latency was prolonged in the PyMT/Fet-/- and PyMT/Fet+/- mice.
  • The majority of the PyMT/Fet-/- mice were tumor-free at the end of the study, at approximately 40 weeks.
  • The pathology of the mammary tumors in the Fet-null mice showed extensive fibrosis, necrosis, and squamous metaplasia.
  • Likewise, p19ARF and p53 were highly expressed in tumor tissues of PyMT/Fet-/- mice relative to the controls in the absence of Fet.

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  • (PMID = 20847285.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / SC1 CA134018
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AHSG protein, human; 0 / Ahsg protein, mouse; 0 / Antigens, Polyomavirus Transforming; 0 / Blood Proteins; 0 / Transforming Growth Factor beta; 0 / alpha-2-HS-Glycoprotein; EC 2.7.1.137 / Phosphatidylinositol 3-Kinase
  • [Other-IDs] NLM/ PMC2966818
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6. Panner A, Parsa AT, Pieper RO: Translational regulation of TRAIL sensitivity. Cell Cycle; 2006 Jan;5(2):147-50
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  • TNF-related apoptosis-inducing ligand (TRAIL) is a peptide that induces apoptosis to varying degrees in tumor cells.
  • While TRAIL sensitivity in tumors has been linked to c-myc- and MEK/Erk-induced enhancement of caspase activation, our recent study identified a third input controlling TRAIL sensitivity, namely the Akt-mTOR pathway.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Gene Expression Regulation. Membrane Glycoproteins / metabolism. Protein Biosynthesis. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16397410.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 115638; United States / NCI NIH HHS / CA / CA100011; United States / NCI NIH HHS / CA / P50CA097257
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / DIABLO protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Mitochondrial Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.6.5.2 / ral GTP-Binding Proteins
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7. Murphy JF, Lennon F, Steele C, Kelleher D, Fitzgerald D, Long AC: Engagement of CD44 modulates cyclooxygenase induction, VEGF generation, and proliferation in human vascular endothelial cells. FASEB J; 2005 Mar;19(3):446-8
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  • [Title] Engagement of CD44 modulates cyclooxygenase induction, VEGF generation, and proliferation in human vascular endothelial cells.
  • CD44 is a receptor for hyaluronic acid and is found on the surface of hematopoetic cells and in mesenchymal tissue.
  • It is also expressed on endothelial cells (EC).
  • Results from this study may have important and widespread implications for the development of novel therapeutic agents for modulating blood vessel growth during ischemic heart disease, during inflammation, or around solid tumors.
  • [MeSH-major] Antigens, CD44 / physiology. Cell Division / physiology. Endothelial Cells / metabolism. Prostaglandin-Endoperoxide Synthases / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] 6-Ketoprostaglandin F1 alpha / biosynthesis. Antibodies, Monoclonal / pharmacology. Cells, Cultured. Cyclooxygenase 2. Epoprostenol / biosynthesis. Humans. Hyaluronic Acid / metabolism. Hyaluronic Acid / pharmacology. Membrane Proteins. Signal Transduction. Umbilical Veins

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  • (PMID = 15640281.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD44; 0 / Membrane Proteins; 0 / Vascular Endothelial Growth Factor A; 58962-34-8 / 6-Ketoprostaglandin F1 alpha; 9004-61-9 / Hyaluronic Acid; DCR9Z582X0 / Epoprostenol; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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8. Sjöö F, Hassan Z, Abedi-Valugerdi M, Griskevicius L, Nilsson C, Remberger M, Aschan J, Concha H, Gaughan U, Hassan M: Myeloablative and immunosuppressive properties of treosulfan in mice. Exp Hematol; 2006 Jan;34(1):115-21
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  • OBJECTIVE: Treosulfan is a prodrug with a specific clinical activity in ovarian carcinoma and other solid tumors.
  • Due to its myeloablative and immunosuppressive effects, its use in conditioning regimens prior to allogeneic stem cell treatment (SCT) has been proposed.
  • At different intervals, colony-forming unit granulocyte macrophage assay was performed on marrow cells.
  • Additionally, immunological analyses were performed using spleen cells.
  • Moreover, treosulfan was more effective in depletion of splenic B and T cells in comparison with busulfan and cyclophosphamide.
  • Furthermore, T cells isolated from the spleens of treosulfan- or busulfan-treated mice were not responsive to allogeneic cells compared with that observed in controls and cyclophosphamide-treated mice.
  • Treatment with treosulfan induced only interleukin-2 production in spleen cells for a short time and had no significant effect on synthesis of tumor necrosis factor-alpha and/or interferon-gamma as compared with that observed in splenic T cells isolated from mice treated with either busulfan or cyclophosphamide.
  • [MeSH-minor] Animals. Cell Count. Cyclophosphamide / pharmacology. Cytokines / biosynthesis. Drug Evaluation, Preclinical. Female. Mice. Mice, Inbred BALB C. Spleen / cytology. Spleen / drug effects. Spleen / physiology. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. Time Factors

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  • (PMID = 16413398.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; CO61ER3EPI / treosulfan; G1LN9045DK / Busulfan
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9. Fine B, Hodakoski C, Koujak S, Su T, Saal LH, Maurer M, Hopkins B, Keniry M, Sulis ML, Mense S, Hibshoosh H, Parsons R: Activation of the PI3K pathway in cancer through inhibition of PTEN by exchange factor P-REX2a. Science; 2009 Sep 4;325(5945):1261-5
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  • PTEN (phosphatase and tensin homolog on chromosome 10) is a tumor suppressor whose cellular regulation remains incompletely understood.
  • P-REX2a mRNA was more abundant in human cancer cells and significantly increased in tumors with wild-type PTEN that expressed an activated mutant of PIK3CA encoding the p110 subunit of phosphoinositide 3-kinase subunit alpha (PI3Kalpha).
  • P-REX2a stimulated cell growth and cooperated with a PIK3CA mutant to promote growth factor-independent proliferation and transformation.
  • Depletion of P-REX2a reduced amounts of phosphorylated AKT and growth in human cell lines with intact PTEN.
  • Thus, P-REX2a is a component of the PI3K pathway that can antagonize PTEN in cancer cells.

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  • (PMID = 19729658.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA082783-08; United States / NCI NIH HHS / CA / P01 CA097403; United States / NCI NIH HHS / CA / CA082783-09; United States / NCI NIH HHS / CA / CA082783-07; United States / NCI NIH HHS / CA / R01 CA082783-07; United States / NCI NIH HHS / CA / CA082783-10; United States / NCI NIH HHS / CA / CA097403-06A1; United States / NCI NIH HHS / CA / P01 CA097403-01A10003; United States / NCI NIH HHS / CA / CA082783-08; United States / NCI NIH HHS / CA / CA097403-01A10003; United States / NCI NIH HHS / CA / R01 CA082783-09; United States / NCI NIH HHS / CA / R01 CA082783-06; United States / NCI NIH HHS / CA / CA097403; United States / NCI NIH HHS / CA / R01 CA082783; United States / NCI NIH HHS / CA / P01 CA097403-06A1; United States / NCI NIH HHS / CA / CA082783-06; United States / NCI NIH HHS / CA / R01 CA082783-10
  • [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 / GTPase-Activating Proteins; 0 / Guanine Nucleotide Exchange Factors; 0 / PREX2 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ NIHMS226733; NLM/ PMC2936784
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10. Meng Y, Mauceri HJ, Khodarev NN, Darga TE, Pitroda SP, Beckett MA, Kufe DW, Weichselbaum RR: Ad.Egr-TNF and local ionizing radiation suppress metastases by interferon-beta-dependent activation of antigen-specific CD8+ T cells. Mol Ther; 2010 May;18(5):912-20
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  • [Title] Ad.Egr-TNF and local ionizing radiation suppress metastases by interferon-beta-dependent activation of antigen-specific CD8+ T cells.
  • Ad.Egr-TNF is a radioinducible adenovector currently in phase 3 trials for inoperable pancreatic cancer.
  • The combination of Ad.Egr-TNF and ionizing radiation (IR) contributes to local tumor control through the production of tumor necrosis factor-alpha (TNFalpha) in the tumor microenvironment.
  • Moreover, clinical and preclinical studies with Ad.Egr-TNF/IR have suggested that this local approach suppresses the growth of distant metastatic disease; however, the mechanisms responsible for this effect remain unclear.
  • The results demonstrate that production of TNFalpha in the tumor microenvironment induces expression of interferon (IFNbeta).
  • In turn, IFNbeta stimulates the production of chemokines that recruit CD8(+) T cells to the tumor.
  • The results further demonstrate that activation of tumor antigen-specific CD8(+) CTLs contributes to local antitumor activity and suppression of DLN metastases.
  • These findings support a model in which treatment of tumors with Ad.Egr-TNF and IR is mediated by local and distant immune-mediated antitumor effects that suppress the development of metastases.
  • [MeSH-major] CD8-Positive T-Lymphocytes / metabolism. Neoplasm Metastasis / prevention & control. Neoplasm Metastasis / therapy. Radiation, Ionizing. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Proliferation. Genetic Vectors / genetics. Humans. Interferon-beta / metabolism. Lymphocyte Activation. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Mutant Strains. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20197756.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / R01 CA111423; United States / NCI NIH HHS / CA / R0-1 CA111423
  • [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 / Tumor Necrosis Factor-alpha; 77238-31-4 / Interferon-beta
  • [Other-IDs] NLM/ PMC2890103
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11. Wu K, Nie Y, Guo C, Chen Y, Ding J, Fan D: Molecular basis of therapeutic approaches to gastric cancer. J Gastroenterol Hepatol; 2009 Jan;24(1):37-41
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  • As the majority of cases present with advanced disease, conventional therapies (surgery, chemotherapy, and radiotherapy) have limited efficacy to reduce mortality.
  • Numerous molecules have been shown potential to target specific pathways for tumor cell growth.
  • Cyclooxygenase-2 (COX-2) is overexpressed in and correlated with gastric cancer, and knockdown of COX-2 or administration of COX-2 inhibitors suppresses tumor formation in models of gastric cancer.
  • Runt-related transcription factor 3 (RUNX3) is a candidate tumor suppressor gene whose deficiency is causally related to gastric cancer.
  • RUNX3 activation inhibits angiogenesis in xenograft tumors in nude mice.
  • Tumor microenvironment modulation also provides a powerful tool to inhibit cancer development and progress; details of the potential roles of angiopoietins are discussed in this review.
  • A tumor-specific antigen MG7-Ag has been identified with great potential for inducing immune response in gastric cancer.
  • Using HLA-A-matched allogeneic gastric cancer cells to induce tumor-specific cytotoxic T lymphocytes appeared to be an alternative option of immunotherapy for gastric cancer.
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Angiogenic Proteins / genetics. Angiogenic Proteins / metabolism. Animals. Core Binding Factor Alpha 3 Subunit / genetics. Core Binding Factor Alpha 3 Subunit / metabolism. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Cyclooxygenase 2 Inhibitors / therapeutic use. Humans. Potassium Channel Blockers / therapeutic use. Protein Kinase Inhibitors / therapeutic use. RNA Interference. RNA, Small Interfering / therapeutic use

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  • (PMID = 19196394.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 3 Subunit; 0 / Cyclooxygenase 2 Inhibitors; 0 / Potassium Channel Blockers; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 0 / Runx3 protein, human; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Number-of-references] 48
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12. Mahadevan D, Cooke L, Riley C, Swart R, Simons B, Della Croce K, Wisner L, Iorio M, Shakalya K, Garewal H, Nagle R, Bearss D: A novel tyrosine kinase switch is a mechanism of imatinib resistance in gastrointestinal stromal tumors. Oncogene; 2007 Jun 7;26(27):3909-19
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  • [Title] A novel tyrosine kinase switch is a mechanism of imatinib resistance in gastrointestinal stromal tumors.
  • KIT or alpha-platelet-derived growth factor receptor (alpha-PDGFR) activating mutations are the pathogenic mechanisms that characterize gastrointestinal stromal tumors (GIST).
  • We developed an IM-resistant GIST cell line (GIST-R) from the IM-sensitive GIST882 cell line (GIST-S) by growing these cells in IM.
  • Gene expression profiling (GEP) of GIST-S, GIST-R cells and two IM resistant GIST patients demonstrated that KIT is downregulated implying a major role in IM resistance.
  • Instead, GIST-R cells have acquired IM resistance by overexpressing the oncogenic receptor tyrosine kinase - AXL - in a 'kinase switch'.
  • Real time reverse transcriptase-polymerase chain reaction and Western blotting of the GIST-S and GIST-R cells confirmed the switch from Kit to AXL.
  • MP470 synergizes with docetaxel (taxotere) and is cytotoxic to GIST cells.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Gastrointestinal Stromal Tumors / genetics. Oncogene Proteins / genetics. Piperazines / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Benzamides. Blotting, Western. Cell Line, Tumor. Cell Shape / drug effects. Cell Survival / drug effects. Drug Synergism. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Imatinib Mesylate. Models, Molecular. Mutation. Oligonucleotide Array Sequence Analysis. Phosphorylation / drug effects. Protein Kinase Inhibitors / chemistry. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Proto-Oncogene Proteins. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Taxoids / pharmacology

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  • (PMID = 17325667.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA23074
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / MP470; 0 / Oncogene Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / Taxoids; 147336-22-9 / Green Fluorescent Proteins; 15H5577CQD / docetaxel; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / axl receptor tyrosine kinase
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13. Earel JK Jr, VanOosten RL, Griffith TS: Histone deacetylase inhibitors modulate the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand-resistant bladder tumor cells. Cancer Res; 2006 Jan 1;66(1):499-507
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  • [Title] Histone deacetylase inhibitors modulate the sensitivity of tumor necrosis factor-related apoptosis-inducing ligand-resistant bladder tumor cells.
  • The large majority of tumors are superficial at diagnosis and, after local surgical therapy, have a high rate of local recurrence and progression.
  • Current treatments extend time to recurrence but do not alter disease survival.
  • The objective of the present study was to investigate the tumoricidal potential of combining the apoptosis-inducing protein tumor necrosis factor-related apoptosis inducing ligand (TRAIL) with histone deacetylase inhibitors (HDACi) against TRAIL-resistant bladder tumor cells.
  • Pretreatment with HDACi at nontoxic doses, followed by incubation with TRAIL, resulted in a marked increase in TRAIL-induced apoptosis of T24 cells but showed no significant increase in toxicity to SV40 immortalized normal human uroepithelial cell-1.
  • The increased TRAIL-R2 levels also resulted in accelerated death-inducing signaling complex (DISC) formation, caspase activation, and loss of mitochondrial membrane potential, which all contributed to the increase in tumor cell death.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis Regulatory Proteins / pharmacology. Histone Deacetylase Inhibitors. Membrane Glycoproteins / pharmacology. Tumor Necrosis Factor-alpha / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Caspases / metabolism. Cell Line, Tumor. Drug Synergism. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / pharmacology. Humans. Intracellular Membranes / drug effects. Intracellular Membranes / physiology. Membrane Potentials / drug effects. Membrane Potentials / physiology. Mitochondria / drug effects. Mitochondria / physiology. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / biosynthesis. Receptors, Tumor Necrosis Factor / genetics. Receptors, Tumor Necrosis Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand. Transcription, Genetic

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  • (PMID = 16397266.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109446
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10B protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspases
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14. Spada A, Lania A, Mantovani G: Hormonal signaling and pituitary adenomas. Neuroendocrinology; 2007;85(2):101-9
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  • [Title] Hormonal signaling and pituitary adenomas.
  • In recent years the demonstration that human pituitary adenomas are monoclonal in origin provides further evidence that pituitary neoplasia arise from the replication of a single mutated cell in which growth advantage results from either activation of proto-oncogenes or inactivation of tumor suppressor genes.
  • Mutations in common oncogenes and tumor suppressor genes are only exceptionally involved in pituitary tumors.
  • Since pituicytes may proliferate in response to hypothalamic neurohormones, locally produced growth factors and peripheral hormones, it has been speculated that dysregulation of the signaling molecules that constitute these pathways may confer growth advantage to the target cell, finally resulting in tumor formation.
  • The only mutational change so far recognized to be unequivocally associated with pituitary tumors occur in the Gs alpha gene (GNAS1) and cause constitutive activation of the cAMP-dependent pathway.
  • [MeSH-major] Adenoma / etiology. Hormones / physiology. Pituitary Neoplasms / etiology. Signal Transduction / physiology

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  • (PMID = 17337884.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Hormones; 0 / Hypothalamic Hormones; 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, G-Protein-Coupled
  • [Number-of-references] 66
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15. Morris PG, Abrey LE: Novel targeted agents for platelet-derived growth factor receptor and c-KIT in malignant gliomas. Target Oncol; 2010 Sep;5(3):193-200
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  • Malignant gliomas are a heterogeneous group of tumors with a varying natural history and response to treatment.
  • Despite current therapeutic strategies, these tumors almost universally recur after excision and are associated with a poor survival.
  • Increasingly, the true heterogeneity of these tumors is being correlated with distinct molecular subgroups.
  • Platelet-derived growth factor receptor (PDGFR) alpha is almost universally expressed on glioma cells; expression of the proto-oncogene c-KIT has also been reported.

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  • (PMID = 20844972.001).
  • [ISSN] 1776-260X
  • [Journal-full-title] Targeted oncology
  • [ISO-abbreviation] Target Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
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16. Gururaj AE, Singh RR, Rayala SK, Holm C, den Hollander P, Zhang H, Balasenthil S, Talukder AH, Landberg G, Kumar R: MTA1, a transcriptional activator of breast cancer amplified sequence 3. Proc Natl Acad Sci U S A; 2006 Apr 25;103(17):6670-5
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  • Here we define a function of metastasis-associated protein 1 (MTA1), a presumed corepressor of estrogen receptor alpha (ERalpha), as a transcriptional activator of Breast Cancer Amplified Sequence 3 (BCAS3), a gene amplified and overexpressed in breast cancers.
  • MTA1 stimulation of BCAS3 transcription required ERalpha and involved a functional ERE half-site in BCAS3.
  • BCAS3 expression was elevated in mammary tumors from MTA1 transgenic mice and 60% of the human breast tumors, and correlated with the coexpression of MTA1 as well as with tumor grade and proliferation of primary breast tumor samples.
  • These findings reveal a previously unrecognized function of MTA1 in stimulating BCAS3 expression and suggest an important role for MTA1-BCAS3 pathway in promoting cancerous phenotypes in breast tumor cells.

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  • [ErratumIn] Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):4147-8
  • (PMID = 16617102.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / U01 CA065746; United States / NCI NIH HHS / CA / R01 CA098823; United States / NCI NIH HHS / CA / CA098823; United States / NCI NIH HHS / CA / CA109379; United States / NCI NIH HHS / CA / R01 CA065746; United States / NCI NIH HHS / CA / R01 CA109379; United States / NCI NIH HHS / CA / CA65746
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCAS3 protein, human; 0 / DNA, Neoplasm; 0 / Estrogen Receptor alpha; 0 / Neoplasm Proteins; 0 / Repressor Proteins; 0 / Trans-Activators; 4TI98Z838E / Estradiol; EC 3.5.1.- / Mta1 protein, human; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC1458939
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17. Vajtai I, Sahli R, Kappeler A, Christ ER, Seiler RW: Leiomyomatoid angiomatous neuroendocrine tumor (LANT) of the pituitary: a distinctive biphasic neoplasm with primitive secretory phenotype and smooth muscle-rich stroma. Acta Neuropathol; 2006 Mar;111(3):278-83
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  • [Title] Leiomyomatoid angiomatous neuroendocrine tumor (LANT) of the pituitary: a distinctive biphasic neoplasm with primitive secretory phenotype and smooth muscle-rich stroma.
  • We describe a hitherto undocumented variant of dimorphic pituitary neoplasm composed of an admixture of neurosecretory cells and profuse leiomyomatous stroma around intratumoral vessels.
  • At the term of a yearlong history of amenorrhea and progressive bitemporal visual loss, subtotal resection was performed via transsphenoidal microsurgery.
  • Histologically, solid sheets, nests and cords of epithelial-looking, yet cytokeratin-negative cells were seen growing in a richly vascularized stroma of spindle cells.
  • Architectural patterns varied from monomorphous stroma-dominant zones through biphasic neuroendocrine-leiomyomatous areas, to pseudopapillary fronds along vascular cores.
  • Staining for S100 protein and GFAP, characteristics of sustentacular cells, as well as bcl-2 and c-kit was absent.
  • Except for alpha-subunit, anterior pituitary hormones tested negative in tumor cells, as did a panel of peripheral endocrine markers, including serotonin, somatostatin, calcitonin, parathormone and vasoactive intestinal polypeptide.
  • While assignment of this lesion to any established neoplastic entity is not forthcoming, we propose it is being considered as a low-grade neuroendocrine tumor possibly related to null cell adenoma.
  • [MeSH-major] Neuroendocrine Tumors / pathology. Pituitary Neoplasms / pathology. Stromal Cells / pathology


18. Ishida M, Hasegawa M, Kanao K, Oyama M, Nakajima Y: Non-palpable testicular embryonal carcinoma diagnosed by ultrasound: a case report. Jpn J Clin Oncol; 2009 Feb;39(2):124-6
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  • With the extensive use of scrotal ultrasound (US), incidental non-palpable testicular tumors have thus been unexpectedly discovered.
  • This report documents the case of 24-year-old male with a non-palpable testicular tumor that contained non-seminomatous germ cell components detected by US.
  • Radical orchiectomy was performed and histological examinations confirmed a diagnosis of a mixed tumor of seminoma and embryonal carcinoma.
  • Serum alpha-fetoprotein (AFP) rose from 7.8 to 43 ng/ml and CT scan revealed multiple metastases only 1 month after the operation.
  • The obscurity and implications of such a diagnosis are also discussed.

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  • (PMID = 19066212.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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19. Tiedemann RE, Schmidt J, Keats JJ, Shi CX, Zhu YX, Palmer SE, Mao X, Schimmer AD, Stewart AK: Identification of a potent natural triterpenoid inhibitor of proteosome chymotrypsin-like activity and NF-kappaB with antimyeloma activity in vitro and in vivo. Blood; 2009 Apr 23;113(17):4027-37
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  • [Title] Identification of a potent natural triterpenoid inhibitor of proteosome chymotrypsin-like activity and NF-kappaB with antimyeloma activity in vitro and in vivo.
  • As multiple myeloma tumors universally dysregulate cyclin D genes we conducted high-throughput chemical library screens for compounds that induce suppression of cyclin D2 promoter transcription.
  • Strikingly, the early transcriptional response of cells treated with pristimerin closely resembles cellular responses elicited by proteosome inhibitors, with rapid induction of heat shock proteins, activating transcription factor 3 (ATF3), and CHOP.
  • Notably, cytotoxic triterpenoids including pristimerin inhibit NF-kappaB activation via inhibition of IKK alpha or IKK beta, whereas proteosome inhibitors instead suppress NF-kappaB function by impairing degradation of ubiquitinated I kappaB.
  • By inhibiting both IKK and the proteosome, pristimerin causes overt suppression of constitutive NF-kappaB activity in myeloma cells that may mediate its suppression of cyclin D.
  • Consistent with this, pristimerin is potently and selectively lethal to primary myeloma cells (IC(50) < 100 nM), inhibits xenografted plasmacytoma tumors in mice, and is synergistically cytotoxic with bortezomib--providing the rationale for pharmaceutical development of triterpenoid dual-function proteosome/NF-kappaB inhibitors as therapeutics for human multiple myeloma and related malignancies.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Cell Lineage. Cells, Cultured. Coculture Techniques. Combinatorial Chemistry Techniques. Cyclin D. Cyclins / genetics. Cyclins / metabolism. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Molecular Structure. Proteasome Endopeptidase Complex / metabolism. Transcriptional Activation / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 19096011.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA133115
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biological Products; 0 / Cyclin D; 0 / Cyclins; 0 / NF-kappa B; 0 / Proteasome Inhibitors; 0 / Triterpenes; 1258-84-0 / pristimerin; EC 3.4.21.39 / Chymases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC3952546
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20. van der Groep P, Bouter A, Menko FH, van der Wall E, van Diest PJ: High frequency of HIF-1alpha overexpression in BRCA1 related breast cancer. Breast Cancer Res Treat; 2008 Oct;111(3):475-80
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  • 19/30 (63%) of BRCA1 tumors showed perinecrotic (hypoxia induced) and 8/30 (27%) a diffuse HIF-1alpha overexpression pattern, the latter more likely related to genetic alterations in oncogenes and tumor suppressor genes.
  • In contrast, sporadic breast cancer HIF-1 expressing tumors showed an inverse ratio of perinecrotic/diffuse expression (31 vs. 69%, P = 0.0002).
  • [MeSH-major] BRCA1 Protein / genetics. Breast Neoplasms / chemistry. Germ-Line Mutation. Hypoxia-Inducible Factor 1, alpha Subunit / analysis
  • [MeSH-minor] Cell Hypoxia. Female. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Humans. Necrosis. Neoplasm Invasiveness. Up-Regulation

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  • (PMID = 18030615.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / BRCA1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
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21. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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22. Chen C, Sun J, Liu G, Chen J: Effect of small interference RNA targeting HIF-1alpha mediated by rAAV combined L: -ascorbate on pancreatic tumors in athymic mice. Pathol Oncol Res; 2009 Mar;15(1):109-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of small interference RNA targeting HIF-1alpha mediated by rAAV combined L: -ascorbate on pancreatic tumors in athymic mice.
  • To study the effect of recombinant adeno-associated virus (rAAV) vector bearing small inference RNA (siRNA) targeting hypoxia inducible factor 1alpha (HIF-1alpha) combined L: -ascorbate on pancreatic tumors in athymic mice primarily.
  • In vitro, rAAV-hrGFP, rAAV-siHIF and L: -ascorbate which were used alone or in combination were delivered to exponentially growing MiaPaCa2 cells.
  • Then, we examined the expression of HIF-1alpha mRNA and protein, the secretion of VEGF in MiaPaCa2 cells under hypoxic condition with Real-time PCR, Western Blot, ELISA, respectively.
  • In vivo, MiaPaCa2 cells were inoculated subcutaneously on the back of nude mice.
  • Nude mice with xenograft tumor were randomly divided into equal groups and were injected with rAAV-hrGFP or rAAV-siHIF or were fed with L: -ascorbate.
  • Then, we measured the size of tumor every 3 days and drew a tumor growth curve.
  • After 30 days, all mice were sacrificed and the tumors were dissected.
  • In vitro, we found that rAAV-siHIF could inhibit the expression of HIF-1alpha mRNA and protein in MiaPaCa2 human pancreatic cancer cells but L: -ascorbate could only restrain the expression of HIF-1alpha protein.
  • In vivo, we found that rAAV-siHIF could inhibit the growth of nude mice xenograft tumor and the expression of HIF-1alpha and VEGF and MVD while L: -ascorbate can only inhibit the growth of xenograft tumor in the early and middle stage.
  • These results suggest that rAAV-siHIF and L: -ascorbate can inhibit the growth of nude mice xenograft tumor and HIF-1alpha could be a target of pancreatic cancer genetic and pharmacological therapy.
  • [MeSH-major] Antioxidants / pharmacology. Ascorbic Acid / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Pancreatic Neoplasms / prevention & control. RNA, Small Interfering / pharmacology

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  • (PMID = 18509748.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Vascular Endothelial Growth Factor A; PQ6CK8PD0R / Ascorbic Acid
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23. He L, Hou M, Li G, Wen S, Yang H, Chen P, Xu N: [The clinical signifcance of expression of ERCC1 and PkCalpha in non-small cell lung cancer]. Zhongguo Fei Ai Za Zhi; 2010 Mar;13(3):270-3
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  • [Title] [The clinical signifcance of expression of ERCC1 and PkCalpha in non-small cell lung cancer].
  • BACKGROUND AND OBJECTIVE: Excision repair cross-complementing 1 (Excision-Repair Cross-Complementing 1, ERCC1), an important member of the DNA repair gene family, plays a key role in nucleotide excision repair and apoptosis of tumor cells.
  • Protein kinase C-alpha (Protein kinase C, PKCalpha), an isozyme in protein kinase C family, is an important signaling molecule in signal transduction pathways of tumors, which has been implicated in malignant transformation and proliferation.
  • The aim of this study was to explore the clinical significance of ERCC1 and PKCalpha in non-small cell lung cancer (NSCLC).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / pathology. DNA-Binding Proteins / metabolism. Endonucleases / metabolism. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Protein Kinase C-alpha / metabolism

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  • (PMID = 20673527.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; EC 2.7.11.13 / Protein Kinase C-alpha; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases
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24. Thangapazham RL, Rajeshkumar NV, Sharma A, Warren J, Singh AK, Ives JA, Gaddipati JP, Maheshwari RK, Jonas WB: Effect of homeopathic treatment on gene expression in Copenhagen rat tumor tissues. Integr Cancer Ther; 2006 Dec;5(4):350-5
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  • [Title] Effect of homeopathic treatment on gene expression in Copenhagen rat tumor tissues.
  • Agents that induce apoptosis may inhibit tumor growth and provide therapeutic benefit.
  • MATERIALS AND METHODS: The authors investigated the effect of a homeopathic treatment regimen containing Conium maculatum, Sabal serrulata, Thuja occidentalis, and a MAT-LyLu Carcinosin nosode on the expression of cytokines and genes that regulate apoptosis.
  • RESULTS: There were no significant changes in mRNA levels of the apoptotic genes bax, bcl-2, bcl-x, caspase-1, caspase-2, caspase-3, Fas, FasL, or the cytokines interleukin (IL)-1alpha, IL-1beta, tumor necrosis factor (TNF)-beta, IL-3, IL-4, IL-5, IL-6, IL-10, TNF-alpha, IL-2, and interferon-gamma in prostate tumor and lung metastasis after treatment with homeopathic medicines.
  • CONCLUSIONS: This study indicates that treatment with the highly diluted homeopathic remedies does not alter the gene expression in primary prostate tumors or in lung metastasis.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Cell Line, Tumor. Cytokines / genetics. Disease Models, Animal. Male. RNA, Messenger / metabolism. Rats. Rats, Inbred Strains. Reverse Transcriptase Polymerase Chain Reaction


25. Yunokawa M, Tanimoto K, Nakamura H, Nagai N, Kudo Y, Kawamoto T, Kato Y, Hiyama E, Hiyama K, Nishiyama M: Differential regulation of DEC2 among hypoxia-inducible genes in endometrial carcinomas. Oncol Rep; 2007 Apr;17(4):871-8
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  • In this study, we demonstrate an important role of activation of the hypoxia-inducible factor-1 (HIF-1) pathway in endometrial carcinogenesis and tumor phenotype development of endometrial carcinoma, and suggest a unique role of the HIF-1-target gene, differentiated embryo chondrocyte 2 (DEC2), in carcinogenesis.
  • Hypoxia caused an increase in HIF-1alpha protein expression in 4 endometrial carcinoma cell lines.
  • The expressions of its 5 target genes - DEC1, DEC2, carbonic anhydrase-9 (CA9), vascular endothelial growth factor (VEGF), and solute carrier family 2, member 1 (SLC2A1) - also reactively increased in most of the cell lines, except for DEC2 in the SNG-M cells.
  • The expression levels of CA9 and VEGF were significantly higher in the tumors of post- as opposed to pre-menopausal patients.
  • [MeSH-major] Anoxia / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Carcinoma / genetics. Endometrial Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, Neoplasm / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • [MeSH-minor] Antigens, Neoplasm / genetics. Carbonic Anhydrases / genetics. Female. Gene Expression Profiling. Glucose Transporter Type 1 / genetics. Humans. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 17342330.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / BHLHE41 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DEC1 protein, human; 0 / Glucose Transporter Type 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / SLC2A1 protein, human; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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26. Paniagua RT, Sharpe O, Ho PP, Chan SM, Chang A, Higgins JP, Tomooka BH, Thomas FM, Song JJ, Goodman SB, Lee DM, Genovese MC, Utz PJ, Steinman L, Robinson WH: Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis. J Clin Invest; 2006 Oct;116(10):2633-42
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  • Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor developed to treat Bcr/Abl-expressing leukemias and subsequently found to treat c-Kit-expressing gastrointestinal stromal tumors.
  • We further show that micromolar concentrations of imatinib abrogate multiple signal transduction pathways implicated in RA pathogenesis, including mast cell c-Kit signaling and TNF-alpha release, macrophage c-Fms activation and cytokine production, and fibroblast PDGFR signaling and proliferation.
  • In our studies, imatinib attenuated PDGFR signaling in fibroblast-like synoviocytes (FLSs) and TNF-alpha production in synovial fluid mononuclear cells (SFMCs) derived from human RA patients.
  • Imatinib-mediated inhibition of a spectrum of signal transduction pathways and the downstream pathogenic cellular responses may provide a powerful approach to treat RA and other inflammatory diseases.
  • [MeSH-minor] Animals. Autoantigens / immunology. B-Lymphocytes / drug effects. B-Lymphocytes / immunology. B-Lymphocytes / metabolism. Benzamides. Cell Proliferation / drug effects. Collagen Type II / immunology. Humans. Imatinib Mesylate. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / metabolism. Male. Mast Cells / drug effects. Mast Cells / metabolism. Mast Cells / pathology. Mice. Mice, Inbred DBA. Mice, Transgenic. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-kit / metabolism. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism. Signal Transduction / drug effects. Stem Cell Factor / pharmacology. Synovial Fluid / cytology. Synovial Fluid / drug effects. Synovial Fluid / metabolism. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16981009.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI051614; United States / NIAID NIH HHS / AI / T32 AI007290; United States / NHLBI NIH HHS / HV / N01 HV028183; United States / NIAMS NIH HHS / AR / K08 AR002133; United States / NIAMS NIH HHS / AR / R21 AR049328; United States / NIAMS NIH HHS / AR / AR49328; United States / NIAMS NIH HHS / AR / R01 AR054822; United States / NIAID NIH HHS / AI / AI051614; United Kingdom / Multiple Sclerosis Society / / 835; United States / NHLBI NIH HHS / HV / N01-HV-28183; United States / NIAMS NIH HHS / AR / K08 AR02133; United States / NHLBI NIH HHS / HL / N01HV28183
  • [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 / Autoantigens; 0 / Benzamides; 0 / Collagen Type II; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Stem Cell Factor; 0 / Tumor Necrosis Factor-alpha; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC1564430
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27. Papaetis GS, Syrigos KN: Sunitinib: a multitargeted receptor tyrosine kinase inhibitor in the era of molecular cancer therapies. BioDrugs; 2009;23(6):377-89
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  • These include vascular endothelial growth factor receptors (VEGFR type 1 and 2), platelet-derived growth factor receptors (PDGFR-alpha and PDGFR-beta), stem cell factor receptor (KIT), FMS-like tyrosine kinase-3 (FLT3), glial cell-line derived neurotrophic factor receptor (RET) and the receptor of macrophage-colony stimulating factor (CSF1R).
  • Examination of the antitumor effect of sunitinib in a variety of cell lines in vitro suggested an antiproliferative activity that is dependent on the presence of constitutively active RTK targets.
  • The use of sunitinib as first-line therapy in advanced renal cell carcinoma (RCC) has improved the overall survival compared with that observed after cytokine therapy, while its administration in patients with gastrointestinal stromal tumors (GISTs) after progression or intolerance to imatinib achieved an objective response of 7%.
  • An interesting antitumor activity of sunitinib was reported in phase II studies of patients with a variety of malignancies, such as hepatocellular cancer, pancreatic neuroendocrine tumors, and non-small cell lung cancer; results of phase III studies are urgently anticipated.
  • A variety of skin adverse effects have been described with the use of sunitinib such as hand-foot syndrome, yellow discoloration of the skin, dry skin, subungual splinter hemorrhages, acral erythema, and generalized skin rashes.

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  • (PMID = 19894779.001).
  • [ISSN] 1179-190X
  • [Journal-full-title] BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy
  • [ISO-abbreviation] BioDrugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Indoles; 0 / Protein Kinase Inhibitors; 0 / Pyrroles; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; V99T50803M / sunitinib
  • [Number-of-references] 123
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28. Stratakis CA: New genes and/or molecular pathways associated with adrenal hyperplasias and related adrenocortical tumors. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):152-7
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  • [Title] New genes and/or molecular pathways associated with adrenal hyperplasias and related adrenocortical tumors.
  • Over the course of the last 10 years, we have studied the genetic and molecular mechanisms leading to disorders that affect the adrenal cortex, with emphasis on those that are developmental, hereditary and associated with adrenal hypoplasia or hyperplasia, multiple tumors and abnormalities in other endocrine glands.
  • On the basis of this work, we propose an hypothesis on how adrenocortical tumors form and the importance of the cyclic AMP-dependent signaling pathway in this process.
  • The regulatory subunit type 1-alpha (RIalpha) of protein kinase A (PKA) (the PRKAR1A gene) is mutated in most patients with Carney complex and primary pigmented nodular adrenocortical disease (PPNAD).
  • Phosphodiesterase-11A (the PDE11A gene) and -8B (the PDE8B gene) mutations were found in patients with isolated adrenal hyperplasia and Cushing syndrome, as well in patients with PPNAD.
  • PKA effects on tumor suppression and/or development and the cell cycle are becoming clear: PKA and/or cAMP act as a coordinator of growth and proliferation in the adrenal cortex.
  • Genome-wide searches for other genes responsible for adrenal tumors and related diseases are ongoing; recent evidece of the involvement of the mitochondrial oxidation pathway in adrenocortical tumorigenesis is derived from our study of rare associations such as those of disorders predisposing to adrenomedullary and related tumors (Carney triad, the dyad of paragangliomas and gastric stromal sarcomas or Carney-Stratakis syndrome, hereditary leiomyomatosis and renal cancer syndrome) which appear to be associated with adrenocortical lesions.

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  • (PMID = 19063937.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z01 HD000642-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.1.4.- / Phosphoric Diester Hydrolases
  • [Number-of-references] 29
  • [Other-IDs] NLM/ NIHMS99078; NLM/ PMC2668239
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29. Perrone F, Da Riva L, Orsenigo M, Losa M, Jocollè G, Millefanti C, Pastore E, Gronchi A, Pierotti MA, Pilotti S: PDGFRA, PDGFRB, EGFR, and downstream signaling activation in malignant peripheral nerve sheath tumor. Neuro Oncol; 2009 Dec;11(6):725-36
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  • [Title] PDGFRA, PDGFRB, EGFR, and downstream signaling activation in malignant peripheral nerve sheath tumor.
  • We investigated the activation of platelet-derived growth factor (PDGF) receptor A (PDGFRA), PDGF receptor B (PDGFRB), epidermal growth factor receptor (EGFR), and their downstream pathways in malignant peripheral nerve sheath tumors (MPNSTs).
  • The activation of the downstream receptor pathways was also studied by means of v-akt murine thymoma viral oncogene homolog (AKT), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR) Western blotting experiments, as well as rat sarcoma viral oncogene homolog (RAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), phosphoinositide-3-kinase, catalytic, alpha polypeptide (PI3KCA), and phosphatase and tensin homolog deleted on chromosome ten (PTEN) mutational analysis and fluorescence in situ hybridization.
  • [MeSH-major] Nerve Sheath Neoplasms / metabolism. Receptor, Epidermal Growth Factor / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism. Signal Transduction


30. Viswanathan AN, Schernhammer ES: Circulating melatonin and the risk of breast and endometrial cancer in women. Cancer Lett; 2009 Aug 18;281(1):1-7
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  • Melatonin interacts with membrane and nuclear receptors, and may be linked to the regulation of tumor growth.
  • Similarly, both case-control and prospective cohort studies have consistently linked night shift work with breast cancer risk and, more recently, endometrial cancer - another tumor highly sensitive to estrogens.
  • While, to date, the evidence for an association between sleep duration and breast cancer risk is less convincing, overall, there is increasing support for a potentially important link between melatonin and breast cancer risk and perhaps the risk of other tumors.

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  • (PMID = 19070424.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114534; United States / NCI NIH HHS / CA / CA117979-04; United States / NCI NIH HHS / CA / K07 CA117979-04; United States / NCI NIH HHS / CA / K07 CA117979-01; United States / NCI NIH HHS / CA / CA114534; United States / NCI NIH HHS / CA / CA117979-02; United States / NCI NIH HHS / CA / CA117979-01; United States / NCI NIH HHS / CA / K07 CA117979; United States / NCI NIH HHS / CA / K07 CA117979-02; United States / NCI NIH HHS / CA / K07 CA117979-03; United States / NCI NIH HHS / CA / CA117979-03; United States / NCI NIH HHS / CA / 5K07 CA117979-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 333DO1RDJY / Serotonin; 4TI98Z838E / Estradiol; EC 1.14.14.1 / Aromatase; JL5DK93RCL / Melatonin
  • [Number-of-references] 85
  • [Other-IDs] NLM/ NIHMS127367; NLM/ PMC2735793
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31. Choi HJ, Eun JS, Kim DK, Li RH, Shin TY, Park H, Cho NP, Soh Y: Icariside II from Epimedium koreanum inhibits hypoxia-inducible factor-1alpha in human osteosarcoma cells. Eur J Pharmacol; 2008 Jan 28;579(1-3):58-65
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  • [Title] Icariside II from Epimedium koreanum inhibits hypoxia-inducible factor-1alpha in human osteosarcoma cells.
  • Hypoxia-inducible factor-1 (HIF-1) is an important tumor-selective therapeutic target for solid tumors.
  • Icariside II attenuated the protein level of HIF-1alpha induced by hypoxia in human osteosarcoma (HOS) cells in a concentration-dependent manner, probably by enhancing the interaction rate between von Hippel-Lindau (VHL) and HIF-1alpha.
  • Furthermore, Icariside II down-regulated the levels of HIF-inducible genes involved in angiogenesis, metastasis, and glucose metabolism, such as vascular endothelial growth factor (VEGF), urokinase plasminogen activator receptor (uPAR), adrenomedullin (ADM), matrix metalloproteinase 2 (MMP2), aldolase A, and enolase 1 in HOS cells.
  • Icariside II also inhibited the migration rate in HOS cells and tube formation rate in human umbilical vein endothelium cells (HUVECs).
  • [MeSH-major] Epimedium / chemistry. Flavonoids / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Hypoxia-Inducible Factor 1, alpha Subunit / drug effects
  • [MeSH-minor] Adrenomedullin / drug effects. Adrenomedullin / genetics. Bone Neoplasms / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Fructose-Bisphosphate Aldolase / drug effects. Fructose-Bisphosphate Aldolase / genetics. Humans. Matrix Metalloproteinase 2 / drug effects. Matrix Metalloproteinase 2 / genetics. Osteosarcoma / metabolism. Phosphopyruvate Hydratase / drug effects. Phosphopyruvate Hydratase / genetics. Receptors, Cell Surface / drug effects. Receptors, Cell Surface / genetics. Receptors, Urokinase Plasminogen Activator. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / genetics. Von Hippel-Lindau Tumor Suppressor Protein / drug effects. Von Hippel-Lindau Tumor Suppressor Protein / metabolism

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  • (PMID = 17980359.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 0 / Vascular Endothelial Growth Factor A; 113558-15-9 / baohuoside I; 148498-78-6 / Adrenomedullin; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 4.1.2.13 / Fructose-Bisphosphate Aldolase; EC 4.2.1.11 / Phosphopyruvate Hydratase; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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32. Masjosthusmann K, Bielack SS, Köhler G, Florax A, Schiborr M, Bruch J, Reinhardt D, Kuhn N, Paulussen M, Jürgens H: Concomitant Ewing sarcoma and acute lymphoblastic leukemia in a 5-year-old girl. Pediatr Blood Cancer; 2005 Nov;45(6):846-9
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  • Malignancies from the Ewing family of tumors and acute lymphoblastic leukemia (ALL) are not known to be associated with each other.
  • The simultaneous presence of two distinct neoplasms was confirmed by RT-PCR, with EWS/FLI1 type 1 rearrangement in the bone tumor and TEL/AML1 rearrangement in the marrow.
  • She was treated with chemotherapy, radiotherapy, and surgery and was in remission of both diseases 31 months after diagnosis.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Sarcoma, Ewing / complications
  • [MeSH-minor] Child, Preschool. Combined Modality Therapy. Core Binding Factor Alpha 2 Subunit. Disease-Free Survival. Female. Humans. Oncogene Proteins, Fusion. Polymerase Chain Reaction. Proto-Oncogene Protein c-fli-1. RNA-Binding Protein EWS. Translocation, Genetic

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15926159.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / EWS-FLI fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Protein c-fli-1; 0 / RNA-Binding Protein EWS; 0 / TEL-AML1 fusion protein
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33. Yan H, Blackburn AC, McLary SC, Tao L, Roberts AL, Xavier EA, Dickinson ES, Seo JH, Arenas RB, Otis CN, Cao QJ, Lawlor RG, Osborne BA, Kittrell FS, Medina D, Jerry DJ: Pathways contributing to development of spontaneous mammary tumors in BALB/c-Trp53+/- mice. Am J Pathol; 2010 Mar;176(3):1421-32
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  • [Title] Pathways contributing to development of spontaneous mammary tumors in BALB/c-Trp53+/- mice.
  • Here we use BALB/c-Trp53+/- mice as a model to examine the sequence of events leading to mammary tumors.
  • Among the 28 mammary tumors collected from BALB/c-Trp53+/- mice, loss of heterozygosity for Trp53 was detected in more than 90% of invasive mammary tumors.
  • Moreover, expression of biomarkers such as estrogen receptor alpha, progesterone receptor, Her2/Neu, and activated Notch1 varied among mammary tumors, suggesting that multiple oncogenic lesions collaborate with loss of p53 function.
  • Expression of biomarkers was retained when tumor fragments were transplanted to syngeneic hosts.
  • Tumors expressing solely luminal or basal keratins were also observed (27 and 11%, respectively), but the largest class of tumors expressed both luminal and basal keratins (62%).
  • Overall, this panel of transplantable tumors provides a resource for detailed evaluation of the cell lineages undergoing transformation and preclinical testing of therapeutic agents targeting a variety of oncogenic pathways including cancer stem cells.

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  • (PMID = 20110418.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES015739; United States / NCI NIH HHS / CA / R01-CA105452; United States / NCI NIH HHS / CA / R01 CA095164; United States / NCI NIH HHS / CA / R01 CA105452; United States / NCI NIH HHS / CA / R01-CA095164; United States / NIEHS NIH HHS / ES / R01-ES015739
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Notch; 0 / Receptors, Progesterone; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2832161
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34. Lee YJ, Moon MS, Kwon SJ, Rhee JG: Hypoxia and low glucose differentially augments TRAIL-induced apoptotic death. Mol Cell Biochem; 2005 Feb;270(1-2):89-97
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  • Tumor microenvironment, which is characterized by hypoxia, low-glucose concentrations, high-lactate concentrations, low-extracellular pH, can alter the therapeutic response in tumors.
  • When human prostate adenocarcinoma DU-145 cells were treated with 50 ng/mL TRAIL or hypoxia for 4 h, the survival was 45.7 and 32.5%, respectively.
  • The combination of TRAIL and hypoxia synergistically increased cell death.
  • Similar results were observed in human prostate adenocarcinoma LNCaP cells.
  • [MeSH-major] Apoptosis. Glucose / metabolism. Hypoxia. Membrane Glycoproteins / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Apoptosis Regulatory Proteins. Blotting, Western. Caspase 3. Caspase 9. Caspases / metabolism. Cell Line, Tumor. Cell Survival. Electrophoresis, Polyacrylamide Gel. Enzyme Activation. Humans. Hydrogen-Ion Concentration. Immunoblotting. Signal Transduction. TNF-Related Apoptosis-Inducing Ligand. Time Factors

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  • (PMID = 15792357.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA96989; United States / NCI NIH HHS / CA / R01 CA096989; United States / NCI NIH HHS / CA / CA48000; United States / NCI NIH HHS / CA / R01 CA095191; United States / NCI NIH HHS / CA / CA95191
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases; IY9XDZ35W2 / Glucose
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35. Corvaisier M, Moreau-Aubry A, Diez E, Bennouna J, Mosnier JF, Scotet E, Bonneville M, Jotereau F: V gamma 9V delta 2 T cell response to colon carcinoma cells. J Immunol; 2005 Oct 15;175(8):5481-8
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  • [Title] V gamma 9V delta 2 T cell response to colon carcinoma cells.
  • During analysis of CD8 T cells derived from ascites of a colon cancer patient, we isolated a Vgamma9Vdelta2 T cell clone showing strong reactivity against autologous tumor cell lines.
  • This clone killed a large fraction of allogeneic colon carcinoma and melanoma cell lines, but did not affect a normal colon cell line, colon fibroblasts, or melanocytes.
  • Tumor cell recognition was TCR and NKG2D dependent and induced TNF-alpha and IFN-gamma secretion by the clone; accordingly, tumor targets expressed several NKG2D ligands, such as MHC class I chain-related gene A and UL16-binding protein molecules.
  • Colon tumor recognition by Vgamma9Vdelta2 T cells was highly dependent on isopentenyl pyrophosphate production and ICAM-1 expression by target cells.
  • Finally, similar reactivity patterns against colon carcinoma cell lines were observed using polyclonal Vgamma9Vdelta2 T cells of various origins, and Vgamma9Vdelta2 lymphocytes were present in the majority of colon tumor samples studied.
  • Together, these results suggest that Vgamma9Vdelta2 T cells contribute to the natural immune surveillance against colon cancers.
  • Therefore, this study provides a strong rationale for the use of Vgamma9Vdelta2 T cell agonists in immunotherapies targeting colon tumors.
  • [MeSH-major] Colonic Neoplasms / immunology. Cytotoxicity, Immunologic. Receptors, Antigen, T-Cell, gamma-delta / immunology. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Antigens / immunology. Caco-2 Cells. Cell Line, Tumor. Clone Cells. HCT116 Cells. HT29 Cells. Humans. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. NK Cell Lectin-Like Receptor Subfamily K. Receptors, Immunologic / immunology. Receptors, Natural Killer Cell

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  • (PMID = 16210656.001).
  • [ISSN] 0022-1767
  • [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 / Antigens; 0 / KLRK1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell; 126547-89-5 / Intercellular Adhesion Molecule-1
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36. Postovit LM, Abbott DE, Payne SL, Wheaton WW, Margaryan NV, Sullivan R, Jansen MK, Csiszar K, Hendrix MJ, Kirschmann DA: Hypoxia/reoxygenation: a dynamic regulator of lysyl oxidase-facilitated breast cancer migration. J Cell Biochem; 2008 Apr 1;103(5):1369-78
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  • Fluctuating oxygen levels characterize the microenvironment of many cancers and tumor hypoxia is associated with increased invasion and metastatic potential concomitant with a poor prognosis.
  • Similarly, the expression of lysyl oxidase (LOX) in breast cancer facilitates tumor cell migration and is associated with estrogen receptor negative status and reduced patient survival.
  • Here we demonstrate that hypoxia/reoxygenation drives poorly invasive breast cancer cells toward a more aggressive phenotype by up-regulating LOX expression and catalytic activity.
  • Moreover, poorly invasive breast cancer cells displayed a marked increase in LOX-dependent FAK/Src activation and cell migration following hypoxia/reoxygenation, but not in response to hypoxia alone.
  • Furthermore, LOX expression is only partially dependent on hypoxia inducible factor-1 (HIF-1alpha) in poorly invasive breast cancer cells, as hypoxia mimetics and overexpression of HIF-1alpha could not up-regulate LOX expression to the levels observed under hypoxia.
  • Clinically, LOX expression positively correlates with tumor progression and co-localization with hypoxic regions (defined by HIF-1alpha expression) in ductal carcinoma in situ and invasive ductal carcinoma primary tumors.
  • However, positive correlation is lost in metastatic tumors, suggesting that LOX expression is independent of a hypoxic environment at later stages of tumor progression.
  • This work demonstrates that both hypoxia and reoxygenation are necessary for LOX catalytic activity which facilitates breast cancer cell migration through a hydrogen peroxide-mediated mechanism; thereby illuminating a potentially novel mechanism by which poorly invasive cancer cells can obtain metastatic competency.
  • [MeSH-major] Breast Neoplasms / enzymology. Carcinoma, Ductal, Breast / enzymology. Cell Movement. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Protein-Lysine 6-Oxidase / biosynthesis
  • [MeSH-minor] Cell Hypoxia. Cell Line, Tumor. Female. Humans. Hydrogen Peroxide / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Neoplasm Invasiveness. Neoplasm Metastasis

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  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17685448.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 P50 CA089018; United States / NIAMS NIH HHS / AR / AR047713; United States / NCRR NIH HHS / RR / RR003061
  • [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 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; BBX060AN9V / Hydrogen Peroxide; EC 1.4.3.13 / Protein-Lysine 6-Oxidase
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37. Wollmann G, Robek MD, van den Pol AN: Variable deficiencies in the interferon response enhance susceptibility to vesicular stomatitis virus oncolytic actions in glioblastoma cells but not in normal human glial cells. J Virol; 2007 Feb;81(3):1479-91
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  • [Title] Variable deficiencies in the interferon response enhance susceptibility to vesicular stomatitis virus oncolytic actions in glioblastoma cells but not in normal human glial cells.
  • With little improvement in the poor prognosis for humans with high-grade glioma brain tumors, alternative therapeutic strategies are needed.
  • Here we test the hypothesis that defects in the interferon (IFN) pathway could be exploited to enhance the selective oncolytic profile of vesicular stomatitis virus (VSV) in glioblastoma cells.
  • Two green fluorescent protein-expressing VSV strains, recombinant VSV and the glioma-adapted recombinant VSV-rp30a, were used to study infection of a variety of human glioblastoma cell lines compared to a panel of control cells, including normal human astrocytes, oligodendrocyte precursor cells, and primary explant cultures from human brain tissue.
  • Infection rate, cell viability, viral replication, and IFN-alpha/beta-related gene expression were compared in the absence and presence of IFN-alpha or polyriboinosinic polyribocytidylic acid [poly(I:C)], a synthetic inducer of the IFN-alpha/beta pathway.
  • Both VSV strains caused rapid and total infection and death of all tumor cell lines tested.
  • To a lesser degree, normal cells were also subject to VSV infection.
  • In contrast, IFN-alpha or poly(I:C) completely attenuated the infection of all primary control brain cells, whereas most glioblastoma cell lines treated with IFN-alpha or poly(I:C) showed little or no sign of protection and were killed by VSV.
  • Together, our results demonstrate that activation of the interferon pathway protects normal human brain cells from VSV infection while maintaining the vulnerability of human glioblastoma cells to viral destruction.

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  • (PMID = 17108037.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / K22 AI064757; United States / NIAID NIH HHS / AI / R01 AI048854; United States / NIAID NIH HHS / AI / AI48854
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 9008-11-1 / Interferons
  • [Other-IDs] NLM/ PMC1797501
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38. Gagliano N, Donne ID, Torri C, Migliori M, Grizzi F, Milzani A, Filippi C, Annoni G, Colombo P, Costa F, Ceva-Grimaldi G, Bertelli AA, Giovannini L, Gioia M: Early cytotoxic effects of ochratoxin A in rat liver: a morphological, biochemical and molecular study. Toxicology; 2006 Aug 15;225(2-3):214-24
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  • We characterized the overall early effect of chronic ochratoxin A (OTA) treatment on rat liver, analyzing different aspects related to: (i) fibrosis, by measuring collagen content and turnover, and alpha-smooth muscle actin (alphaSMA);.
  • (iii) the possible tumor promoter effect, evaluating cadherin and connexin (CX) mRNA levels.
  • In conclusion, these in vivo results show that OTA-induced liver injury involves a reduction in the ability to counterbalance oxidative stress, maybe leading to altered gap junction intercellular communication and loss of cell adhesion and polarity.
  • This suggests that mild oxidative damage might be a key factor, in combination with other cytotoxic effects, in triggering the promotion of liver tumors after exposure to OTA.

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  • (PMID = 16857307.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cadherins; 0 / Carcinogens; 0 / Connexins; 0 / HSP70 Heat-Shock Proteins; 0 / Mycotoxins; 0 / Ochratoxins; 0 / RNA, Messenger; 1779SX6LUY / ochratoxin A; 9007-34-5 / Collagen; EC 1.15.1.1 / Superoxide Dismutase
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39. Banning A, Kipp A, Schmitmeier S, Löwinger M, Florian S, Krehl S, Thalmann S, Thierbach R, Steinberg P, Brigelius-Flohé R: Glutathione Peroxidase 2 Inhibits Cyclooxygenase-2-Mediated Migration and Invasion of HT-29 Adenocarcinoma Cells but Supports Their Growth as Tumors in Nude Mice. Cancer Res; 2008 Dec 1;68(23):9746-53
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  • [Title] Glutathione Peroxidase 2 Inhibits Cyclooxygenase-2-Mediated Migration and Invasion of HT-29 Adenocarcinoma Cells but Supports Their Growth as Tumors in Nude Mice.
  • The selenoprotein gastrointestinal glutathione peroxidase 2 (GPx2) is up-regulated in a variety of cancer cells with thus far unknown consequences.
  • Therefore, two clones of a human colon cancer cell line (HT-29) in which GPx2 was stably knocked down by small interfering RNA (siRNA; siGPx2) were used to test whether cancer-relevant processes are affected by GPx2.
  • The capacity to grow anchorage independently in soft agar was significantly reduced in siGPx2 cells when compared with controls (i.e., HT-29 cells stably transfected with a scramble siRNA).
  • The weight of tumors derived from siGPx2 cells injected into nude mice was lower in 9 of 10 animals.
  • In contrast, in a wound-healing assay, wound closure was around 50% in controls and 80% in siGPx2 cells, indicating an enhanced capacity of the knockdown cells to migrate.
  • Similarly, invasion of siGPx2 cells in a Transwell assay was significantly increased.
  • Migration and invasion of siGPx2 cells were inhibited by celecoxib, a cyclooxygenase-2 (COX-2)-specific inhibitor, but not by alpha-tocopherol.
  • Selenium supplementation of cell culture medium did not influence the results obtained with siGPx2 cells, showing that none of the other selenoproteins could replace GPx2 regarding the described effects.
  • The data show that GPx2 inhibits malignant characteristics of tumor cells, such as migration and invasion, obviously by counteracting COX-2 expression but is required for the growth of transformed intestinal cells and may, therefore, facilitate tumor cell growth.
  • The data also shed new light on the use of selenium as a chemopreventive trace element: a beneficial effect may depend on the stage of tumor development.
  • [MeSH-major] Adenocarcinoma / enzymology. Cell Movement / physiology. Colonic Neoplasms / enzymology. Cyclooxygenase 2 / physiology. Glutathione Peroxidase / physiology
  • [MeSH-minor] Animals. Celecoxib. Cell Growth Processes / physiology. Cyclooxygenase 2 Inhibitors / pharmacology. HT29 Cells. Humans. Male. Mice. Mice, Knockout. Mice, Nude. Neoplasm Invasiveness. Pyrazoles / pharmacology. Sulfonamides / pharmacology

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  • (PMID = 19047153.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.11.1.- / GPX2 protein, human; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
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40. Seagroves TN, Peacock DL, Liao D, Schwab LP, Krueger R, Handorf CR, Haase VH, Johnson RS: VHL deletion impairs mammary alveologenesis but is not sufficient for mammary tumorigenesis. Am J Pathol; 2010 May;176(5):2269-82
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  • Overexpression of hypoxia inducible factor-1 (HIF-1)alpha, which is common in most solid tumors, correlates with poor prognosis and high metastatic risk in breast cancer patients.
  • Because HIF-1alpha protein stability is tightly controlled by the tumor suppressor von Hippel-Lindau (VHL), deletion of VHL results in constitutive HIF-1alpha expression.
  • During first pregnancy, loss of Vhl resulted in decreased mammary epithelial cell proliferation and impaired alveolar differentiation; despite these phenotypes, lactation was sufficient to support pup growth.
  • Deletion of Vhl in the epithelium also impacted the mammary stroma, as there was increased microvessel density accompanied by hemorrhage and increased immune cell infiltration.

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  • (PMID = 20382704.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / S10 RR025665; United States / NCI NIH HHS / CA / R01 CA082515; United States / NCI NIH HHS / CA / R01 CA100787-06; United States / NCI NIH HHS / CA / CA100787-06; United States / NCI NIH HHS / CA / R01 CA100787; United States / NCRR NIH HHS / RR / 1S10RR025665-01; United States / NCI NIH HHS / CA / R01CA082515
  • [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] EC 6.3.2.19 / Vhlh protein, mouse; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC2861092
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41. Borgman MP, Ray A, Kolhatkar RB, Sausville EA, Burger AM, Ghandehari H: Targetable HPMA copolymer-aminohexylgeldanamycin conjugates for prostate cancer therapy. Pharm Res; 2009 Jun;26(6):1407-18
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  • PURPOSE: This study focuses on the synthesis and characterization of N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-cyclo-RGD (Arg-Gly-Asp) conjugates for delivery of geldanamycin to prostate tumors.
  • Competitive binding of copolymer conjugates to alpha(v)beta(3) integrin was evaluated in prostate cancer (PC-3) and endothelial (HUVEC) cell lines and in vitro growth inhibition was assessed.
  • RESULTS: HPMA copolymers containing AH-GDM and RGDfK showed active binding to the alpha(v)beta(3) integrin similar to that of free peptide.
  • Similarly, growth inhibition of cells by conjugates was comparable to that of the free drug.

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  • (PMID = 19225872.001).
  • [ISSN] 1573-904X
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB007171; United States / NIBIB NIH HHS / EB / R01 EB 007171
  • [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 / Acrylamides; 0 / Benzoquinones; 0 / Integrin alpha Chains; 0 / Integrin beta Chains; 0 / Lactams, Macrocyclic; 0 / Peptides, Cyclic; 0 / cyclic (arginyl-glycyl-aspartyl-phenylalanyl-lysyl); 21442-01-3 / N-(2-hydroxypropyl)methacrylamide; EC 3.4.22.1 / Cathepsin B; Z3K3VJ16KU / geldanamycin
  • [Other-IDs] NLM/ NIHMS529278; NLM/ PMC3952876
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42. Becher OJ, Hambardzumyan D, Walker TR, Helmy K, Nazarian J, Albrecht S, Hiner RL, Gall S, Huse JT, Jabado N, MacDonald TJ, Holland EC: Preclinical evaluation of radiation and perifosine in a genetically and histologically accurate model of brainstem glioma. Cancer Res; 2010 Mar 15;70(6):2548-57
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  • Brainstem gliomas (BSG) are a rare group of central nervous system tumors that arise mostly in children and usually portend a particularly poor prognosis.
  • We report the development of a genetically engineered mouse model of BSG using the RCAS/tv-a system and its implementation in preclinical trials.
  • Using immunohistochemistry, we found that platelet-derived growth factor (PDGF) receptor alpha is overexpressed in 67% of pediatric BSGs.
  • We show that the likely cells of origin for these mouse BSGs exist on the floor of the fourth ventricle and cerebral aqueduct.
  • Irradiation of these high-grade BSGs shows that although single doses of 2, 6, and 10 Gy significantly increased the percent of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive nuclei, only 6 and 10 Gy significantly induce cell cycle arrest.
  • [MeSH-major] Brain Stem Neoplasms / drug therapy. Brain Stem Neoplasms / radiotherapy. Disease Models, Animal. Glioma / drug therapy. Glioma / radiotherapy. Phosphorylcholine / analogs & derivatives
  • [MeSH-minor] Animals. Combined Modality Therapy. Genetic Engineering. Inbreeding. Mice. Mice, Inbred BALB C. Receptor, Platelet-Derived Growth Factor alpha / biosynthesis

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  • (PMID = 20197468.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100688; United States / NCI NIH HHS / CA / R01 CA100688; United States / NCI NIH HHS / CA / U01 CA141502; United States / NCI NIH HHS / CA / U01 CA141502; United States / NCI NIH HHS / CA / U54 CA126518; United States / NCI NIH HHS / CA / U54 CA126518
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 107-73-3 / Phosphorylcholine; 2GWV496552 / perifosine; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ NIHMS171774; NLM/ PMC3831613
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43. Spiess PE, Brown GA, Pisters LL, Liu P, Tu SM, Evans JG, Kamat AM, Black P, Tannir NM: Viable malignant germ cell tumor in the postchemotherapy retroperitoneal lymph node dissection specimen: can it be predicted using clinical parameters? Cancer; 2006 Oct 1;107(7):1503-10
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  • [Title] Viable malignant germ cell tumor in the postchemotherapy retroperitoneal lymph node dissection specimen: can it be predicted using clinical parameters?
  • BACKGROUND: The presence of viable tumor in the surgical specimen after postchemotherapy retroperitoneal lymph node dissection (PC-RPLND) is associated with an increased risk of disease progression.
  • The objective of this study was to determine whether the presence of viable tumor in the surgical specimen could be predicted.
  • METHODS: Between 1980 and 2003, 236 patients underwent PC-RPLND for clinical Stage IIA or III nonseminomatous germ cell tumors (NSGCT).
  • A multivariate logistic regression analysis was used to evaluate whether clinical parameters were capable of predicting the presence of viable tumor in the surgical specimen.
  • RESULTS: International Germ Cell Consensus Classification (IGCCC) risk categories could be assigned to 218 patients, with 101 patients in the good-risk category, 32 patients in the intermediate-risk category, and 85 patients in the poor-risk category.
  • The incidence of viable tumor in the good-risk, intermediate-risk, and poor-risk categories was similar (17.8%, 15.6%, and 15.3%, respectively); however, the risk categories predicted disease-specific and recurrence-free survival (P = .022 and P < .0001, respectively).
  • On multivariate analysis, an elevated serum alpha-fetoprotein (AFP) level prior to PC-RPLND (P = .05) and the size of the retroperitoneal mass on pathology review (P = .02) were predictive of viable tumor in the surgical specimen.
  • CONCLUSIONS: Although IGCCC risk categories were correlated with disease-related outcomes, the risk groups had similar incidences of viable tumor.
  • Elevated serum AFP levels prior to surgery and the size of the retroperitoneal mass in the resected specimen may help to predict viable tumor in the PC-RPLND specimen.
  • [MeSH-major] Lymph Nodes / pathology. Neoplasms, Germ Cell and Embryonal / pathology. Testicular Neoplasms / drug therapy. Testicular Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / blood. Disease-Free Survival. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Middle Aged. Pathology, Surgical. Prognosis. Retroperitoneal Space. Risk. alpha-Fetoproteins / analysis

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 16944534.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
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44. Niu G, Xiong Z, Cheng Z, Cai W, Gambhir SS, Xing L, Chen X: In vivo bioluminescence tumor imaging of RGD peptide-modified adenoviral vector encoding firefly luciferase reporter gene. Mol Imaging Biol; 2007 May-Jun;9(3):126-34
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  • [Title] In vivo bioluminescence tumor imaging of RGD peptide-modified adenoviral vector encoding firefly luciferase reporter gene.
  • PURPOSE: The goal of this study is to demonstrate the feasibility of chemically modified human adenovirus (Ad) vectors for tumor retargeting.
  • PROCEDURES: E1- and E3-deleted Ad vectors carrying firefly luciferase reporter gene under cytomegalovirus promoter (AdLuc) was surface-modified with cyclic arginine-glycine-aspartic acid (RGD) peptides through a bifunctional poly(ethyleneglycol) linker (RGD-PEG-AdLuc) for integrin alpha(v)beta(3) specific delivery.
  • The Coxsackie and adenovirus viral receptor (CAR) and integrin alpha(v)beta(3) expression in various tumor cell lines was determined by reverse transcriptase PCR and fluorescence-activated cell sorting.
  • RESULTS: RGD-PEG-AdLuc abrogated the native CAR tropism and exhibited significantly enhanced transduction efficiency of integrin-positive tumors than AdLuc through intravenous administration.
  • CONCLUSION: This approach provides a robust platform for site-specific gene delivery and noninvasive monitoring of the transgene delivery efficacy and homing.

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  • (PMID = 17297551.001).
  • [ISSN] 1536-1632
  • [Journal-full-title] Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging
  • [ISO-abbreviation] Mol Imaging Biol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA102123; United States / NCI NIH HHS / CA / R24 CA93862; United States / NIBIB NIH HHS / EB / R21 EB001785; United States / NCI NIH HHS / CA / U54 CA119367; United States / NCI NIH HHS / CA / P50 CA114747
  • [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 / CLMP protein, human; 0 / CLMP protein, mouse; 0 / Coxsackie and Adenovirus Receptor-Like Membrane Protein; 0 / DNA Primers; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 0 / Receptors, Virus; 0 / Recombinant Proteins; 30IQX730WE / Polyethylene Glycols; 99896-85-2 / arginyl-glycyl-aspartic acid; EC 1.13.12.7 / Luciferases, Firefly
  • [Other-IDs] NLM/ NIHMS622064; NLM/ PMC4165526
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45. Santen R, Cavalieri E, Rogan E, Russo J, Guttenplan J, Ingle J, Yue W: Estrogen mediation of breast tumor formation involves estrogen receptor-dependent, as well as independent, genotoxic effects. Ann N Y Acad Sci; 2009 Feb;1155:132-40
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  • [Title] Estrogen mediation of breast tumor formation involves estrogen receptor-dependent, as well as independent, genotoxic effects.
  • One involves the binding of estradiol to estrogen receptor (ER) alpha with stimulation of cell proliferation.
  • Estradiol and its catechol-estrogen metabolite 4-OH-estradiol causes mutations in cell culture systems and can transform benign MCF-10F cells, allowing them to cause tumors in SCID mice.
  • The depurinated estradiol-guanine and -adenine adducts are measurable in MCF-7 breast cancer cells in culture and in mouse mammary tissue.
  • The double transgenic, alpha estrogen receptor knockout/Wnt-1 knockin mouse model allows us to dissect out the separate effects of ER-mediated and ER-independent actions of estradiol.
  • Knock out of the ER alpha delays the onset of breast tumors in this model, demonstrating a role of receptor-mediated actions.
  • Oophorectomy delays the onset of tumors and reduces overall incidence, providing evidence for an ER-independent effect.
  • [MeSH-major] Breast Neoplasms / pathology. Estrogen Receptor alpha / physiology. Estrogens / physiology. Mutation

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  • (PMID = 19250200.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Estrogens, Catechol; 4TI98Z838E / Estradiol; C3ZO03450E / 4-hydroxyestradiol
  • [Number-of-references] 22
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46. Abdel-Motal UM, Wigglesworth K, Galili U: Intratumoral injection of alpha-gal glycolipids induces a protective anti-tumor T cell response which overcomes Treg activity. Cancer Immunol Immunother; 2009 Oct;58(10):1545-56
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  • [Title] Intratumoral injection of alpha-gal glycolipids induces a protective anti-tumor T cell response which overcomes Treg activity.
  • alpha-Gal glycolipids capable of converting tumors into endogenous vaccines, have alpha-gal epitopes (Gal alpha 1-3 Gal beta 1-4GlcNAc-R) and are extracted from rabbit RBC membranes. alpha-Gal epitopes bind anti-Gal, the most abundant natural antibody in humans constituting 1% of immunoglobulins. alpha-Gal glycolipids insert into tumor cell membranes, bind anti-Gal and activate complement.
  • The complement cleavage peptides C5a and C3a recruit inflammatory cells and APC into the treated lesion.
  • Anti-Gal further opsonizes the tumor cells and targets them for effective uptake by recruited APC, via Fc gamma receptors.
  • These APC transport internalized tumor cells to draining lymph nodes, and present immunogenic tumor antigen peptides for activation of tumor specific T cells.
  • The present study demonstrates the ability of alpha-gal glycolipids treatment to prevent development of metastases at distant sites and to protect against tumor challenge in the treated mice.
  • Adoptive transfer studies indicate that this protective immune response is mediated by CD8+ T cells, activated by tumor lesions turned vaccine.
  • This T cell activation is potent enough to overcome the suppressive activity of Treg cells present in tumor bearing mice, however it does not elicit an autoimmune response against antigens on normal cells.
  • Insertion of alpha-gal glycolipids and subsequent binding of anti-Gal are further demonstrated with human melanoma cells, suggesting that intratumoral injection of alpha-gal glycolipids is likely to elicit a protective immune response against micrometastases also in cancer patients.

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  • (PMID = 19184002.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122019-02; United States / NCI NIH HHS / CA / R01 CA122019; United States / NCI NIH HHS / CA / CA122019; United States / NCI NIH HHS / CA / R01 CA122019-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Trisaccharides; 0 / alpha-galactosyl epitope; EC 2.4.1.- / Galactosyltransferases; EC 2.4.1.87 / N-acetyllactosaminide alpha-1,3-galactosyltransferase
  • [Other-IDs] NLM/ NIHMS165243; NLM/ PMC3233201
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47. Bae MK, Kim SH, Jeong JW, Lee YM, Kim HS, Kim SR, Yun I, Bae SK, Kim KW: Curcumin inhibits hypoxia-induced angiogenesis via down-regulation of HIF-1. Oncol Rep; 2006 Jun;15(6):1557-62
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  • Hypoxia-inducible factor-1 (HIF-1) has a central role in cellular responses to hypoxia, including the transcriptional activation of a number of genes involved in angiogenesis in tumors.
  • We found that curcumin, a natural, biologically active compound isolated from the commonly used spice turmeric, significantly decreases hypoxia-induced HIF-1alpha protein levels in HepG2 hepatocellular carcinoma cells.
  • Curcumin also blocked hypoxia-stimulated angiogenesis in vitro and down-regulated HIF-1alpha and VEGF expression in vascular endothelial cells.
  • These findings suggest that curcumin may play pivotal roles in tumor suppression via the inhibition of HIF-1alpha-mediated angiogenesis.
  • [MeSH-major] Curcumin / pharmacology. Hepatoblastoma / blood supply. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Liver Neoplasms / blood supply
  • [MeSH-minor] Cell Growth Processes / drug effects. Cell Hypoxia / drug effects. Cell Hypoxia / physiology. Down-Regulation / drug effects. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Endothelial Cells / pathology. Humans. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transcriptional Activation / drug effects. Transfection. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 16685395.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; IT942ZTH98 / Curcumin
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48. Bellezza G, Colella R, Sidoni A, Del Sordo R, Ferri I, Cioccoloni C, Cavaliere A: Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding. Histol Histopathol; 2008 09;23(9):1127-30
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  • [Title] Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding.
  • Granular cell tumor (GCT) is a relatively rare neoplasm, usually located in the upper aerodigestive tract, skin and soft tissue.
  • Because of its uncertain histogenesis, GCT has been the object of many immunohistochemical and ultrastructural studies that have suggested a Schwann cell origin.
  • Our recent observation of a case of GCT immunoreactive for Galectin-3 and HBME-1 led us to further investigate the immunohistochemical profile of these neoplasms.
  • We evaluated the immunohistochemical expression of the traditional markers for GCT (S-100, CD68) along with new markers (Galectin-3, HBME-1, Calretinina and Inhibin-alpha) in 22 granular cell tumors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Galectin 3 / metabolism. Granular Cell Tumor / metabolism. Head and Neck Neoplasms / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 18581283.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3; 0 / HBME-1 antigen
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49. McCluggage WG, McKenna M, McBride HA: CD56 is a sensitive and diagnostically useful immunohistochemical marker of ovarian sex cord-stromal tumors. Int J Gynecol Pathol; 2007 Jul;26(3):322-7
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  • [Title] CD56 is a sensitive and diagnostically useful immunohistochemical marker of ovarian sex cord-stromal tumors.
  • Ovarian sex cord-stromal tumors comprise a heterogeneous group of neoplasms with wide morphological diversity, and they can be mistaken for a variety of other tumors.
  • Some types, including granulosa and Sertoli cell tumor, may be confused with a neuroendocrine neoplasm.
  • CD56 is a widely used neuroendocrine marker with a high sensitivity for neuroendocrine tumors and is commonly used as part of a panel to distinguish between a neuroendocrine neoplasm and other tumors in the differential diagnosis.
  • In this study, we investigate CD56 staining in ovarian sex cord-stromal tumors.
  • Neoplasms studied were adult granulosa cell tumor (n = 40), juvenile granulosa cell tumor (n = 8), Sertoli cell tumor (n = 1), Sertoli-Leydig cell tumor (n = 14), Leydig cell tumor (n = 2), steroid cell tumor, not otherwise specified (n = 2), sclerosing stromal tumor (n = 1), sex cord tumor with annular tubules (n = 2), and fibroma (n = 15).
  • Three uterine tumors resembling ovarian sex cord tumor were also studied.
  • Nonneoplastic ovaries, including 3 cases of pregnancy-related granulosa or Sertoli cell proliferation, were also included.
  • In nontumorous ovaries, granulosa cells of follicular and corpus luteum cysts were consistently negative.
  • All sex cord-stromal tumors except one were positive with CD56; staining ranged from focal to diffuse but was usually diffuse involving more than 50% of tumor cells.
  • CD56 immunoreactivity is almost universal in ovarian sex cord-stromal tumors of all the major morphological types and is of no value in distinguishing a sex cord-stromal and a neuroendocrine neoplasm.
  • Since CD56 is an extremely sensitive marker of ovarian sex cord-stromal tumors, it may be useful in the diagnosis of this group of neoplasms, especially in cases which are alpha inhibin or calretinin negative, and in distinguishing these from mimics which are CD56 negative.
  • [MeSH-major] Antigens, CD56 / metabolism. Biomarkers, Tumor / metabolism. Ovarian Neoplasms / metabolism. Sex Cord-Gonadal Stromal Tumors / metabolism

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  • (PMID = 17581419.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Biomarkers, Tumor
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50. Zaffaroni N, Villa R, Pastorino U, Cirincione R, Incarbone M, Alloisio M, Curto M, Pilotti S, Daidone MG: Lack of telomerase activity in lung carcinoids is dependent on human telomerase reverse transcriptase transcription and alternative splicing and is associated with long telomeres. Clin Cancer Res; 2005 Apr 15;11(8):2832-9
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  • PURPOSE: Preliminary evidence indicates that telomerase activity is significantly less expressed in typical carcinoids than in large cell neuroendocrine carcinomas or in small cell lung cancers.
  • Knowledge of the mechanisms by which telomerase is differentially regulated in neuroendocrine lung tumors is important for a better understanding of the pathogenesis of these malignancies.
  • EXPERIMENTAL DESIGN: We investigated telomerase activity in 86 neuroendocrine lung tumors and correlated the enzyme activity with the expression of the enzyme subunits [human RNA component (hTR), human telomerase reverse transcriptase (hTERT), and alternatively spliced hTERT variants], with the telomere-associated protein human protection of telomere-1, and with the telomere length pattern.
  • RESULTS: A significantly (P = 0.0001) lower frequency of telomerase-positive cases was found in typical carcinoids (14%) than in large cell neuroendocrine carcinomas (87%) and small cell lung cancers (92%).
  • Telomerase-negative carcinoids were characterized by the absence of any hTERT transcript, only displayed the beta(-) alternatively spliced variant, or concomitantly expressed the alpha(+)beta(+) full-length message with different combinations of alternatively spliced variants.
  • However, in these tumors, a more abundant level of alternatively spliced transcripts than that of the alpha(+)beta(+) full-length transcript was generally found.
  • However, alternative lengthening of telomeres, as shown by associated promyelocytic leukemia bodies, was not observed in these tumors.
  • [MeSH-major] Alternative Splicing. Carcinoid Tumor / pathology. Lung Neoplasms / pathology. Telomerase / genetics. Telomere / genetics

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  • (PMID = 15837730.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / Telomerase
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51. Ernst DS, Brasher P, Venner PM, Czaykowski P, Moore MJ, Reyno L, Winquist E, Segal R, Hao D: Compliance and outcome of patients with stage 1 non-seminomatous germ cell tumors (NSGCT) managed with surveillance programs in seven Canadian centres. Can J Urol; 2005 Apr;12(2):2575-80
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  • [Title] Compliance and outcome of patients with stage 1 non-seminomatous germ cell tumors (NSGCT) managed with surveillance programs in seven Canadian centres.
  • Histological characteristics of the primary tumor were recorded for each patient.
  • Surveillance protocols consisted of clinical assessments, chest X-rays, serum beta HCG (bHCG), alpha feto-protein (aFP), and abdominopelvic CT.
  • Either CT, tumor markers, or CXR detected 90% of all relapses.
  • The mean rate of compliance with clinic visit (which included CXR and tumor markers) was 78% (range: 68.4-94.2%).
  • An abnormal CT was the most frequent identifier of disease relapse, and in combination with tumor markers and CXR, 90% of relapses were detected within 2 years of orchiectomy.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / surgery. Orchiectomy. Patient Compliance. Testicular Neoplasms / surgery

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  • (PMID = 15877938.001).
  • [ISSN] 1195-9479
  • [Journal-full-title] The Canadian journal of urology
  • [ISO-abbreviation] Can J Urol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Canada
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52. Yang Z, Zheng S, Harrison WJ, Harder J, Wen X, Gelovani JG, Qiao A, Li C: Long-circulating near-infrared fluorescence core-cross-linked polymeric micelles: synthesis, characterization, and dual nuclear/optical imaging. Biomacromolecules; 2007 Nov;8(11):3422-8
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  • With an average diameter of 24 +/- 8.9 nm, CCPMs exhibited a prolonged blood half-life (t1/2,alpha = 1.25 h; t1/2,beta = 46.18 h) and moderate uptake by the mononuclear phagocytic system.
  • Significant accumulation of CCPMs in human breast tumor xenografts allowed noninvasive monitoring of the uptake kinetics with both NIRF optical and gamma imaging techniques.
  • Our data suggest that Cy7-entrapped CCPM nanoparticles are suitable for NIRF imaging of solid tumors and have potential applications in the imaging of tumor-associated molecular markers.

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  • (PMID = 17958440.001).
  • [ISSN] 1525-7797
  • [Journal-full-title] Biomacromolecules
  • [ISO-abbreviation] Biomacromolecules
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA119387-02; United States / NCI NIH HHS / CA / R01 CA119387-01; United States / NCI NIH HHS / CA / R01 CA 119387; United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / CA119387-02; United States / NCI NIH HHS / CA / R01 CA119387-03; United States / NCI NIH HHS / CA / CA119387-03; United States / NCI NIH HHS / CA / R01 CA119387; United States / NCI NIH HHS / CA / CA119387-01
  • [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 / Chelating Agents; 0 / Cross-Linking Reagents; 0 / Fluorescent Dyes; 0 / Micelles; 0 / Polymers; 7A314HQM0I / Pentetic Acid
  • [Other-IDs] NLM/ NIHMS62709; NLM/ PMC2542943
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53. Munot K, Bell SM, Lane S, Horgan K, Hanby AM, Speirs V: Pattern of expression of genes linked to epigenetic silencing in human breast cancer. Hum Pathol; 2006 Aug;37(8):989-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We used immunohistochemistry to study expression of the tumor suppressor gene p16, estrogen receptor (ER) alpha, ERbeta, progesterone receptor (PR), and the DNA repair gene MGMT (O6 -methylguanine-DNA methyltransferase) in a panel of 200 breast cancers.
  • A significant correlation was seen between grade III tumor and loss of expression of ERalpha, ERbeta, PR (all P < .0001), and MGMT (P = .04), whereas loss of expression of p16 was associated with grades I and II tumors (P < .001).
  • In conclusion, there is silencing of several key genes in breast cancer affecting molecular pathways involved in cell immortalization, DNA repair, and hormonal regulation, and this correlates significantly with risk of cancer-specific death.
  • [MeSH-minor] Biomarkers, Tumor / metabolism. DNA Methylation. DNA, Neoplasm / analysis. Female. Great Britain / epidemiology. Humans. Immunoenzyme Techniques. Lymph Nodes / pathology. Lymphatic Metastasis. Mammary Glands, Human / metabolism. Mammary Glands, Human / pathology. Middle Aged. Neoplasm Staging. O(6)-Methylguanine-DNA Methyltransferase / genetics. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Polymerase Chain Reaction. Survival Rate

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  • (PMID = 16867861.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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54. Holmquist L, Jögi A, Påhlman S: Phenotypic persistence after reoxygenation of hypoxic neuroblastoma cells. Int J Cancer; 2005 Aug 20;116(2):218-25
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  • [Title] Phenotypic persistence after reoxygenation of hypoxic neuroblastoma cells.
  • Fast-growing solid tumors are usually insufficiently vascularized, leading to areas with necrosis and/or poorly oxygenated cells.
  • Tumor cells adapt to acute hypoxic stress.
  • Hypoxic (1% O2) neuroblastoma cells downregulate sympathetic nervous system marker genes, whereas neural crest cell markers are upregulated, suggesting that hypoxic tumor cells adopt a less mature phenotype, which in the clinical setting would translate to more aggressive tumors with increased metastatic potential.
  • Here, we compared gene expression patterns in neuroblastoma cells grown at 1%, 5% (a physiologic oxygen level) and 21% O2.
  • At 5% O2, cells developed a weak hypoxic phenotype and HIF-2 alpha, but not HIF-1 alpha, was acutely stabilized.
  • At 1% O2, HIF-2 alpha protein remained present in long-term cultures, while HIF-1 alpha was present only transiently.
  • The stability of the hypoxia-induced dedifferentiated phenotype in cells acutely reoxygenated at either 21% or 5% O2 persisted for at least 24 hr.
  • Thus, if these culture conditions are viewed as models for acute reoxygenation of metastasizing hypoxic tumor cells, our data suggest that an aggressive hypoxic phenotype persists for 24 hr or more, which might be long enough for the cells to be able to home to secondary sites, in part as a consequence of their immature hypoxic characteristics.
  • [MeSH-major] Cell Hypoxia. Gene Expression Regulation, Neoplastic. Neuroblastoma / genetics. Neuroblastoma / pathology. Oxygen / metabolism
  • [MeSH-minor] Adaptation, Physiological. Basic Helix-Loop-Helix Transcription Factors. Cell Survival. Down-Regulation. Gene Expression Profiling. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Neoplasm Metastasis. Phenotype. Transcription Factors / biosynthesis. Tumor Cells, Cultured. Up-Regulation

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15800931.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / endothelial PAS domain-containing protein 1; S88TT14065 / Oxygen
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55. Moschovi M, Alexiou GA, Dastamani A, Stefanaki K, Prodromou N, Hatzigiorgi H, Karamolegou K, Tzortzatou-Stathopoulou F: Alpha-fetoprotein secretion in a craniopharyngioma. Are craniopharyngiomas part of the germ cell tumor family? Acta Neurol Belg; 2010 Sep;110(3):272-5
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  • [Title] Alpha-fetoprotein secretion in a craniopharyngioma. Are craniopharyngiomas part of the germ cell tumor family?
  • These findings were suggestive for a brain germ cell tumor.
  • After two courses there was a reduction in the levels of AFP but the tumor size remained unchanged.
  • Subtotal tumor excision was performed that revealed the presence of a craniopharyngioma.
  • One month later there was enlargement of the cystic part of the tumor, while serum AFP was elevated.
  • The child received again systemic chemotherapy and placement of a reservoir into the cystic part of the tumor.
  • These observations support the theory of a germ cell tumor family, in which craniopharyngioma and germ cell tumor present the two sides of the same entity, while between them a wide variety of tumors, with variable type of secretion of AFP and/or beta-HCG, may exist.
  • [MeSH-major] Craniopharyngioma. Neoplasms, Germ Cell and Embryonal / classification. Pituitary Neoplasms. alpha-Fetoproteins / secretion

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  • (PMID = 21114138.001).
  • [ISSN] 0300-9009
  • [Journal-full-title] Acta neurologica Belgica
  • [ISO-abbreviation] Acta Neurol Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / AFP protein, human; 0 / alpha-Fetoproteins
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56. Datta J, Majumder S, Kutay H, Motiwala T, Frankel W, Costa R, Cha HC, MacDougald OA, Jacob ST, Ghoshal K: Metallothionein expression is suppressed in primary human hepatocellular carcinomas and is mediated through inactivation of CCAAT/enhancer binding protein alpha by phosphatidylinositol 3-kinase signaling cascade. Cancer Res; 2007 Mar 15;67(6):2736-46
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  • [Title] Metallothionein expression is suppressed in primary human hepatocellular carcinomas and is mediated through inactivation of CCAAT/enhancer binding protein alpha by phosphatidylinositol 3-kinase signaling cascade.
  • Here, we report that the levels of MT-1 and MT-2A are drastically reduced in primary human hepatocellular carcinomas (HCCs) and in diethylnitrosamine-induced liver tumors in mice, which is primarily due to transcriptional repression.
  • Inhibitors of both phosphatidylinositol 3-kinase (PI3K) and its downstream target AKT increased expression of MT genes in HCC cells but not in liver epithelial cells.
  • Further, treatment of cells with a specific inhibitor of glycogen synthase kinase-3 (GSK-3), a downstream effector of PI3K/AKT, inhibited MT expression specifically in HCC cells.
  • Short interfering RNA-mediated depletion of CCAAT/enhancer binding protein alpha (C/EBPalpha), a target of GSK-3, impeded MT expression, which could not be reversed by PI3K inhibitors.
  • DNA binding activity of C/EBPalpha and its phosphorylation at T222 and T226 by GSK-3 are required for MT expression.

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  • (PMID = 17363595.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA086978; United States / NCI NIH HHS / CA / CA086978-04; United States / NCI NIH HHS / CA / R01 CA086978-01A2; United States / NCI NIH HHS / CA / R01 CA086978-02; United States / NCI NIH HHS / CA / CA122523-01A1; United States / NCI NIH HHS / CA / CA086978-02; United States / NCI NIH HHS / CA / R01 CA086978-03; United States / NCI NIH HHS / CA / CA086978-06A1; United States / NCI NIH HHS / CA / R01 CA086978-06A1; United States / NCI NIH HHS / CA / R21 CA122523; United States / NCI NIH HHS / CA / CA122523; United States / NCI NIH HHS / CA / R01 CA086978-04; United States / NCI NIH HHS / CA / CA86978; United States / NCI NIH HHS / CA / CA086978-05; United States / NCI NIH HHS / CA / CA086978-03; United States / NCI NIH HHS / CA / R01 CA086978-05; United States / NCI NIH HHS / CA / R21 CA122523-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / DNA-Binding Proteins; 0 / Transcription Factors; 0 / transcription factor MTF-1; 9038-94-2 / Metallothionein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Oncogene Protein v-akt
  • [Other-IDs] NLM/ NIHMS39093; NLM/ PMC2276570
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57. Argani P, Laé M, Ballard ET, Amin M, Manivel C, Hutchinson B, Reuter VE, Ladanyi M: Translocation carcinomas of the kidney after chemotherapy in childhood. J Clin Oncol; 2006 Apr 1;24(10):1529-34
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  • Renal cell carcinoma (RCC) occurring as a secondary malignancy is uncommon.
  • RESULTS: The ages at time of diagnosis of the RCC ranged from 6 to 22 years.
  • Histologically, these tumors showed typical features previously described for translocation RCCs.
  • At the molecular level, three tumors contained the ASPL-TFE3 fusion, two contained Alpha-TFEB, and one contained PRCC-TFE3.
  • The intervals between chemotherapy and the diagnosis of RCC ranged from 4 to 13 years.
  • The indications for the antecedent chemotherapy were varied and included acute promyelocytic leukemia, acute myeloid leukemia with t(9;11), bilateral Wilms' tumor, systemic lupus erythematosus, and conditioning regimen of bone marrow transplant for Hurler's syndrome.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics. Carcinoma, Renal Cell / genetics. Kidney Neoplasms / genetics. Neoplasm Proteins / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic

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  • (PMID = 16575003.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA95785
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Neoplasm Proteins; 0 / TFE3 protein, human; 0 / TFEB protein, human
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58. D'Assoro AB, Busby R, Acu ID, Quatraro C, Reinholz MM, Farrugia DJ, Schroeder MA, Allen C, Stivala F, Galanis E, Salisbury JL: Impaired p53 function leads to centrosome amplification, acquired ERalpha phenotypic heterogeneity and distant metastases in breast cancer MCF-7 xenografts. Oncogene; 2008 Jun 26;27(28):3901-11
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  • In this study, we establish an MCF-7 xenograft model that mimics the progression of human breast carcinomas typified by loss of p53 integrity, development of centrosome amplification, acquired estrogen receptor (ERalpha) heterogeneity, overexpression of Mdm2 and metastatic spread from the primary tumor to distant organs.
  • MCF-7 cells with abrogated p53 function (vMCF-7(Dnp53)) maintained nuclear ERalpha expression and normal centrosome characteristics in vitro.
  • In contrast to the parental MCF-7 cells, when introduced into nude mice as xenografts, tumors derived from the vMCF-7(DNp53) cell line developed a strikingly altered phenotype characterized by increased tumor growth, higher tumor histopathology grade, centrosome amplification, loss of nuclear ERalpha expression, increased expression of Mdm-2 oncoprotein and resistance to the antiestrogen tamoxifen.
  • Importantly, while MCF-7 xenografts did not develop distant metastases, primary tumors derived from vMCF-7(DNp53) cells gave rise to lung metastases.
  • Taken together, these observations indicate that abrogation of p53 function and consequent deregulation of the G1/S cell cycle transition leads to centrosome amplification responsible for breast cancer progression.

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  • (PMID = 18264135.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA072836-09; United States / NCI NIH HHS / CA / CA72836; United States / NCI NIH HHS / CA / R01 CA072836; None / None / / R01 CA072836-09; United States / NCI NIH HHS / BC / BC022276
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS57313; NLM/ PMC2526020
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59. Gong J, Morishita A, Kurokohchi K, Tani J, Kato K, Miyoshi H, Inoue H, Kobayashi M, Liu S, Murota M, Muramatsu A, Izuishi K, Suzuki Y, Yoshida H, Uchida N, Deguchi K, Iwama H, Ishimaru I, Masaki T: Use of protein array to investigate receptor tyrosine kinases activated in gastric cancer. Int J Oncol; 2010 Jan;36(1):101-6
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  • Our study used protein array technology to analyze the expression status of various activated receptor tyrosine kinases (RTKs) in gastric carcinoma; then, we sought to discover an effective therapeutic receptor tyrosine kinase for this disease and investigated the anti-tumor mechanism of the therapeutic RTK.
  • In addition to the expressions of activated RTKs in human gastric cancer and adjacent normal mucosa, the expression of activated RTKs in gastric cancer cell lines, MKN74, MKN45, MKN7 and MKN1, were also studied.
  • Among the RTKs activated in gastric cancer tissues, EGFR and ErbB2 were also activated in all gastric cell lines examined in this study.
  • Moreover, using an angiogenesis protein array, the expressions of Ang I, FGF-alpha, FGF-beta TGF-beta and IL-8 in MKN74 xenograft tumors were found to be significantly reduced by treatment with trastuzumab, indicating that trastuzumab may inhibit the expression of angiogenic molecules in MKN74 cells in vivo.
  • [MeSH-minor] Aged. Animals. Cell Line, Tumor. Female. Humans. Male. Mice. Mice, Nude. Middle Aged. Neoplasm Transplantation


60. Kang SH, Cho HT, Devi S, Zhang Z, Escuin D, Liang Z, Mao H, Brat DJ, Olson JJ, Simons JW, Lavallee TM, Giannakakou P, Van Meir EG, Shim H: Antitumor effect of 2-methoxyestradiol in a rat orthotopic brain tumor model. Cancer Res; 2006 Dec 15;66(24):11991-7
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  • [Title] Antitumor effect of 2-methoxyestradiol in a rat orthotopic brain tumor model.
  • Grade 4 malignant glioma (GBM) is a fatal disease despite aggressive surgical and adjuvant therapies.
  • The hallmark of GBM tumors is the presence of pseudopalisading necrosis and microvascular proliferation.
  • These tumor cells are hypoxic and express hypoxia-inducible factor-1 (HIF-1), a prosurvival transcription factor that promotes formation of neovasculature through activation of target genes, such as vascular endothelial growth factor.
  • Here, we evaluated whether 2-methoxyestradiol, a microtubule and HIF-1 inhibitor, would have therapeutic potential for this disease in a 9L rat orthotopic gliosarcoma model using a combination of noninvasive imaging methods: magnetic resonance imaging to measure the tumor volume and bioluminescence imaging for HIF-1 activity.
  • Treatment with 2-methoxyestradiol (60-600 mg/kg/d) resulted in a dose-dependent inhibition of tumor growth.
  • This effect was also associated with improved tumor oxygenation as assessed by pimonidazole staining, decreased HIF-1alpha protein levels, and microtubule destabilization as assessed by deacetylation.
  • In addition to showing tumor growth inhibition, we identified three potential surrogate biomarkers to determine the efficacy of 2-methoxyestradiol therapy: decreased HIF-1alpha levels, alpha-tubulin acetylation, and degree of hypoxia as determined by pimonidazole staining.
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Disease Models, Animal. Magnetic Resonance Imaging. Rats. Rats, Inbred F344

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  • (PMID = 17178898.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA114335-01
  • [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 / Antineoplastic Agents; 0 / Tubulin Modulators; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
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61. Provenzano PP, Inman DR, Eliceiri KW, Knittel JG, Yan L, Rueden CT, White JG, Keely PJ: Collagen density promotes mammary tumor initiation and progression. BMC Med; 2008 Apr 28;6:11
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  • [Title] Collagen density promotes mammary tumor initiation and progression.
  • METHODS: To study the effects of collagen density on mammary tumor formation and progression, we utilized a bi-transgenic tumor model with increased stromal collagen in mouse mammary tissue.
  • Imaging of the tumors and tumor-stromal interface in live tumor tissue was performed with multiphoton laser-scanning microscopy to generate multiphoton excitation and spectrally resolved fluorescent lifetimes of endogenous fluorophores.
  • RESULTS: Herein we demonstrate that increased stromal collagen in mouse mammary tissue significantly increases tumor formation approximately three-fold (p < 0.00001) and results in a significantly more invasive phenotype with approximately three times more lung metastasis (p < 0.05).
  • Furthermore, the increased invasive phenotype of tumor cells that arose within collagen-dense mammary tissues remains after tumor explants are cultured within reconstituted three-dimensional collagen gels.
  • To better understand this behavior we imaged live tumors using nonlinear optical imaging approaches to demonstrate that local invasion is facilitated by stromal collagen re-organization and that this behavior is significantly increased in collagen-dense tissues.
  • In addition, using multiphoton fluorescence and spectral lifetime imaging we identify a metabolic signature for flavin adenine dinucleotide, with increased fluorescent intensity and lifetime, in invading metastatic cells.
  • CONCLUSION: This study provides the first data causally linking increased stromal collagen to mammary tumor formation and metastasis, and demonstrates that fundamental differences arise and persist in epithelial tumor cells that progressed within collagen-dense microenvironments.

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  • (PMID = 18442412.001).
  • [ISSN] 1741-7015
  • [Journal-full-title] BMC medicine
  • [ISO-abbreviation] BMC Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076537; United States / NIBIB NIH HHS / EB / R01 EB000184; United States / NCI NIH HHS / CA / R01-CA076537; United States / NIBIB NIH HHS / EB / R01-EB000184
  • [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] England
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain
  • [Other-IDs] NLM/ PMC2386807
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62. Elander N, Ungerbäck J, Olsson H, Uematsu S, Akira S, Söderkvist P: Genetic deletion of mPGES-1 accelerates intestinal tumorigenesis in APC(Min/+) mice. Biochem Biophys Res Commun; 2008 Jul 18;372(1):249-53
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  • Here we demonstrate that APC(Min/+) mice with genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), which catalyses the terminal conversion of PGH(2) into PGE(2), surprisingly develop more and generally larger intestinal tumors than do mPGES-1 wild type littermates (mean number of tumors/intestine 80 vs. 38, p<0.0005, mean tumor diameter 1.64 vs. 1.12 mm, p<0.0005).
  • PGE(2) levels were suppressed in tumors of mPGES-1 deficient animals, but the concentrations of other PGH(2) derived prostanoids were generally enhanced, being most prominent for TxA(2) and PGD(2).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / genetics. Dinoprostone / metabolism. Gene Deletion. Intramolecular Oxidoreductases / genetics
  • [MeSH-minor] 6-Ketoprostaglandin F1 alpha / analysis. Animals. Female. Male. Mice. Mice, Mutant Strains. RNA, Messenger / metabolism. Thromboxane B2 / analysis


63. Lopez-Beltran A, Cheng L, Prieto R, Blanca A, Montironi R: Lymphoepithelioma-like carcinoma of the prostate. Hum Pathol; 2009 Jul;40(7):982-7
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  • In this report, we summarized the clinicopathologic features of 5 cases of lymphoepithelioma-like carcinoma of the prostate, a rare variant of prostate cancer characterized by a malignant epithelial component densely infiltrated by lymphoid cells.
  • The initial diagnosis of lymphoepithelioma-like carcinoma of the prostate was made on transurethral resection in 3 cases and radical prostatectomy in 2 others.
  • In one case the diagnosis of lymphoepithelioma-like carcinoma admixed with conventional acinar adenocarcinoma was an unexpected finding at time of transurethral resection for benign prostatic hyperplasia.
  • Three patients had clinical stage T3 tumors and another had stage T4 disease; stage T1b was present in the remaining case.
  • Microscopically, all tumors contained lymphoepithelioma-like carcinoma, which comprised 10% to 90% of the entire tumor.
  • The stroma was densely infiltrated by lymphoid cells admixed with some plasma cells and neutrophils; one case had a prominent infiltration of eosinophils.
  • Immunohistochemical staining demonstrated that lymphoepithelioma-like carcinoma was positive for prostate-specific antigen, prostate acid phosphatase, alpha-methylacyl coenzyme A racemase, and epithelial membrane antigen; several cytokeratins (AE1/AE3, 7, 8, and 20 [rare cells]) were also immunoreactive.
  • The lymphoid component was mainly composed of T with a minor subset of B cells, admixed with some dendritic cells and histiocytes as seen by S100 and CD68 immunoreactivity.
  • DNA ploidy of lymphoepithelioma-like carcinoma tumors gave DNA histograms with aneuploid peaks.
  • Four patients died of disease from 8 to 26 months; one patient was lost to follow-up.
  • Morphologic recognition and distinction from other prostatic lesions and tumors with prominent lymphoid stroma is critical for its clinical management.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 19269013.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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64. de Pinho LK, Neto LV, Cardão Chimelli LM, Gasparetto EL, Warszawski L, do Souto AA, Gadelha MR: Germ cell tumor presenting as sellar mass with suprasellar extension and long history of hypopituitarism. Neuro Endocrinol Lett; 2010;31(3):306-9
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  • [Title] Germ cell tumor presenting as sellar mass with suprasellar extension and long history of hypopituitarism.
  • OBJECTIVE: Primary central nervous system germ cell tumors are rare neoplasms usually located in the pineal and/or suprasellar region.
  • Pure germinomas do not usually secrete beta-human chorionic gonadotropin hormone (beta-HCG) or alpha-fetoprotein (AFP) and diagnosis is made a few weeks or months after beginning of symptoms.
  • CASE: Here we report a case of a pure germinoma in a 20 year-old woman presenting as a sellar mass with suprasellar extension, abnormal serum beta-HCG and a long history of polyuria and polydipsia (4 years), that was initially diagnosed as a pituitary macroadenoma.
  • CONCLUSION: This presentation highlights the importance of thinking in alternative diagnosis to pituitary adenoma when diabetes insipidus is the initial symptom.
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Young Adult

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  • (PMID = 20588244.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
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65. Li H, Cherukuri P, Li N, Cowling V, Spinella M, Cole M, Godwin AK, Wells W, DiRenzo J: Nestin is expressed in the basal/myoepithelial layer of the mammary gland and is a selective marker of basal epithelial breast tumors. Cancer Res; 2007 Jan 15;67(2):501-10
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  • [Title] Nestin is expressed in the basal/myoepithelial layer of the mammary gland and is a selective marker of basal epithelial breast tumors.
  • These tumors display a high degree of cellular heterogeneity and lack established molecular targets, such as estrogen receptor-alpha, progesterone receptor, and Her2 overexpression, indicating a need for definitive diagnostic markers.
  • We present evidence that nestin, a previously described marker of regenerative cells in diverse tissues, is expressed in the regenerative compartment of the normal human mammary gland.
  • In the embryonal carcinoma cell line NT2/D1, ectopic DeltaN-p63-alpha disrupts retinoic acid-induced differentiation, thereby preserving expression of nestin; however, small interfering RNA-mediated ablation of nestin is insufficient to promote differentiation, indicating that whereas nestin may identify cells within the regenerative compartment of the mammary gland, it is insufficient to block differentiation and preserve replicative capacity.
  • Immunohistochemical analysis of basal epithelial breast tumors, including those shown to carry BRCA1 mutations, indicates robust expression of nestin and CK14, punctate expression of p63, and low to undetectable levels of desmin expression.
  • Nestin was not detected in other breast cancer subtypes, indicating selectivity for basal epithelial breast tumors.
  • [MeSH-minor] Animals. Carcinoma, Embryonal / metabolism. Carcinoma, Embryonal / pathology. Cell Differentiation / physiology. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / metabolism. Epithelial Cells / metabolism. Female. Humans. Keratin-14 / biosynthesis. Male. Mammary Glands, Animal / metabolism. Mice. Mice, Inbred C57BL. Nestin. Pregnancy. Trans-Activators / biosynthesis. Trans-Activators / metabolism. Transcription Factors. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / metabolism

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  • (PMID = 17234757.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01 CA108539
  • [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 / DNA-Binding Proteins; 0 / Intermediate Filament Proteins; 0 / Keratin-14; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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66. Jiang W, Cazacu S, Xiang C, Zenklusen JC, Fine HA, Berens M, Armstrong B, Brodie C, Mikkelsen T: FK506 binding protein mediates glioma cell growth and sensitivity to rapamycin treatment by regulating NF-kappaB signaling pathway. Neoplasia; 2008 Mar;10(3):235-43
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  • [Title] FK506 binding protein mediates glioma cell growth and sensitivity to rapamycin treatment by regulating NF-kappaB signaling pathway.
  • Using glioma cDNA microarray analysis, we found that FKBP5 was overexpressed in glioma tumors.
  • This finding was further validated by real-time reverse transcription-polymerase chain reaction and Western blot analysis.
  • The roles of FKBP5 in glioma cells were then examined.
  • We found that cell growth was suppressed after FKBP5 expression was inhibited by short interfering RNA transfection and enhanced by FKBP5 overexpression.
  • The expression level of I-kappa B alpha and phosphorylated NF-kappaB was regulated by the expression of FKBP5.
  • These data suggest that FKBP5 is involved in NF-kappaB pathway activation in glioma cells.
  • In addition, FKBP5 overexpression in rapamycin-sensitive U87 cells blocked the cells' response to rapamycin treatment, whereas rapamycin-resistant glioma cells, both PTEN-positive and -negative, were synergistically sensitive to rapamycin after FKBP5 was knocked down, suggesting that the FKBP5 regulates glioma cell response to rapamycin treatment.

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  • (PMID = 18320068.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R24 CA095809; United States / NCI NIH HHS / CA / CA095809; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / NF-kappa B; EC 5.2.1.- / Tacrolimus Binding Proteins; EC 5.2.1.8 / tacrolimus binding protein 5; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2259453
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67. Wieder H, Beer AJ, Poethko T, Meisetschlaeger G, Wester HJ, Rummeny E, Schwaiger M, Stahl AR: PET/CT with Gluc-Lys-([(18)F]FP)-TOCA: correlation between uptake, size and arterial perfusion in somatostatin receptor positive lesions. Eur J Nucl Med Mol Imaging; 2008 Feb;35(2):264-71
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  • This study determinates variability in lesion uptake of the glycosylated sst analogon N(alpha)-(1-deoxy-D-fructosyl)-N(epsilon)-(2-[(18)F]fluoropropionyl)-Lys(0)-Tyr(3)-octreotate (Gluc-Lys([(18)F]FP)-TOCA) and correlates it with lesion size and arterial perfusion as measured on computed tomography (CT).
  • METHODS: Ten patients with metastasized neuroendocrine carcinomas were investigated with positron emission tomography PET/CT (Biograph 16, Siemens, Germany).
  • CONCLUSION: Partial volume effects were a major source of intraindividual variability in tumour tracer uptake.
  • In larger lesions residual variability in uptake must be considered; it may be due to variable sstr2 expression on the tumours' cell surfaces.
  • [MeSH-major] Arteries / metabolism. Fructose / analogs & derivatives. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / metabolism. Peptides, Cyclic / pharmacokinetics. Positron-Emission Tomography / methods. Receptors, Somatostatin / metabolism. Tomography, X-Ray Computed / methods

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  • (PMID = 17912524.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / N(alpha)-(1-deoxy- D-fructosyl)- N(epsilon)-(2-fluoropropionyl)-Lys(0)-Tyr(3)-octreotate; 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 30237-26-4 / Fructose
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68. Barone I, Brusco L, Fuqua SA: Estrogen receptor mutations and changes in downstream gene expression and signaling. Clin Cancer Res; 2010 May 15;16(10):2702-8
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  • Estrogens play a crucial role in regulating the growth and differentiation of breast cancers, with approximately two thirds of all breast tumors expressing the estrogen receptor alpha (ERalpha).
  • However, not all patients respond to endocrine therapies (termed de novo resistance), and a large number of patients who do respond will eventually develop disease progression or recurrence while on therapy (acquired resistance).

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  • [Copyright] Copyright (c) 2010 AACR.
  • (PMID = 20427689.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA072038; United States / NCI NIH HHS / CA / R01 CA72038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Estrogen
  • [Number-of-references] 50
  • [Other-IDs] NLM/ NIHMS701446; NLM/ PMC4477803
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69. Schönleben F, Qiu W, Remotti HE, Hohenberger W, Su GH: PIK3CA, KRAS, and BRAF mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/C) of the pancreas. Langenbecks Arch Surg; 2008 May;393(3):289-96
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  • [Title] PIK3CA, KRAS, and BRAF mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/C) of the pancreas.
  • BACKGROUND AND AIMS: Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-alpha (PIK3CA) gene in various human tumors.
  • The Raf/MEK/ERK (mitogen-activated protein kinase) signal transduction is an important mediator of a number of cellular fates including growth, proliferation, and survival.
  • The BRAF gene is activated by oncogenic RAS, leading to cooperative effects in cells responding to growth factor signals.
  • Here we evaluate the mutational status of PIK3CA, KRAS, and BRAF in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMNC) of the pancreas.
  • CONCLUSION: This data is the first report of PIK3CA mutation in pancreatic cancer and it appears to be the first oncogene to be mutated in IPMN/IPMC but not in conventional ductal adenocarcinoma of the pancreas.

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  • (PMID = 18343945.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095434-05; United States / NCI NIH HHS / CA / R01 CA109525-03; United States / NCI NIH HHS / CA / CA109525-03; United States / NCI NIH HHS / CA / CA109525-04; United States / NCI NIH HHS / CA / R01 CA109525; United States / NCI NIH HHS / CA / R01 CA109525-04; United States / NCI NIH HHS / CA / K01 CA095434; United States / NCI NIH HHS / CA / K01 CA095434-05
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ NIHMS235132; NLM/ PMC3915028
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70. Son DJ, Lee JW, Lee YH, Song HS, Lee CK, Hong JT: Therapeutic application of anti-arthritis, pain-releasing, and anti-cancer effects of bee venom and its constituent compounds. Pharmacol Ther; 2007 Aug;115(2):246-70
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  • Bee venom (BV) therapy (BVT), the therapeutic application of BV, has been used in traditional medicine to treat diseases, such as arthritis, rheumatism, pain, cancerous tumors, and skin diseases.
  • BV contains a variety of peptides, including melittin, apamin, adolapin, the mast-cell-degranulating (MCD) peptide, enzymes (i.e., phospholipase [PL] A(2)), biologically active amines (i.e., histamine and epinephrine), and nonpeptide components which have a variety of pharmaceutical properties.
  • Multiple mechanisms, such as activation of the central and spinal opiod receptor, and alpha(2)-adrenergic activity, as well as activation of the descending serotonergic pathway have been suggested.
  • The inhibition of c-Fos expression in the spinal cord by BV apipuncture in several nociceptive models is also reported to be a possible mechanism.
  • The cell cytotoxic effects through the activation of PLA(2) by melittin have been suggested to be the critical mechanism for the anti-cancer activity of BV.
  • The conjugation of cell lytic peptide (melittin) with hormone receptors and gene therapy carrying melittin can be useful as a novel targeted therapy for some types of cancer, such as prostate and breast cancer.

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  • (PMID = 17555825.001).
  • [ISSN] 0163-7258
  • [Journal-full-title] Pharmacology & therapeutics
  • [ISO-abbreviation] Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Analgesics; 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents; 0 / Antirheumatic Agents; 0 / Bee Venoms; 0 / Peptides; 20449-79-0 / Melitten; 24345-16-2 / Apamin; 51943-80-7 / procamine; 79029-92-8 / adolapin; EC 3.2.1.35 / Hyaluronoglucosaminidase
  • [Number-of-references] 166
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71. Teraishi F, Kagawa S, Watanabe T, Tango Y, Kawashima T, Umeoka T, Nisizaki M, Tanaka N, Fujiwara T: ZD1839 (Gefitinib, 'Iressa'), an epidermal growth factor receptor-tyrosine kinase inhibitor, enhances the anti-cancer effects of TRAIL in human esophageal squamous cell carcinoma. FEBS Lett; 2005 Aug 1;579(19):4069-75
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  • [Title] ZD1839 (Gefitinib, 'Iressa'), an epidermal growth factor receptor-tyrosine kinase inhibitor, enhances the anti-cancer effects of TRAIL in human esophageal squamous cell carcinoma.
  • The EGF (epidermal growth factor) receptor-tyrosine kinase inhibitor ZD1839 (Gefitinib, 'Iressa') blocks the cell signaling pathways involved in cell proliferation, survival, and angiogenesis in various cancer cells.
  • We investigated the antitumor effects of ZD1839 alone or in combination with TRAIL against human esophageal squamous cell cancer (ESCC) lines.
  • Although all ESCC cells expressed EGF receptor at a protein level, the effect of ZD1839 on cell growth did not correlate with the level of EGFR expression and phosphorylation of EGF receptor protein in ESCC lines.
  • As TE8 cells are resistant to TRAIL, we tested whether ZD1839 combined with TRAIL induced apoptosis of TE8 cells via the inhibition of EGF receptor signaling by ZD1839.
  • Our results indicated that ZD1839 has anti-cancer properties against human esophageal cancer cells.
  • ZD1839 also augmented the anti-cancer activity of TRAIL, even in TRAIL-resistant tumors.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Enzyme Inhibitors / pharmacology. Esophageal Neoplasms / drug therapy. Membrane Glycoproteins / physiology. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Apoptosis Regulatory Proteins. Cell Line, Tumor. G1 Phase. Humans. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Signal Transduction. TNF-Related Apoptosis-Inducing Ligand. Up-Regulation


72. Wang LC, Thomsen L, Sutherland R, Reddy CB, Tijono SM, Chen CJ, Angel CE, Dunbar PR, Ching LM: Neutrophil influx and chemokine production during the early phases of the antitumor response to the vascular disrupting agent DMXAA (ASA404). Neoplasia; 2009 Aug;11(8):793-803
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  • 5,6-Dimethylxanthenone-4-acetic acid (DMXAA) acts through tumor vascular disruption and cytokine production and is the first of its class to enter phase 3 trials.
  • We characterized leukocytes and cytokines in murine Colon 38 tumors before and after DMXAA treatment.
  • Tumor mass declined 50% 24 hours after DMXAA administration, but the leukocyte count per gram of tumor increased threefold owing to a large influx of Ly6G(+)CD11b(+)F4/80(-) cells with the morphology of neutrophils.
  • However, B and T lymphocytes, natural killer cells, and macrophages in the tumor all decreased in numbers.
  • Seven chemokines were substantially induced in the tumor, spleen, and serum 4 hours after DMXAA administration.
  • Using cultured spleen cell subpopulations, CD11b(+) cells (largely monocytes and macrophages) were shown to be the primary producers of tumor necrosis factor alpha, interleukin 6 (IL-6), and macrophage inflammatory 1alpha (MIP-1alpha).
  • CD49b(+) natural killer cells produced IP-10, whereas CD45R(+) B lymphocytes produced regulated upon activation normal T cell express sequence.
  • [MeSH-minor] Animals. B-Lymphocytes / drug effects. B-Lymphocytes / immunology. Flow Cytometry. Fluorescent Antibody Technique. Humans. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Lymphocytes, Tumor-Infiltrating / drug effects. Lymphocytes, Tumor-Infiltrating / immunology. Macrophages / drug effects. Macrophages / immunology. Mice. Mice, Inbred C57BL. T-Lymphocytes / drug effects. T-Lymphocytes / immunology

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  • (PMID = 19649209.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Xanthones; 0829J8133H / vadimezan
  • [Other-IDs] NLM/ PMC2713591
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73. Ohshiro K, Mudvari P, Meng QC, Rayala SK, Sahin AA, Fuqua SA, Kumar R: Identification of a novel estrogen receptor-alpha variant and its upstream splicing regulator. Mol Endocrinol; 2010 May;24(5):914-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a novel estrogen receptor-alpha variant and its upstream splicing regulator.
  • Although constitutive and alternative mRNA splicing is temporally and spatially regulated, deregulation of mRNA splicing could cause development, progression, and metastasis of tumors.
  • Through yeast two-hybrid screening of a human breast cDNA library using estrogen receptor-alpha (ERalpha) as bait, we identified a novel nuclear receptor box containing full-length protein, nuclear protein E3-3 (NPE3-3).
  • Accordingly, transient expression of NPE3-3 in cells resulted in expected splicing of the CD44 control minigene.
  • ERalphaV was expressed and sequestered in the cytoplasm in MCF-7 cells stably overexpressing NPE3-3, suggesting its involvement in nongenomic hormone signaling.
  • NPE3-3 clones exhibited up-regulation of ERK1/2 signaling, cyclin D1, and cathepsin D and enhanced tumor cell proliferation, migration, and tumorigenicity.
  • Moreover, direct expression of the ERalphaV in breast cancer cells stimulated ERK1/2 up-regulation and cyclin D1 expression.
  • Interestingly, NPE3-3 was up-regulated in human breast tumors.
  • These findings revealed a role for NPE3-3 in alternative splicing and suggest that ERalpha is a physiological target of NPE3-3, leading to a constitutive nongenomic signaling pathway in breast cancer cells.