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1. Rao R, Nalluri S, Fiskus W, Savoie A, Buckley KM, Ha K, Balusu R, Joshi A, Coothankandaswamy V, Tao J, Sotomayor E, Atadja P, Bhalla KN: Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells. Clin Cancer Res; 2010 Oct 1;16(19):4742-54
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  • [Title] Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells.
  • PURPOSE: Bortezomib induces unfolded protein response (UPR) and endoplasmic reticulum stress, as well as exhibits clinical activity in patients with relapsed and refractory mantle cell lymphoma (MCL).
  • EXPERIMENTAL DESIGN: Immunoblot analyses, reverse transcription-PCR, and immunofluorescent and electron microscopy were used to determine the effects of panobinostat on bortezomib-induced aggresome formation and endoplasmic reticulum stress in MCL cells.
  • RESULTS: Treatment with panobinostat induced heat shock protein 90 acetylation; depleted the levels of heat shock protein 90 client proteins, cyclin-dependent kinase 4, c-RAF, and AKT; and abrogated bortezomib-induced aggresome formation in MCL cells.
  • Conversely, knockdown of CHOP attenuated panobinostat-induced cell death of MCL cells.
  • Cotreatment with panobinostat also increased bortezomib-mediated in vivo tumor growth inhibition and improved survival of mice bearing human Z138C MCL cell xenograft.
  • [MeSH-major] Boronic Acids / pharmacology. Endoplasmic Reticulum / drug effects. Hydroxamic Acids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Pyrazines / pharmacology. Stress, Physiological / drug effects. Transcription Factor CHOP / metabolism
  • [MeSH-minor] Acetylation / drug effects. Animals. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Blotting, Western. Bortezomib. Cell Line, Tumor. Cell Proliferation / drug effects. Fluorescent Antibody Technique. HSP90 Heat-Shock Proteins / antagonists & inhibitors. HSP90 Heat-Shock Proteins / metabolism. Humans. Indoles. Mice. Microscopy, Confocal. Protein Folding / drug effects. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Xenograft Model Antitumor Assays

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  • [Copyright] ©2010 AACR.
  • [Cites] N Engl J Med. 2009 Oct 15;361(16):1570-83 [19828534.001]
  • [Cites] Cancer Biol Ther. 2009 Jul;8(13):1273-80 [19440035.001]
  • [Cites] Cancer Sci. 2010 Jan;101(1):196-200 [19817748.001]
  • [Cites] J Cell Biol. 2001 May 28;153(5):1011-22 [11381086.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):300-7 [11460154.001]
  • [Cites] Eur J Cancer. 2002 Feb;38(3):401-8 [11818206.001]
  • [Cites] EMBO J. 2003 Mar 3;22(5):1180-7 [12606582.001]
  • [Cites] Cell. 2003 Dec 12;115(6):727-38 [14675537.001]
  • [Cites] J Cell Biol. 1998 Dec 28;143(7):1883-98 [9864362.001]
  • [Cites] Genes Dev. 2004 Dec 15;18(24):3066-77 [15601821.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):268-81 [15690081.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8567-72 [15937109.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26729-34 [15937340.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11510-9 [16357160.001]
  • [Cites] Blood. 2006 Jan 1;107(1):257-64 [16166592.001]
  • [Cites] Nat Rev Cancer. 2006 Jan;6(1):38-51 [16397526.001]
  • [Cites] EMBO Rep. 2006 Sep;7(9):880-5 [16953201.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3441-9 [16728695.001]
  • [Cites] Blood. 2007 Jan 1;109(1):31-9 [16960145.001]
  • [Cites] Cancer Cell. 2007 Apr;11(4):349-60 [17418411.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):750-62 [17891190.001]
  • [Cites] Science. 2007 Nov 9;318(5852):944-9 [17991856.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:270-6 [18024640.001]
  • [Cites] Cell Cycle. 2008 Jan 1;7(1):7-10 [18196966.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):549-58 [18223231.001]
  • [Cites] Biochem J. 2008 Mar 15;410(3):439-53 [18290764.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):415-21 [18536582.001]
  • [Cites] Cancer Res. 2008 Jun 15;68(12):4833-42 [18559531.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2917-26 [18641367.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2896-905 [18660379.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29 [17565364.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1337-49 [17604722.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1631-8 [17502456.001]
  • [Cites] Genes Dev. 2007 Sep 1;21(17):2172-81 [17785525.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2641-9 [17525289.001]
  • [Cites] Hematol Oncol Clin North Am. 2008 Oct;22(5):953-63, ix [18954745.001]
  • [Cites] Drug Resist Updat. 2008 Aug-Oct;11(4-5):164-79 [18818117.001]
  • [Cites] Mol Cell Biol. 2008 Dec;28(23):6989-7000 [18794359.001]
  • [Cites] Cancer Biol Ther. 2008 Oct;7(10):1648-62 [18787411.001]
  • [Cites] PLoS One. 2009;4(1):e4170 [19137072.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2200-5 [19164757.001]
  • [Cites] Br J Haematol. 2009 Apr;145(1):34-9 [19220284.001]
  • [Cites] Semin Hematol. 2009 Apr;46(2):166-75 [19389500.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5250-7 [19671864.001]
  • [Cites] Leukemia. 2009 Dec;23(12):2222-32 [19741729.001]
  • (PMID = 20647473.001).
  • [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 CA129962
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / HSP90 Heat-Shock Proteins; 0 / Hydroxamic Acids; 0 / Indoles; 0 / PMAIP1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 147336-12-7 / Transcription Factor CHOP; 69G8BD63PP / Bortezomib; 9647FM7Y3Z / panobinostat
  • [Other-IDs] NLM/ NIHMS222886; NLM/ PMC2948590
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2. Saint-Marc O, Pozzo A, Cohen C, Le Tortorec S, Potier P, Berland B: [Gastric interdigitating reticulum cell sarcoma: unusual presentation of a histiocytic tumor]. Gastroenterol Clin Biol; 2002 May;26(5):526-8
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  • [Title] [Gastric interdigitating reticulum cell sarcoma: unusual presentation of a histiocytic tumor].
  • Diagnosis is based on immunohistochemical and molecular genetic study, which allows to distinguish histiocytic sarcoma from lymphocytic proliferation, such as non-Hodgkin's lymphoma.
  • We report the case of a gastric interdigitating reticulum cell sarcoma, treated by resection and chemotherapy.
  • [MeSH-minor] Antigens, CD / analysis. Antigens, Neoplasm / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Cisplatin / therapeutic use. Cytarabine / therapeutic use. Diagnosis, Differential. Etoposide / therapeutic use. Gastrectomy. Humans. Immunohistochemistry. Male. Methylprednisolone / therapeutic use. Middle Aged

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  • (PMID = 12122368.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; X4W7ZR7023 / Methylprednisolone; ESAP protocol
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3. Leleu X, Xu L, Jia X, Sacco A, Farag M, Hunter ZR, Moreau AS, Ngo HT, Hatjiharissi E, Ho AW, Santos DD, Adamia S, O'Connor K, Ciccarelli B, Soumerai J, Manning RJ, Patterson CJ, Roccaro AM, Ghobrial IM, Treon SP: Endoplasmic reticulum stress is a target for therapy in Waldenstrom macroglobulinemia. Blood; 2009 Jan 15;113(3):626-34
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  • [Title] Endoplasmic reticulum stress is a target for therapy in Waldenstrom macroglobulinemia.
  • Waldenstrom macroglobulinemia (WM) is an incurable low-grade lymphoma characterized by bone marrow (BM) involvement of IgM secreting lymphoplasmacytic cells.
  • The induction of unfolded protein response (UPR) genes ("physiologic" UPR) enables cells to differentiate into professional secretory cells capable of production of high amounts of endoplasmic reticulum (ER)-processed proteins, such as immunoglobulins.
  • Tunicamycin induced significant cytotoxicity, apoptosis and cell-cycle arrest, and inhibited DNA synthesis in WM cell lines and primary BM CD19(+) cells from patients with WM with an inhibitory concentration (IC(50)) of 0.5 microg/mL to 1 microg/mL, but not in healthy donor cells.
  • Finally, we demonstrate that ER stress inducer synergizes with other agents used in the treatment of WM.
  • These preclinical studies provide a framework for further evaluation of ER stress inducing agents as therapeutic agents in WM.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Endoplasmic Reticulum / drug effects. Tunicamycin / pharmacology. Waldenstrom Macroglobulinemia / drug therapy
  • [MeSH-minor] B-Lymphocytes / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Flow Cytometry. Gene Expression. Humans. Immunoblotting. Protein Folding / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Stress, Physiological

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  • (PMID = 18981296.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 11089-65-9 / Tunicamycin
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4. Chen ST, Thomas S, Gaffney KJ, Louie SG, Petasis NA, Schönthal AH: Cytotoxic effects of celecoxib on Raji lymphoma cells correlate with aggravated endoplasmic reticulum stress but not with inhibition of cyclooxygenase-2. Leuk Res; 2010 Feb;34(2):250-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxic effects of celecoxib on Raji lymphoma cells correlate with aggravated endoplasmic reticulum stress but not with inhibition of cyclooxygenase-2.
  • Inhibition of cyclooxygenase 2 (COX-2) by the selective COX-2 inhibitor celecoxib has been suggested as potentially useful for B-cell lymphoma therapy.
  • However, additional pharmacological activities of celecoxib have been discovered and have challenged the notion that its antitumor effects are mediated primarily via the inhibition of COX-2.
  • To shed light on this issue, we have investigated the effects of different pharmacological agents with greatly varying COX-2 inhibitory potency in Raji lymphoma cells in vitro.
  • Instead, the cytotoxic outcome was closely aligned with these agents' ability to trigger endoplasmic reticulum (ER) stress, which could be further enhanced by bortezomib, an agent with known ER stress-inducing potency.
  • Together, these results indicate that celecoxib's cytotoxic effects on Raji lymphoma cells do not involve the inhibition of COX-2.
  • [MeSH-major] Cyclooxygenase 2 / drug effects. Endoplasmic Reticulum / pathology. Lymphoma / drug therapy. Pyrazoles / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Boronic Acids / pharmacology. Bortezomib. Celecoxib. Cell Death / drug effects. Cell Line, Tumor. Cyclooxygenase 2 Inhibitors / pharmacology. Drug Synergism. Humans. Pyrazines / pharmacology. Stress, Physiological / drug effects

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19833390.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazines; 0 / Pyrazoles; 0 / Sulfonamides; 69G8BD63PP / Bortezomib; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
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5. Nakamura M, Gotoh T, Okuno Y, Tatetsu H, Sonoki T, Uneda S, Mori M, Mitsuya H, Hata H: Activation of the endoplasmic reticulum stress pathway is associated with survival of myeloma cells. Leuk Lymphoma; 2006 Mar;47(3):531-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation of the endoplasmic reticulum stress pathway is associated with survival of myeloma cells.
  • The endoplasmic reticulum (ER) is an organelle in which proteins are modified.
  • When unfolded proteins accumulate in the ER under various stresses, ER stress (ERS) pathways, including the induction of chaperones, are activated to protect the cell.
  • However, when ERS is excessive, the cell undergoes apoptosis.
  • This study investigated ERS in multiple myeloma cells (MMCs) because they contain a well-developed ER due to M-protein production.
  • The myeloma cell line 12-PE underwent apoptosis via caspase-3 after treatment with thapsigargin (thap), an ERS inducer, while another cell line, U266, did not.
  • Chaperones were up-regulated in U266 cells but down-regulated in 12-PE cells, suggesting that chaperones contribute to cell survival under ERS.
  • Analysis of XBP-1, a transcriptional inducer of chaperones, in freshly isolated MMCs from 22 myeloma cases revealed 10 cases with active XBP-1, who also showed significantly poorer survival (p < 0.05), suggesting that chaperone expression protects MMCs from apoptosis, thereby allowing tumor cell expansion.
  • Inhibition of chaperones could be a new target for myeloma therapy.
  • [MeSH-major] Drug Resistance, Neoplasm. Endoplasmic Reticulum / metabolism. Multiple Myeloma / metabolism. Oxidative Stress
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA-Binding Proteins / drug effects. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Middle Aged. Molecular Chaperones / metabolism. Nuclear Proteins / drug effects. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Prognosis. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Retrospective Studies. Survival Analysis. Thapsigargin / pharmacology. Transcription Factors

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  • (PMID = 16396777.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Molecular Chaperones; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / regulatory factor X transcription factors; 67526-95-8 / Thapsigargin
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6. Carew JS, Nawrocki ST, Krupnik YV, Dunner K Jr, McConkey DJ, Keating MJ, Huang P: Targeting endoplasmic reticulum protein transport: a novel strategy to kill malignant B cells and overcome fludarabine resistance in CLL. Blood; 2006 Jan 1;107(1):222-31
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  • [Title] Targeting endoplasmic reticulum protein transport: a novel strategy to kill malignant B cells and overcome fludarabine resistance in CLL.
  • Here we report that CLL cells and multiple myeloma cells are highly sensitive to brefeldin A, an inhibitor of endoplasmic reticulum (ER) to Golgi protein transport currently being developed as a novel anticancer agent in a prodrug formulation.
  • Such ER stress and blockage of secretory protein traffic eventually resulted in Golgi collapse, activation of caspases, and cell death.
  • Taken together, these findings suggest that malignant B cells may be highly dependent on ER-Golgi protein transport and that targeting this process may be a promising therapeutic strategy for B-cell malignancies, especially for those that respond poorly to conventional treatments.

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  • [Cites] Leukemia. 1987 Sep;1(9):638-43 [3478543.001]
  • [Cites] J Biol Chem. 1988 Dec 5;263(34):18545-52 [3192548.001]
  • [Cites] Eur J Cell Biol. 1991 Feb;54(1):38-54 [2032551.001]
  • [Cites] Science. 1991 Nov 22;254(5035):1197-9 [1957170.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6408-12 [1631136.001]
  • [Cites] Nature. 1992 Nov 26;360(6402):350-2 [1448151.001]
  • [Cites] Nature. 1992 Nov 26;360(6402):352-4 [1448152.001]
  • [Cites] Nature. 1993 Apr 15;362(6421):648-52 [8464517.001]
  • [Cites] Leuk Lymphoma. 1993 May;10(1-2):49-56 [8374523.001]
  • [Cites] Cell Immunol. 1994 Aug;157(1):263-76 [7913665.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3148-57 [7949187.001]
  • [Cites] Br J Haematol. 1996 Sep;94(4):612-8 [8826882.001]
  • [Cites] Exp Cell Res. 1996 Sep 15;227(2):190-6 [8831555.001]
  • [Cites] Blood. 1998 May 1;91(9):3379-89 [9558396.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4342-9 [9596683.001]
  • [Cites] Curr Opin Oncol. 2000 Jan;12(1):22-9 [10687725.001]
  • [Cites] J Immunol. 2000 Apr 15;164(8):3961-70 [10754286.001]
  • [Cites] J Cell Biol. 2000 May 1;149(3):603-12 [10791974.001]
  • [Cites] J Pharm Biomed Anal. 1998 Apr;16(8):1301-9 [9777604.001]
  • [Cites] Clin Cancer Res. 1995 Sep;1(9):1005-13 [9816073.001]
  • [Cites] Exp Cell Res. 1998 Nov 25;245(1):57-68 [9828101.001]
  • [Cites] J Immunol. 1999 Jan 15;162(2):1042-8 [9916731.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):399-408 [10458259.001]
  • [Cites] Br J Haematol. 1999 Sep;106(4):995-1004 [10520003.001]
  • [Cites] J Biol Chem. 2004 Nov 26;279(48):49575-8 [15475367.001]
  • [Cites] Leukemia. 2004 Dec;18(12):1934-40 [15483672.001]
  • [Cites] Leuk Lymphoma. 2004 Dec;45(12):2365-72 [15621749.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):268-81 [15690081.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Apr 1;158(1):88-91 [15771912.001]
  • [Cites] Leukemia. 2005 Apr;19(4):513-23 [15703780.001]
  • [Cites] Leukemia. 2005 Apr;19(4):524-30 [15674425.001]
  • [Cites] Leukemia. 2005 Apr;19(4):531-2 [15861177.001]
  • [Cites] Mol Biol Cell. 2005 Jun;16(6):3019-27 [15829563.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1795-801 [12176902.001]
  • [Cites] Science. 2002 Aug 23;297(5585):1352-4 [12193789.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2973-9 [12351410.001]
  • [Cites] Adv Cancer Res. 2000;79:157-73 [10818680.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2240-5 [10979972.001]
  • [Cites] Blood. 2000 Nov 1;96(9):3181-7 [11050001.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):795-9 [11309324.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):300-7 [11460154.001]
  • [Cites] EMBO Rep. 2001 Oct;2(10):945-51 [11571266.001]
  • [Cites] Nat Cell Biol. 2001 Nov;3(11):E255-63 [11715037.001]
  • [Cites] Nature. 2002 Jan 3;415(6867):92-6 [11780124.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1030-7 [11807009.001]
  • [Cites] Clin Pharmacokinet. 2002;41(2):93-103 [11888330.001]
  • [Cites] Leukemia. 2002 May;16(5):911-9 [11986954.001]
  • [Cites] Semin Cancer Biol. 2002 Apr;12(2):149-55 [12027587.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1045-52 [12040436.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21836-42 [11919205.001]
  • [Cites] Biochem J. 2002 Aug 15;366(Pt 1):15-22 [11985495.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3749-56 [12411322.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2002;:193-213 [12446424.001]
  • [Cites] J Cell Biol. 2002 Dec 9;159(5):739-45 [12460989.001]
  • [Cites] Nat Immunol. 2003 Apr;4(4):321-9 [12612580.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1466-71 [12697868.001]
  • [Cites] Cell Death Differ. 2003 Apr;10(4):477-84 [12719725.001]
  • [Cites] Blood. 2003 May 15;101(10):4098-104 [12531810.001]
  • [Cites] Br J Haematol. 2003 May;121(4):578-85 [12752098.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4561-8 [12560233.001]
  • [Cites] Oncology. 2003;64(4):459-67 [12759546.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1437-47 [12886229.001]
  • [Cites] Transpl Int. 2003 Jul;16(7):537-42 [12819863.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37832-9 [12853461.001]
  • [Cites] Leuk Res. 2004 Mar;28(3):221-2 [14687614.001]
  • [Cites] Leuk Res. 2004 Mar;28(3):243-8 [14687619.001]
  • [Cites] Am J Hematol. 2004 Jan;75(1):22-33 [14695629.001]
  • [Cites] Trends Immunol. 2004 Jan;25(1):17-24 [14698280.001]
  • [Cites] Blood. 2004 Jan 15;103(2):679-88 [14504101.001]
  • [Cites] Trends Cell Biol. 2004 Jan;14(1):20-8 [14729177.001]
  • [Cites] Mol Cancer Ther. 2004 Jan;3(1):59-70 [14749476.001]
  • [Cites] J Natl Cancer Inst. 2004 May 5;96(9):673-82 [15126604.001]
  • [Cites] Science. 2004 May 7;304(5672):843-6 [15073321.001]
  • [Cites] EMBO Rep. 2004 Jun;5(6):643-8 [15153933.001]
  • [Cites] Blood. 2004 Aug 1;104(3):788-94 [14996703.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1391-400 [15175625.001]
  • [Cites] J Chem Neuroanat. 2004 Sep;28(1-2):93-100 [15363494.001]
  • [Cites] Cell Death Differ. 2004 Nov;11(11):1234-41 [15297885.001]
  • [Cites] Cancer Cell. 2004 Oct;6(4):399-408 [15488762.001]
  • [Cites] Blood. 1983 Aug;62(2):495-504 [6603243.001]
  • [Cites] Clin Immunol Immunopathol. 1985 Mar;34(3):296-303 [3871678.001]
  • [Cites] Cancer Chemother Pharmacol. 1986;18(2):145-52 [2431803.001]
  • (PMID = 16144803.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA081534; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA109041; United States / NCI NIH HHS / CA / CA85563; United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA100428
  • [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 / Membrane Proteins; 0 / TNFSF13 protein, human; 0 / Tumor Necrosis Factor Ligand Superfamily Member 13; 0 / Tumor Necrosis Factor-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 20350-15-6 / Brefeldin A; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC1895341
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7. Kurtoglu M, Philips K, Liu H, Boise LH, Lampidis TJ: High endoplasmic reticulum activity renders multiple myeloma cells hypersensitive to mitochondrial inhibitors. Cancer Chemother Pharmacol; 2010 May;66(1):129-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High endoplasmic reticulum activity renders multiple myeloma cells hypersensitive to mitochondrial inhibitors.
  • Multiple myeloma (MM) cells continuously secrete large amounts of immunoglobulins that are folded in the endoplasmic reticulum (ER) whose function depend on the Ca(2+) concentration inside its lumen.
  • Here, we indeed find that Ca(2+) leak is greater in 3 MM, when compared to 2 B-cell leukemia cell lines.
  • Consistent with our hypothesis, CCCP is more potent in inducing the unfolded protein response marker, CHOP/GADD153 in MM versus B-cell leukemia lines.
  • Overall, our results demonstrate that the unusually high ER activity in MM cells may be exploited for therapeutic benefit through the use of mitochondrial inhibitors including troglitazone and fenofibrate.

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  • [Cites] Redox Rep. 2004;9(3):173-8 [15327748.001]
  • [Cites] Diabetes. 2004 Apr;53(4):1052-9 [15047621.001]
  • [Cites] J Biol Chem. 2003 Nov 7;278(45):44769-79 [12941956.001]
  • [Cites] J Cell Sci. 2004 Aug 15;117(Pt 18):4135-42 [15280427.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Oct;311(1):109-14 [15166256.001]
  • [Cites] Agents Actions. 1984 Dec;15(5-6):660-3 [6532186.001]
  • [Cites] Annu Rev Biochem. 1987;56:395-433 [3304139.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8800-4 [3194391.001]
  • [Cites] J Biol Chem. 1993 Jul 5;268(19):13765-8 [8390976.001]
  • [Cites] Mol Cell Biol. 1996 Aug;16(8):4273-80 [8754828.001]
  • [Cites] EMBO J. 1998 Apr 1;17(7):1986-95 [9524121.001]
  • [Cites] J Cell Biol. 1998 Sep 7;142(5):1235-43 [9732284.001]
  • [Cites] EMBO J. 1999 Jan 4;18(1):96-108 [9878054.001]
  • [Cites] Am J Physiol. 1999 May;276(5 Pt 2):F786-93 [10330061.001]
  • [Cites] J Biol Chem. 1999 Jun 4;274(23):16188-97 [10347173.001]
  • [Cites] Environ Health Perspect. 1999 Feb;107 Suppl 1:25-35 [10229704.001]
  • [Cites] Biochim Biophys Acta. 2004 Dec 6;1742(1-3):119-31 [15590062.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):101-12 [15621787.001]
  • [Cites] J Biol Chem. 2005 Apr 1;280(13):12114-22 [15659398.001]
  • [Cites] Annu Rev Biochem. 2005;74:739-89 [15952902.001]
  • [Cites] Biochem Pharmacol. 2005 Jul 15;70(2):177-88 [15925327.001]
  • [Cites] Apoptosis. 2006 Jan;11(1):5-13 [16374548.001]
  • [Cites] Toxicology. 2006 May 15;222(3):233-9 [16621215.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4907-16 [16507771.001]
  • [Cites] FASEB J. 2006 Jun;20(8):1215-7 [16611832.001]
  • [Cites] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1391-418 [16986999.001]
  • [Cites] Drug Metab Pharmacokinet. 2006 Oct;21(5):347-56 [17072088.001]
  • [Cites] Cell Calcium. 2006 Nov-Dec;40(5-6):553-60 [17074387.001]
  • [Cites] Pflugers Arch. 2007 Mar;453(6):797-808 [17171366.001]
  • [Cites] Apoptosis. 2007 May;12(5):857-68 [17294079.001]
  • [Cites] Arch Biochem Biophys. 2007 Jun 1;462(1):115-21 [17481572.001]
  • [Cites] Toxicol Appl Pharmacol. 2007 Sep 15;223(3):277-87 [17658574.001]
  • [Cites] PLoS One. 2007;2(9):e835 [17848986.001]
  • [Cites] Toxicol Appl Pharmacol. 2007 Oct 15;224(2):138-46 [17681577.001]
  • [Cites] Pflugers Arch. 2007 Dec;455(3):375-96 [17611770.001]
  • [Cites] Mol Cancer Ther. 2007 Nov;6(11):3049-58 [18025288.001]
  • [Cites] Semin Cell Dev Biol. 2007 Dec;18(6):716-31 [18023214.001]
  • [Cites] Int J Hematol. 2007 Dec;86(5):429-37 [18192112.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2008 May;246(5):677-83 [18278507.001]
  • [Cites] Free Radic Biol Med. 2008 Jul 1;45(1):50-9 [18394432.001]
  • [Cites] Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):808-16 [18573473.001]
  • [Cites] Biochem Pharmacol. 2008 Sep 1;76(5):569-81 [18555207.001]
  • [Cites] J Oral Pathol Med. 2008 Sep;37(8):490-8 [18631371.001]
  • [Cites] Cancer Res. 2009 Feb 15;69(4):1545-52 [19190324.001]
  • [Cites] Immunol Today. 1999 Dec;20(12):582-8 [10562710.001]
  • [Cites] J Biol Chem. 2001 Aug 3;276(31):29430-9 [11358971.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):381-9 [14685163.001]
  • (PMID = 19779717.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA37109; United States / NCI NIH HHS / CA / R01 CA127910; United States / NCI NIH HHS / CA / CA037109-21; United States / NCI NIH HHS / CA / R01 CA037109-21; United States / NCI NIH HHS / CA / R01 CA037109
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chromans; 0 / Peroxisome Proliferator-Activated Receptors; 0 / Thiazolidinediones; 0 / Uncoupling Agents; 147336-12-7 / Transcription Factor CHOP; 555-60-2 / Carbonyl Cyanide m-Chlorophenyl Hydrazone; I66ZZ0ZN0E / troglitazone; SY7Q814VUP / Calcium; U202363UOS / Fenofibrate
  • [Other-IDs] NLM/ NIHMS211134; NLM/ PMC2918425
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8. Wright G, Tan B, Rosenwald A, Hurt EH, Wiestner A, Staudt LM: A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma. Proc Natl Acad Sci U S A; 2003 Aug 19;100(17):9991-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma.
  • We used this method to classify diffuse large B cell lymphoma (DLBCL) biopsy samples into two gene expression subgroups based on data obtained from spotted cDNA microarrays.
  • The germinal center B cell-like (GCB) DLBCL subgroup expressed genes characteristic of normal germinal center B cells whereas the activated B cell-like (ABC) DLBCL subgroup expressed a subset of the genes that are characteristic of plasma cells, particularly those encoding endoplasmic reticulum and golgi proteins involved in secretion.
  • The GCB and ABC DLBCL subgroups identified in this data set had significantly different 5-yr survival rates after multiagent chemotherapy (62% vs. 26%; P < or = 0.0051), in accord with analyses of other DLBCL cohorts.
  • [MeSH-major] Gene Expression Profiling / methods. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / genetics. Oligonucleotide Array Sequence Analysis / methods

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  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] J Comput Biol. 2002;9(3):505-11 [12162889.001]
  • [Cites] Science. 2002 Sep 20;297(5589):2066-70 [12242446.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Nat Med. 2002 Jan;8(1):68-74 [11786909.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1166-70 [11158612.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):300-7 [11460154.001]
  • [Cites] Immunity. 2001 Sep;15(3):375-85 [11567628.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54 [11742071.001]
  • [Cites] Nature. 2002 Jan 3;415(6867):92-6 [11780124.001]
  • [CommentIn] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10585-7 [12963810.001]
  • (PMID = 12900505.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC187912
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9. Jie H, Donghua H, Xingkui X, Liang G, Wenjun W, Xiaoyan H, Zhen C: Homoharringtonine-induced apoptosis of MDS cell line MUTZ-1 cells is mediated by the endoplasmic reticulum stress pathway. Leuk Lymphoma; 2007 May;48(5):964-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Homoharringtonine-induced apoptosis of MDS cell line MUTZ-1 cells is mediated by the endoplasmic reticulum stress pathway.
  • Here we showed that the endoplasmic reticulum (ER) may be the initial site of apoptotic signal induced by homoharringtonine in MUTZ-1 cells.
  • After incubation with homoharringtonine, the percentage of apoptotic MUTZ-1 cells increased in a time-dependent manner, Ca(2+) translocated from ER pool to cytosol, the mitochondrial membrane potential decreased, and Bid protein translocated from ER to mitochondria.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis. Harringtonines / pharmacology. Leukemia / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] BH3 Interacting Domain Death Agonist Protein / metabolism. Calcium / metabolism. Cell Line, Tumor. Cytosol / metabolism. Endoplasmic Reticulum / metabolism. Humans. K562 Cells. Membrane Potentials. Mitochondria / metabolism. Time Factors

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  • [RetractionIn] Leuk Lymphoma. 2016 May;57(5):1241 [27096892.001]
  • (PMID = 17487741.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Harringtonines; 6FG8041S5B / homoharringtonine; SY7Q814VUP / Calcium
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10. Daniels I, Turzanski J, Haynes AP: A requirement for calcium in the caspase-independent killing of Burkitt lymphoma cell lines by Rituximab. Br J Haematol; 2008 Jul;142(3):394-403
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A requirement for calcium in the caspase-independent killing of Burkitt lymphoma cell lines by Rituximab.
  • The therapeutic monoclonal antibody rituximab has previously been shown to kill B cells in a caspase-independent manner.
  • The present study showed that rituximab treatment of Burkitt lymphoma cell lines induced a slow rise in intracellular calcium ([Ca(2+)](i)).
  • This rise was only witnessed in cell lines that were killed by antibody, suggesting a critical role for Ca(2+) in mediating rituximab-driven caspase-independent cell death.
  • In sharp contrast, inhibition of Ca(2+) entry via plasma membrane channels with (2-aminoethoxy) diphenylborate or SKF-96365 or complete chelation of extracellular Ca(2+) with ethyleneglycol bis (aminoethylether) tetra-acetate inhibited the rise in [Ca(2+)](i) and increased cell viability.
  • Together, these data suggest that ligation of the CD20 receptor with rituximab allows a slow sustained influx of Ca(2+) from the external environment that under certain conditions can lead to cell death.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Burkitt Lymphoma / drug therapy. Calcium / metabolism
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / immunology. B-Lymphocytes / drug effects. B-Lymphocytes / metabolism. B-Lymphocytes / pathology. Calcium Channel Blockers / pharmacology. Caspases / metabolism. Cell Death. Cell Line. Cell Membrane / metabolism. Dantrolene / pharmacology. Endoplasmic Reticulum / drug effects. Endoplasmic Reticulum / metabolism. Flow Cytometry. Humans. Imidazoles / pharmacology. Inositol 1,4,5-Trisphosphate Receptors / metabolism. Macrocyclic Compounds / pharmacology. Oxazoles / pharmacology. Rituximab. Ryanodine / metabolism

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  • (PMID = 18544085.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / Calcium Channel Blockers; 0 / Imidazoles; 0 / Inositol 1,4,5-Trisphosphate Receptors; 0 / Macrocyclic Compounds; 0 / Oxazoles; 0 / xestospongin C; 130495-35-1 / 1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; 15662-33-6 / Ryanodine; 4F4X42SYQ6 / Rituximab; EC 3.4.22.- / Caspases; F64QU97QCR / Dantrolene; SY7Q814VUP / Calcium
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11. Wlodkowic D, Skommer J, Pelkonen J: Brefeldin A triggers apoptosis associated with mitochondrial breach and enhances HA14-1- and anti-Fas-mediated cell killing in follicular lymphoma cells. Leuk Res; 2007 Dec;31(12):1687-700
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  • [Title] Brefeldin A triggers apoptosis associated with mitochondrial breach and enhances HA14-1- and anti-Fas-mediated cell killing in follicular lymphoma cells.
  • Follicular lymphoma (FL) remains a fatal disease of increasing worldwide incidence.
  • Since patients with FL eventually develop resistance to conventional anticancer agents, and due to BCL-2 overexpression present with profoundly compromised execution of mitochondrial pathway of apoptosis, targeting alternative pathways of cell demise may appear therapeutically beneficial.
  • Herein we report for the first time the effects of an ER-Golgi transport inhibitor, Brefeldin A (BFA), alone and in combination with a small molecule Bcl-2 inhibitor HA14-1 or agonistic anti-Fas mAb, in the recently established human FL cell lines.
  • All cell lines tested were sensitive to BFA-induced cytotoxicity and apoptosis.
  • Moreover BFA-induced cell death was associated with profound ER stress, mitochondrial breach and subsequent caspase cascade activation, including caspase 2 activation.
  • Of importance, small molecule Bcl-2 antagonist, HA14-1 and agonistic anti-Fas mAb significantly enhanced BFA-mediated cytotoxicity and apoptosis, revealing novel and previously unexplored means to enhance ER stress-mediated cell killing in follicular lymphoma cells.
  • [MeSH-major] Antigens, CD95 / antagonists & inhibitors. Apoptosis / drug effects. Benzopyrans / pharmacology. Brefeldin A / pharmacology. Lymphoma, Follicular / drug therapy. Lymphoma, Follicular / pathology. Nitriles / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Caspases / metabolism. Cell Line, Tumor. Endoplasmic Reticulum / pathology. Humans. Mitochondria / drug effects. Oxidative Stress / drug effects. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors

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  • (PMID = 17428536.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD95; 0 / Benzopyrans; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; 20350-15-6 / Brefeldin A; EC 3.4.22.- / Caspases
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12. Yagita M, Tabata R, Konaka Y, Ohno T, Takatsuki K: [Intravascular large B-cell lymphoma associated with hypoalbuminemia and hypoxemia]. Rinsho Ketsueki; 2000 Nov;41(11):1189-94

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intravascular large B-cell lymphoma associated with hypoalbuminemia and hypoxemia].
  • A 67-year-old man was referred to our hospital for treatment of hemophagocytic syndrome.
  • Hypotension, hypoxemia, pleural effusion, severe anasarca, and splenomegaly were noticed at the time of admission.
  • Bone marrow aspiration revealed an increase of reticulum cells with active hemophagocytosis and the presence of immature lymphocytes (6.0%).
  • Lymphoma was suspected, but effective chemotherapy could not be performed because of progressive hypoxemia and severe hypoalbuminemia, and the patient died of the disease 2 weeks after admission.
  • The postmortem diagnosis was intravascular large B-cell lymphoma.
  • Hypoalbuminemia and hypoxemia appear to be important clinical features of intravascular large B-cell lymphoma.
  • [MeSH-major] Anoxia / complications. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Serum Albumin / analysis. Vascular Neoplasms / pathology
  • [MeSH-minor] Aged. Histiocytosis, Non-Langerhans-Cell / pathology. Humans. Male

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  • (PMID = 11193438.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Serum Albumin
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13. van der Luit AH, Vink SR, Klarenbeek JB, Perrissoud D, Solary E, Verheij M, van Blitterswijk WJ: A new class of anticancer alkylphospholipids uses lipid rafts as membrane gateways to induce apoptosis in lymphoma cells. Mol Cancer Ther; 2007 Aug;6(8):2337-45
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new class of anticancer alkylphospholipids uses lipid rafts as membrane gateways to induce apoptosis in lymphoma cells.
  • Single-chain alkylphospholipids, unlike conventional chemotherapeutic drugs, act on cell membranes to induce apoptosis in tumor cells.
  • We tested four different alkylphospholipids, i.e., edelfosine, perifosine, erucylphosphocholine, and compound D-21805, as inducers of apoptosis in the mouse lymphoma cell line S49.
  • We compared their mechanism of cellular entry and their potency to induce apoptosis through inhibition of de novo biosynthesis of phosphatidylcholine at the endoplasmic reticulum.
  • Similar to edelfosine, perifosine accumulated in (isolated) lipid rafts independent on raft sphingomyelin content per se.
  • However, perifosine was more susceptible than edelfosine to back-extraction by fatty acid-free serum albumin, suggesting a more peripheral location in the cell due to less effective internalization.
  • Overall, our results suggest that lipid rafts are critical membrane portals for cellular entry of alkylphospholipids depending on SMS1 activity and, therefore, are potential targets for alkylphospholipid anticancer therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Lymphoma / pathology. Membrane Microdomains / drug effects. Phospholipids / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Endocytosis / drug effects. HeLa Cells. Humans. Mice. Phosphatidylcholines / biosynthesis. Phospholipid Ethers / chemistry. Phospholipid Ethers / pharmacology. Phosphorylcholine / analogs & derivatives. Phosphorylcholine / chemistry. Phosphorylcholine / pharmacology. Sphingomyelins / biosynthesis. Time Factors

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  • (PMID = 17699729.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phosphatidylcholines; 0 / Phospholipid Ethers; 0 / Phospholipids; 0 / Sphingomyelins; 107-73-3 / Phosphorylcholine; 1Y6SNA8L5S / edelfosine; 2GWV496552 / perifosine
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14. Zismanov V, Lishner M, Tartakover-Matalon S, Radnay J, Shapiro H, Drucker L: Tetraspanin-induced death of myeloma cell lines is autophagic and involves increased UPR signalling. Br J Cancer; 2009 Oct 20;101(8):1402-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tetraspanin-induced death of myeloma cell lines is autophagic and involves increased UPR signalling.
  • BACKGROUND: Multiple myeloma (MM) therapy is hindered by the interaction of the heterogeneous malignant plasma cells with their microenvironment and evolving drug resistance.
  • METHODS: Multiple myeloma cell lines were transiently transfected with eGFP-CD81N1/CD82N1 fusion proteins and assessed for death mode by flow cytometry (propidium iodide, ZVAD-fmk, 3MA), activation of unfolded protein response (UPR), and autophagy (immunoblot, RT-PCR).
  • RESULTS: Cell death induced by CD81N1 and CD82N1 in MM cell lines was autophagic and involved endoplasmic reticulum (ER)-stress manifested by activation of UPR pathways, PERK (protein kinase-like ER kinase) and IRE1 (inositol-requiring 1).
  • We also established the relative X-box binding protein 1 baseline expression levels in a panel of MM cell lines and their general dependence on autophagy for survival.
  • Timeline of UPR cascades and cell fate supported our results.
  • Integration of our findings with published data highlights the unifying dependence of MM cells on ER-Golgi homoeostasis, and underscores the potential of tetraspanin complexes and ER-stress as leverage for MM therapy.
  • [MeSH-major] Antigens, CD / physiology. Antigens, CD82 / physiology. Apoptosis. Autophagy. Endoplasmic Reticulum / metabolism. Multiple Myeloma / pathology. Protein Folding. Signal Transduction
  • [MeSH-minor] Antigens, CD81. Cell Line, Tumor. Cell Survival. Humans

  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
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  • [Cites] Blood. 2003 Apr 15;101(8):3126-35 [12515720.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):300-7 [11460154.001]
  • [Cites] Tissue Antigens. 2004 Sep;64(3):235-42 [15304003.001]
  • [Cites] Eur J Cell Biol. 2004 Oct;83(10):583-90 [15679103.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10501-8 [15634669.001]
  • [Cites] Blood. 2006 Jan 1;107(1):222-31 [16144803.001]
  • [Cites] Leuk Lymphoma. 2006 Mar;47(3):531-9 [16396777.001]
  • [Cites] Carcinogenesis. 2006 Feb;27(2):197-204 [16113057.001]
  • [Cites] Mol Cell Biol. 2006 Dec;26(24):9220-31 [17030611.001]
  • [Cites] Biochem Soc Symp. 2007;(74):107-16 [17233584.001]
  • [Cites] FASEB J. 2007 Mar;21(3):691-9 [17210782.001]
  • [Cites] Curr Top Dev Biol. 2007;78:217-45 [17338918.001]
  • [Cites] Exp Hematol. 2007 Apr;35(4 Suppl 1):155-62 [17379101.001]
  • [Cites] Cancer Cell. 2007 Apr;11(4):349-60 [17418411.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29 [17565364.001]
  • [Cites] J Cell Sci. 2007 Aug 1;120(Pt 15):2479-87 [17646672.001]
  • [Cites] Am J Pathol. 2007 Aug;171(2):513-24 [17620365.001]
  • [Cites] FEBS Lett. 2007 Jul 31;581(19):3652-7 [17475256.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2385-8 [17786234.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2641-9 [17525289.001]
  • [Cites] Cancer Sci. 2007 Nov;98(11):1666-77 [17727684.001]
  • [Cites] Autophagy. 2007 Nov-Dec;3(6):542-5 [17611390.001]
  • [Cites] Autophagy. 2007 Nov-Dec;3(6):663-6 [17622797.001]
  • [Cites] Cell Res. 2007 Oct;17(10):839-49 [17893711.001]
  • [Cites] Antioxid Redox Signal. 2007 Dec;9(12):2373-87 [17883326.001]
  • [Cites] Science. 2007 Nov 9;318(5852):944-9 [17991856.001]
  • [Cites] Nature. 2008 Feb 28;451(7182):1069-75 [18305538.001]
  • [Cites] Curr Mol Med. 2008 Mar;8(2):78-91 [18336289.001]
  • [Cites] Curr Mol Med. 2008 Mar;8(2):92-101 [18336290.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 May;61(6):923-32 [17624530.001]
  • [Cites] Blood. 2008 May 1;111(9):4690-9 [18305219.001]
  • [Cites] Hematol Oncol. 2008 Jun;26(2):73-81 [18324639.001]
  • [Cites] Autophagy. 2008 Aug;4(6):770-82 [18594198.001]
  • [Cites] Diabetes. 2008 Nov;57(11):2967-76 [18728232.001]
  • [Cites] Cell Signal. 2008 Dec;20(12):2309-16 [18804164.001]
  • [Cites] Cell Signal. 2009 Jan;21(1):169-77 [18950706.001]
  • [Cites] Biochem J. 2000 Nov 1;351 Pt 3:629-37 [11042117.001]
  • [Cites] Acta Pharmacol Sin. 2004 Feb;25(2):148-51 [14769201.001]
  • (PMID = 19755988.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD81; 0 / Antigens, CD82; 0 / CD81 protein, human; 0 / CD82 protein, human
  • [Other-IDs] NLM/ PMC2768457
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15. Traini R, Ben-Josef G, Pastrana DV, Moskatel E, Sharma AK, Antignani A, Fitzgerald DJ: ABT-737 overcomes resistance to immunotoxin-mediated apoptosis and enhances the delivery of pseudomonas exotoxin-based proteins to the cell cytosol. Mol Cancer Ther; 2010 Jul;9(7):2007-15
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABT-737 overcomes resistance to immunotoxin-mediated apoptosis and enhances the delivery of pseudomonas exotoxin-based proteins to the cell cytosol.
  • Pseudomonas exotoxin (PE)-based immunotoxins (antibody-toxin fusion proteins) have achieved frequent complete remissions in patients with hairy cell leukemia but far fewer objective responses in other cancers.
  • To address possible mechanisms of resistance, we investigated immunotoxin activity in a model system using the colon cancer cell line, DLD1.
  • In other epithelial cell lines, ABT-737 enhanced the cytotoxicity of PE-related immunotoxins by as much as 20-fold, but did not enhance diphtheria toxin or cycloheximide.
  • Because PE translocates to the cytosol via the endoplasmic reticulum (ER) and the other toxins do not, ABT-737-mediated effects on the ER were investigated.
  • ABT-737 treatment stimulated increased levels of ER stress response factor, ATF4.
  • Because of its activity in the ER, ABT-737 might be particularly well suited for enhancing the activity of immunotoxins that translocate from the ER to the cell cytosol.
  • [MeSH-major] Apoptosis / drug effects. Biphenyl Compounds / pharmacology. Immunotoxins / pharmacology. Nitrophenols / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Activating Transcription Factor 4 / metabolism. Blotting, Western. Caspases / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cytosol / drug effects. Cytosol / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Synergism. Endoplasmic Reticulum / metabolism. Exotoxins / metabolism. Exotoxins / pharmacology. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / pathology. Piperazines / pharmacology. Protein Biosynthesis / drug effects. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pseudomonas / metabolism

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  • [Cites] Biochemistry. 1998 Dec 1;37(48):16934-42 [9836586.001]
  • [Cites] Biochemistry. 1997 Sep 16;36(37):11051-4 [9333321.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):105-10 [15613488.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]
  • [Cites] J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911.001]
  • [Cites] Traffic. 2006 Apr;7(4):379-93 [16536737.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2005;70:469-77 [16869785.001]
  • [Cites] Annu Rev Cell Dev Biol. 2006;22:487-508 [16822172.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):389-99 [17097561.001]
  • [Cites] Annu Rev Med. 2007;58:221-37 [17059365.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):782-91 [17234790.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6192-200 [17200126.001]
  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3421-8 [18451170.001]
  • [Cites] Cell Death Differ. 2009 Mar;16(3):360-7 [18806758.001]
  • [Cites] Trends Mol Med. 2009 May;15(5):225-33 [19362056.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873.001]
  • [Cites] Mol Pharmacol. 2009 Sep;76(3):667-78 [19561125.001]
  • [Cites] Cancer Biol Ther. 2009 Aug;8(16):1587-95 [19556859.001]
  • [Cites] Br J Haematol. 2010 Jan;148(1):99-109 [19821820.001]
  • [Cites] Cancer Immunol Immunother. 2010 May;59(5):737-46 [20091030.001]
  • [Cites] Blood. 2010 Apr 22;115(16):3304-13 [20197552.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6101-10 [11085534.001]
  • [Cites] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3092-9 [12374676.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3520-6 [12429643.001]
  • [Cites] Science. 2003 Apr 4;300(5616):135-9 [12624178.001]
  • [Cites] Semin Oncol. 2003 Aug;30(4):545-57 [12939723.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2718-26 [14525789.001]
  • [Cites] Int J Cancer. 2004 Nov 10;112(3):475-83 [15382075.001]
  • [Cites] Cell. 1978 Sep;15(1):245-50 [699044.001]
  • [Cites] J Cell Biol. 1980 Dec;87(3 Pt 1):828-32 [7462324.001]
  • [Cites] J Cell Biol. 1980 Dec;87(3 Pt 1):849-54 [7462326.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):2200-5 [2005905.001]
  • [Cites] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422.001]
  • [Cites] Leukemia. 2000 May;14(5):853-8 [10803517.001]
  • [Cites] J Immunol. 1991 Oct 15;147(8):2609-16 [1918981.001]
  • [Cites] Leuk Lymphoma. 1997 Jul;26(3-4):287-98 [9322891.001]
  • [Cites] J Cell Sci. 1999 Feb;112 ( Pt 4):467-75 [9914159.001]
  • (PMID = 20587662.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC008757-20
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / ATF4 protein, human; 0 / Biphenyl Compounds; 0 / Exotoxins; 0 / Immunotoxins; 0 / Nitrophenols; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Sulfonamides; 145891-90-3 / Activating Transcription Factor 4; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS231519; NLM/ PMC2943340
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16. Balasubramanian S, Ramos J, Luo W, Sirisawad M, Verner E, Buggy JJ: A novel histone deacetylase 8 (HDAC8)-specific inhibitor PCI-34051 induces apoptosis in T-cell lymphomas. Leukemia; 2008 May;22(5):1026-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel histone deacetylase 8 (HDAC8)-specific inhibitor PCI-34051 induces apoptosis in T-cell lymphomas.
  • We have developed a potent, histone deacetylase 8 (HDAC8)-specific inhibitor PCI-34051 with >200-fold selectivity over the other HDAC isoforms.
  • PCI-34051 induces caspase-dependent apoptosis in cell lines derived from T-cell lymphomas or leukemias, but not in other hematopoietic or solid tumor lines.
  • Cells defective in T-cell receptor signaling were still sensitive to PCI-34051-induced apoptosis, whereas a phospholipase C-gamma1 (PLCgamma1)-defective line was resistant.
  • Jurkat cells showed a dose-dependent decrease in PCI-34051-induced apoptosis upon treatment with a PLC inhibitor U73122, but not with an inactive analog.
  • We found that rapid intracellular calcium mobilization from endoplasmic reticulum (ER) and later cytochrome c release from mitochondria are essential for the apoptotic mechanism.
  • These studies show that HDAC8-selective inhibitors have a unique mechanism of action involving PLCgamma1 activation and calcium-induced apoptosis, and could offer benefits including a greater therapeutic index for treating T-cell malignancies.
  • [MeSH-major] Apoptosis / drug effects. Histone Deacetylase Inhibitors. Indoles / pharmacology. Lymphoma, T-Cell / drug therapy. Repressor Proteins / antagonists & inhibitors
  • [MeSH-minor] Calcium / metabolism. Cell Line, Tumor. Histone Deacetylases. Humans. Phospholipase C gamma / metabolism

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  • (PMID = 18256683.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Indoles; 0 / PCI 34051; 0 / Repressor Proteins; EC 3.1.4.3 / Phospholipase C gamma; EC 3.5.1.98 / HDAC8 protein, human; EC 3.5.1.98 / Histone Deacetylases; SY7Q814VUP / Calcium
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17. Kovar L, Etrych T, Kabesova M, Subr V, Vetvicka D, Hovorka O, Strohalm J, Sklenar J, Chytil P, Ulbrich K, Rihova B: Doxorubicin attached to HPMA copolymer via amide bond modifies the glycosylation pattern of EL4 cells. Tumour Biol; 2010 Aug;31(4):233-42
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • To avoid the side effects of the anti-cancer drug doxorubicin (Dox), we conjugated this drug to a N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer backbone.
  • In contrast to Dox and Dox-HPMA(HYD), Dox-HPMA(AM) accumulates within the cell's intracellular membranes, including those of the Golgi complex and endoplasmic reticulum, both involved in protein glycosylation.
  • Flow cytometry was used to determine lectin binding and cell death, immunoblot to characterize the presence of CD7, CD43, CD44, and CD45, and high-performance anion exchange chromatography with pulsed amperometric detector analysis for characterization of plasma membrane saccharide composition.
  • In this study, we demonstrate that Dox-HPMA(AM) treatment changes glycosylation of the EL4 T cell lymphoma surface and sensitizes the cells to galectin-1-induced apoptosis.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Doxorubicin / analogs & derivatives. Lymphoma, T-Cell / drug therapy. Polymethacrylic Acids / pharmacology
  • [MeSH-minor] Amides / chemistry. Animals. Antigens, CD43 / metabolism. Apoptosis. Blotting, Western. Cell Line, Tumor / drug effects. Cell Proliferation. Drug Carriers. Endoplasmic Reticulum / metabolism. Flow Cytometry. Galectin 1 / metabolism. Glycosylation. Golgi Apparatus / metabolism. Mice

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  • [Cites] J Control Release. 2003 Aug 28;91(1-2):1-16 [12932633.001]
  • [Cites] Folia Microbiol (Praha). 1997;42(3):277-87 [9246765.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):83-94 [9918206.001]
  • [Cites] J Immunol. 1999 Oct 1;163(7):3801-11 [10490978.001]
  • [Cites] Biomaterials. 1989 Jul;10(5):335-42 [2765631.001]
  • [Cites] J Biol Chem. 2005 Feb 18;280(7):5549-62 [15556936.001]
  • [Cites] Adv Drug Deliv Rev. 2002 Sep 13;54(5):653-74 [12204597.001]
  • [Cites] J Immunol. 2000 Sep 1;165(5):2331-4 [10946254.001]
  • [Cites] J Clin Oncol. 2005 Dec 10;23(35):8932-41 [16219933.001]
  • [Cites] Trends Biotechnol. 2009 Jan;27(1):11-7 [19022512.001]
  • [Cites] Adv Enzyme Regul. 2001;41:189-207 [11384745.001]
  • [Cites] J Control Release. 2001 May 18;73(1):89-102 [11337062.001]
  • [Cites] Expert Opin Biol Ther. 2008 Jan;8(1):45-57 [18081536.001]
  • [Cites] J Control Release. 2005 Dec 10;110(1):119-29 [16269198.001]
  • [Cites] J Control Release. 2002 Apr 23;80(1-3):101-17 [11943391.001]
  • [Cites] Eur J Pharm Biopharm. 2000 Jul;50(1):61-81 [10840193.001]
  • [Cites] J Control Release. 2004 Sep 30;99(2):301-14 [15380639.001]
  • [Cites] Bioconjug Chem. 2007 May-Jun;18(3):894-902 [17402705.001]
  • [Cites] J Exp Med. 1996 Aug 1;184(2):759-64 [8760831.001]
  • [Cites] Cancer Cell. 2004 Mar;5(3):241-51 [15050916.001]
  • [Cites] J Drug Target. 2006 Jul;14 (6):391-403 [17092839.001]
  • [Cites] Biochem Biophys Res Commun. 2008 May 23;370(1):149-53 [18355446.001]
  • [Cites] Pharmacol Rev. 2004 Jun;56(2):185-229 [15169927.001]
  • [Cites] Bioessays. 2005 Jan;27(1):50-6 [15612030.001]
  • [Cites] Scand J Immunol. 2005 Jul;62 Suppl 1:100-5 [15953192.001]
  • [Cites] Anal Biochem. 1988 Apr;170(1):54-62 [3389518.001]
  • [Cites] Cancer Immunol Immunother. 2007 Jan;56(1):35-47 [16636810.001]
  • [Cites] Pharm Res. 1999 Jul;16(7):986-96 [10450921.001]
  • [Cites] Biochim Biophys Acta. 2008 Mar;1780(3):325-46 [17976918.001]
  • [Cites] Nature. 1995 Dec 14;378(6558):736-9 [7501023.001]
  • [Cites] Hum Exp Toxicol. 2001 Sep;20(9):461-70 [11776408.001]
  • [Cites] J Biol Chem. 1986 Aug 5;261(22):10119-26 [3733704.001]
  • [Cites] Glycoconj J. 1998 Aug;15(8):737-47 [9870349.001]
  • [Cites] J Immunol. 2006 Oct 15;177(8):5328-36 [17015718.001]
  • [Cites] J Control Release. 2000 Feb 14;64(1-3):63-79 [10640646.001]
  • [Cites] Bioconjug Chem. 2000 Sep-Oct;11(5):664-73 [10995209.001]
  • [Cites] Anal Biochem. 1994 Jun;219(2):375-8 [8080096.001]
  • [Cites] J Control Release. 2008 Apr 21;127(2):110-20 [18325618.001]
  • (PMID = 20556593.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amides; 0 / Antibiotics, Antineoplastic; 0 / Antigens, CD43; 0 / Drug Carriers; 0 / Galectin 1; 0 / Polymethacrylic Acids; 0 / doxorubicin-N-(2-hydroxypropyl)methacrylamide copolymer conjugate; 80168379AG / Doxorubicin
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18. Wang Q, Mora-Jensen H, Weniger MA, Perez-Galan P, Wolford C, Hai T, Ron D, Chen W, Trenkle W, Wiestner A, Ye Y: ERAD inhibitors integrate ER stress with an epigenetic mechanism to activate BH3-only protein NOXA in cancer cells. Proc Natl Acad Sci U S A; 2009 Feb 17;106(7):2200-5
eagle-i research resources. PMID 19164757 (Special Collections) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The ubiquitin-proteasome system has recently emerged as a major target for drug development in cancer therapy.
  • The proteasome inhibitor bortezomib has clinical activity in multiple myeloma and mantle cell lymphoma.
  • Here we report that Eeyarestatin I (EerI), a chemical inhibitor that blocks endoplasmic reticulum (ER)-associated protein degradation, has antitumor and biologic activities similar to bortezomib and can synergize with bortezomib.
  • Our results identify a class of anticancer agents that integrate ER stress response with an epigenetic mechanism to induce cell death.

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  • [Cites] Mol Biol Cell. 2004 Apr;15(4):1635-46 [14767067.001]
  • [Cites] Bioessays. 2003 Sep;25(9):868-77 [12938176.001]
  • [Cites] Cancer Cell. 2004 May;5(5):417-21 [15144949.001]
  • [Cites] Nature. 2004 Oct 14;431(7010):873-8 [15386022.001]
  • [Cites] Science. 2005 Feb 11;307(5711):935-9 [15705855.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6282-93 [16024630.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6294-304 [16024631.001]
  • [Cites] Blood. 2006 Jan 1;107(1):257-64 [16166592.001]
  • [Cites] J Biol Chem. 2006 Mar 17;281(11):7260-70 [16407291.001]
  • [Cites] J Cell Biol. 2006 Apr 10;173(1):19-26 [16606690.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4907-16 [16507771.001]
  • [Cites] Annu Rev Biochem. 2006;75:243-69 [16756492.001]
  • [Cites] EMBO J. 2006 Jun 21;25(12):2723-34 [16724113.001]
  • [Cites] J Cell Biol. 2006 Sep 25;174(7):963-71 [17000876.001]
  • [Cites] J Struct Biol. 2006 Oct;156(1):29-40 [16529947.001]
  • [Cites] J Biol Chem. 2006 Oct 20;281(42):31440-7 [16928686.001]
  • [Cites] Blood. 2007 Jan 1;109(1):271-80 [16960149.001]
  • [Cites] Blood. 2007 May 15;109(10):4441-9 [17227835.001]
  • [Cites] Cancer Res. 2007 Jun 1;67(11):5418-24 [17545623.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1337-49 [17604722.001]
  • [Cites] Nature. 2007 Oct 25;449(7165):1068-72 [17914355.001]
  • [Cites] Nat Cell Biol. 2007 Dec;9(12):1428-35 [18037880.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19488-93 [18042711.001]
  • [Cites] J Biol Chem. 2008 Mar 21;283(12):7445-54 [18199748.001]
  • [Cites] Mol Cell. 2008 Mar 28;29(6):653-63 [18374642.001]
  • [Cites] Leuk Lymphoma. 2008 Apr;49(4):798-808 [18398749.001]
  • [Cites] J Exp Med. 2008 May 12;205(5):1109-20 [18411339.001]
  • [Cites] Science. 2000 May 12;288(5468):1053-8 [10807576.001]
  • [Cites] Nat Cell Biol. 2001 Feb;3(2):173-82 [11175750.001]
  • [Cites] Cell. 2001 Dec 28;107(7):881-91 [11779464.001]
  • [Cites] Cell. 2001 Dec 28;107(7):893-903 [11779465.001]
  • [Cites] Nature. 2002 Jan 3;415(6867):92-6 [11780124.001]
  • [Cites] Annu Rev Cell Dev Biol. 2002;18:575-99 [12142265.001]
  • [Cites] EMBO J. 2003 May 15;22(10):2309-17 [12743025.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):349-60 [15122206.001]
  • (PMID = 19164757.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE14003
  • [Grant] United States / NCI NIH HHS / CA / R01 CA118306; United States / NIDDK NIH HHS / DK / R01 DK047119; United States / NIEHS NIH HHS / ES / R01 ES008681; United States / NIEHS NIH HHS / ES / ES08681; United States / NIDDK NIH HHS / DK / R37 DK047119; United States / Intramural NIH HHS / / ; United States / NIDDK NIH HHS / DK / R01 DK064938; United States / NIDDK NIH HHS / DK / DK064938; United States / NIDDK NIH HHS / DK / DK47119; United States / NCI NIH HHS / CA / CA118306
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(4-chlorophenyl)-3-(3-(4-chlorophenyl)-5,5-dimethyl-1-(3-(5-nitrofuran-2-yl)allyldienehydrazinocarbonylmethyl)-2-oxoimidazolidin-4-yl)-1-hydroxyurea; 0 / Adaptor Proteins, Vesicular Transport; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Hydrazones; 0 / NOXA1 protein, human; 0 / Pyrazines; 0 / Ubiquitin; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ PMC2629785
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19. Abayomi EA, Sissolak G, Jacobs P: Use of novel proteosome inhibitors as a therapeutic strategy in lymphomas current experience and emerging concepts. Transfus Apher Sci; 2007 Aug;37(1):85-92
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  • [Title] Use of novel proteosome inhibitors as a therapeutic strategy in lymphomas current experience and emerging concepts.
  • Additional changes are mediated in protein folding within the endoplasmic reticulum and contribute to cell death.
  • These concepts are given focus by considering their introduction into treatment of lymphoreticular malignancy.
  • [MeSH-major] Boronic Acids / therapeutic use. Lymphoma / drug therapy. Lymphoma / enzymology. Neoplasm Proteins / antagonists & inhibitors. Protease Inhibitors / therapeutic use. Proteasome Inhibitors. Pyrazines / therapeutic use
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Apoptosis / drug effects. Bortezomib. Cell Adhesion / drug effects. Cell Cycle / drug effects. Cell Differentiation / drug effects. Clinical Trials, Phase II as Topic. Endoplasmic Reticulum / enzymology. Endoplasmic Reticulum / pathology. Humans. NF-kappa B / metabolism. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / enzymology. Proteasome Endopeptidase Complex / metabolism. Ubiquitin / metabolism

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  • (PMID = 17881293.001).
  • [ISSN] 1473-0502
  • [Journal-full-title] Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis
  • [ISO-abbreviation] Transfus. Apher. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Ubiquitin; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease
  • [Number-of-references] 31
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20. Tinhofer I, Anether G, Senfter M, Pfaller K, Bernhard D, Hara M, Greil R: Stressful death of T-ALL tumor cells after treatment with the anti-tumor agent Tetrocarcin-A. FASEB J; 2002 Aug;16(10):1295-7
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  • [Title] Stressful death of T-ALL tumor cells after treatment with the anti-tumor agent Tetrocarcin-A.
  • The T-ALL cell lines CCRF-CEM and Jurkat were studied for their sensitivity toward apoptosis induced by tetrocarcin-A (TC-A), an antibacterial and antitumor agent isolated from the actinomycete Micromonospora.
  • This substance promoted cell death via a mitochondrial signaling pathway, that is, by activation of Bid and Bax, loss of the mitochondrial transmembrane potential, release of cytochrome c, and activation of effector caspases, even under conditions of Bcl-2 overexpression.
  • Furthermore, sensitivity to TC-A was not dependent on expression of wild-type caspase-8.
  • In contrast, this apoptotic pathway was inhibited markedly by pretreatment of cells with cycloheximide, an inhibitor of de novo protein synthesis. cDNA microarray chip analysis revealed that TC-A induced a significant up-regulation of members of the heat shock protein family known to be involved in the endoplasmic reticulum (ER)-stress-induced apoptotic program.
  • The activation of caspase-12, the central inducer caspase involved in ER-stress by TC-A treatment, is in concordance with this result.
  • These results show that, in T-ALL cells, TC-A induces an apoptotic machinery via mitochondrial and ER signaling, which is not inhibited by aberrant expression/function of important regulators of death receptor- and drug-induced apoptosis.
  • [MeSH-major] Aminoglycosides. Anti-Bacterial Agents / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Caspases / metabolism. Endoplasmic Reticulum / metabolism. Heat-Shock Proteins / biosynthesis. Heat-Shock Proteins / genetics. Humans. Jurkat Cells. Mitochondria / drug effects. Mitochondria / metabolism. Models, Biological. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Proto-Oncogene Proteins c-bcl-2 / physiology. Signal Transduction. Transcription Factors / biosynthesis. Transcription Factors / genetics. Tumor Cells, Cultured. Up-Regulation

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  • (PMID = 12060673.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; 0 / Heat-Shock Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 73666-84-9 / tetrocarcin A; EC 3.4.22.- / Caspases
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21. Zhou P, Teruya-Feldstein J, Lu P, Fleisher M, Olshen A, Comenzo RL: Calreticulin expression in the clonal plasma cells of patients with systemic light-chain (AL-) amyloidosis is associated with response to high-dose melphalan. Blood; 2008 Jan 15;111(2):549-57
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  • In high doses with stem-cell transplantation, melphalan is an effective but toxic therapy for patients with systemic light-chain (AL-) amyloidosis, a protein deposition and monoclonal plasma cell disease.
  • Calreticulin is a pleiotropic calcium-binding protein found in the endoplasmic reticulum and the nucleus whose overexpression is associated with increased sensitivity to apoptotic stimuli.
  • Real-time PCR and immunohistochemical staining also showed that expression of calreticulin was higher in the plasma cells of those with a complete response.
  • Furthermore, wild-type murine embryonic fibroblasts were significantly more sensitive to melphalan than calreticulin knock-out murine embryonic fibroblasts.
  • These data have important implications for understanding the activity of melphalan in plasma-cell diseases and support further investigation of calreticulin and its modulation in patients with systemic AL-amyloidosis receiving high-dose melphalan.
  • [MeSH-major] Amyloidosis / metabolism. Endoplasmic Reticulum / metabolism. Immunoglobulin Light Chains. Melphalan / administration & dosage. Myeloablative Agonists / administration & dosage. Plasma Cells / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Calreticulin / biosynthesis. Calreticulin / genetics. Cell Line. Embryo, Mammalian / metabolism. Embryo, Mammalian / pathology. Female. Fibroblasts / metabolism. Fibroblasts / pathology. Gene Expression Regulation / drug effects. Gene Expression Regulation / genetics. Humans. Immunohistochemistry. Male. Mice. Mice, Knockout. Reverse Transcriptase Polymerase Chain Reaction. Stem Cell Transplantation. Transplantation, Autologous

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  • [Cites] Ann Intern Med. 2004 Jan 20;140(2):85-93 [14734330.001]
  • [Cites] Bone Marrow Transplant. 2004 Feb;33(3):259-69 [14647243.001]
  • [Cites] J Intern Med. 2004 Feb;255(2):159-78 [14746554.001]
  • [Cites] Nat Struct Mol Biol. 2004 Feb;11(2):149-56 [14730354.001]
  • [Cites] J Cell Sci. 2004 Aug 1;117(Pt 17):3725-34 [15286174.001]
  • [Cites] Clin Chem. 2005 May;51(5):805-7 [15855664.001]
  • [Cites] Cancer Res. 2005 May 1;65(9):3828-36 [15867381.001]
  • [Cites] FEBS Lett. 2005 Jun 13;579(15):3287-96 [15943973.001]
  • [Cites] Acta Biochim Pol. 2005;52(2):381-95 [15933766.001]
  • [Cites] J Clin Oncol. 2005 Jul 1;23(19):4381-9 [15883412.001]
  • [Cites] Am J Hematol. 2005 Aug;79(4):319-28 [16044444.001]
  • [Cites] Int Rev Cytol. 2005;245:91-121 [16125546.001]
  • [Cites] Bone Marrow Transplant. 2005 Oct;36(7):597-600 [16044137.001]
  • [Cites] Cell. 2005 Oct 21;123(2):321-34 [16239148.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11704-11 [16357182.001]
  • [Cites] Annu Rev Med. 2006;57:223-41 [16409147.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):937-44 [16418495.001]
  • [Cites] Blood. 2006 Apr 1;107(7):2846-54 [16339401.001]
  • [Cites] J Biosci. 2006 Mar;31(1):137-55 [16595883.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3378-83 [16397135.001]
  • [Cites] Cytokine. 2006 Mar 7;33(5):264-73 [16574426.001]
  • [Cites] Mol Cell Proteomics. 2006 Jun;5(6):1033-44 [16522924.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8662-71 [16951181.001]
  • [Cites] Cytogenet Genome Res. 2006;115(1):10-5 [16974078.001]
  • [Cites] Nat Med. 2007 Jan;13(1):54-61 [17187072.001]
  • [Cites] Nat Biotechnol. 2007 Feb;25(2):192-3 [17287754.001]
  • [Cites] J Cell Biol. 2000 Aug 21;150(4):731-40 [10952999.001]
  • [Cites] Amyloid. 2000 Sep;7(3):200-11 [11019861.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):669-78 [11544272.001]
  • [Cites] J Natl Cancer Inst. 2001 Oct 3;93(19):1473-8 [11584063.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):173-7 [11773626.001]
  • [Cites] Blood. 2002 Jul 1;100(1):224-9 [12070031.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(16):5793-800 [12138190.001]
  • [Cites] Biochem J. 2002 Sep 1;366(Pt 2):585-94 [12014989.001]
  • [Cites] Mutagenesis. 2002 Nov;17(6):483-7 [12435845.001]
  • [Cites] Cell Calcium. 2002 Nov-Dec;32(5-6):269-78 [12543089.001]
  • [Cites] J Proteome Res. 2002 Sep-Oct;1(5):435-42 [12645915.001]
  • [Cites] Biochim Biophys Acta. 2003 Jun 17;1641(1):1-12 [12788224.001]
  • [Cites] Mol Cancer Ther. 2003 Jul;2(7):633-40 [12883036.001]
  • [Cites] N Engl J Med. 2003 Aug 7;349(6):583-96 [12904524.001]
  • [Cites] Br J Haematol. 2003 Sep;122(5):728-44 [12930383.001]
  • [Cites] Genome Biol. 2003;4(10):R70 [14519205.001]
  • [Cites] Clin Cancer Res. 2003 Oct 1;9(12):4465-74 [14555520.001]
  • [Cites] Am J Clin Pathol. 2003 Oct;120(4):610-6 [14560572.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7900-6 [14633719.001]
  • [Cites] Mutat Res. 2003 Oct 29;531(1-2):231-51 [14637258.001]
  • [Cites] Blood. 2004 Jan 1;103(1):20-32 [12969978.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5504-10 [15289361.001]
  • [Cites] DNA Repair (Amst). 2004 Nov 2;3(11):1389-407 [15380096.001]
  • [Cites] Cancer Res. 1987 Mar 15;47(6):1542-6 [3815354.001]
  • [Cites] J Natl Compr Canc Netw. 2007 Feb;5(2):179-87 [17335687.001]
  • [Cites] Br J Haematol. 2007 Oct;139(2):224-33 [17897298.001]
  • [Cites] Biochem J. 1999 Dec 1;344 Pt 2:281-92 [10567207.001]
  • [Cites] Leuk Lymphoma. 2000 Apr;37(3-4):245-58 [10752977.001]
  • [Cites] Biochem J. 2000 May 15;348 Pt 1:1-13 [10794707.001]
  • [Cites] Cancer Res. 1988 Apr 1;48(7):1972-6 [3349471.001]
  • [Cites] Hematol Oncol. 1988 Apr-Jun;6(2):173-9 [3292375.001]
  • [Cites] Blood. 1989 Aug 15;74(3):1108-11 [2752156.001]
  • [Cites] J Clin Oncol. 1994 Jan;12(1):194-205 [8270977.001]
  • [Cites] Mayo Clin Proc. 1994 Jul;69(7):684-90 [8015335.001]
  • [Cites] Cancer Res. 1994 Aug 15;54(16):4313-20 [8044778.001]
  • [Cites] J Clin Oncol. 1995 Jul;13(7):1786-99 [7602368.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2801-6 [8839879.001]
  • [Cites] Nucleic Acids Res. 1997 Mar 15;25(6):1211-8 [9092631.001]
  • [Cites] N Engl J Med. 1997 Sep 25;337(13):898-909 [9302305.001]
  • [Cites] Biochemistry. 1998 Apr 14;37(15):5211-9 [9548752.001]
  • [Cites] Biochem J. 1999 Feb 1;337 ( Pt 3):559-66 [9895302.001]
  • [Cites] Br J Haematol. 2005 Mar;128(5):636-44 [15725085.001]
  • [Cites] Br J Haematol. 2004 Feb;124(3):309-14 [14717777.001]
  • (PMID = 17982021.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / PHS HHS / / R03-002174
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calreticulin; 0 / Immunoglobulin Light Chains; 0 / Myeloablative Agonists; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ PMC2200859
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22. Lust S, Vanhoecke B, VAN Gele M, Boelens J, VAN Melckebeke H, Kaileh M, Vanden Berghe W, Haegeman G, Philippé J, Bracke M, Offner F: Xanthohumol activates the proapoptotic arm of the unfolded protein response in chronic lymphocytic leukemia. Anticancer Res; 2009 Oct;29(10):3797-805
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  • BACKGROUND: Chronic lymphocytic leukemia (CLL) is an incurable disease with a natural history of increasing resistance to chemotherapy.
  • A novel approach to overcome chemotherapy resistance may be targeting the endoplasmic reticulum (ER).
  • PATIENTS AND METHODS: The involvement of the unfolded protein response (UPR) in the cell killing effect of xanthohumol (X) was examined in 18 patient samples.
  • The proapoptotic outcome was further demonstrated by the up-regulation of CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), down-regulation of myeloid cell leukemia 1 (Mcl-1) and B-cell lymphoma 2 (Bcl-2), cleavage of poly-(ADP)-ribose polymerase (PARP) and processing of caspase-3, -4 and -9.
  • [MeSH-major] Apoptosis / drug effects. Flavonoids / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Propiophenones / pharmacology. Unfolded Protein Response / drug effects

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  • (PMID = 19846911.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / ATF6 protein, human; 0 / Activating Transcription Factor 6; 0 / Amino Acid Chloromethyl Ketones; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / Flavonoids; 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / Propiophenones; 0 / Proteasome Inhibitors; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 0 / molecular chaperone GRP78; EC 2.7.1.- / ERN2 protein, human; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / eIF-2 Kinase; EC 3.1.- / Endoribonucleases; EC 3.4.22.- / Caspases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; T4467YT1NT / xanthohumol
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23. Dasmahapatra G, Lembersky D, Rahmani M, Kramer L, Friedberg J, Fisher RI, Dent P, Grant S: Bcl-2 antagonists interact synergistically with bortezomib in DLBCL cells in association with JNK activation and induction of ER stress. Cancer Biol Ther; 2009 May;8(9):808-19
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  • Mechanisms underlying interactions between the proteasome inhibitor bortezomib and small molecule Bcl-2 antagonists were examined in GC- and ABC-type human DLBCL (diffuse lymphocytic B-cell lymphoma) cells.
  • Concomitant or sequential exposure to non- or minimally toxic concentrations of bortezomib or other proteasome inhibitors and either HA14-1 or gossypol resulted in a striking increase in Bax/Bak conformational change/translocation, cytochrome c release, caspase activation and synergistic induction of apoptosis in both GC- and ABC-type cells.
  • Pharmacologic or genetic (e.g., shRNA knockdown) interruption of JNK signaling attenuated HA14-1/bortezomib lethality and ER stress induction.
  • They also raise the possibility that such a strategy may be effective in different DLBCL sub-types (e.g., GC- or ABC), and in bortezomib-resistant disease.

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  • [Cites] Science. 2000 May 5;288(5467):870-4 [10797012.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Cell. 2000 Jul 7;102(1):33-42 [10929711.001]
  • [Cites] Cell. 2000 Jul 7;102(1):43-53 [10929712.001]
  • [Cites] Blood. 2001 Aug 15;98(4):945-51 [11493437.001]
  • [Cites] Genes Dev. 2001 Nov 15;15(22):2922-33 [11711427.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):10244-50 [11786558.001]
  • [Cites] Genes Dev. 2002 Jun 1;16(11):1345-55 [12050113.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] J Biol Chem. 2002 Nov 15;277(46):43730-4 [12223490.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):15920-5 [12446838.001]
  • [Cites] N Engl J Med. 2003 Jun 26;348(26):2609-17 [12826635.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3637-45 [12839953.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):33714-23 [12821677.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1180-6 [12937412.001]
  • [Cites] Leukemia. 2003 Oct;17(10):2036-45 [14513055.001]
  • [Cites] Cancer Sci. 2004 Feb;95(2):176-80 [14965369.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(22):9695-704 [15509775.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2244-51 [8630384.001]
  • [Cites] J Biol Chem. 1996 Mar 29;271(13):7440-4 [8631771.001]
  • [Cites] Nature. 1999 Feb 4;397(6718):441-6 [9989411.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8746-53 [15574786.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):667-75 [15613697.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10326-32 [15611068.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1294-305 [15901672.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11658-66 [16357177.001]
  • [Cites] Blood. 2006 Jan 1;107(1):232-40 [16166589.001]
  • [Cites] Mol Pharmacol. 2006 Jan;69(1):288-98 [16219908.001]
  • [Cites] Cancer Cell. 2006 May;9(5):351-65 [16697956.001]
  • [Cites] Science. 2000 Jan 28;287(5453):664-6 [10650002.001]
  • [Cites] Mol Cell. 2000 May;5(5):897-904 [10882126.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2906-16 [18591385.001]
  • [Cites] J Biol Chem. 2006 Jun 30;281(26):17599-611 [16617056.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068.001]
  • [Cites] Blood. 2007 May 15;109(10):4441-9 [17227835.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5430-8 [17332241.001]
  • [Cites] Mol Cell Biol. 2007 Aug;27(15):5499-513 [17548474.001]
  • [Cites] Cell Death Differ. 2007 Sep;14(9):1711-3 [17572662.001]
  • [Cites] J Biol Chem. 2007 Oct 5;282(40):29368-74 [17702754.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2765-75 [18057228.001]
  • [Cites] Cell Death Differ. 2008 May;15(5):820-30 [18309326.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3413-20 [18451169.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3421-8 [18451170.001]
  • [Cites] Cell Death Differ. 2008 Jun;15(6):977-87 [18369371.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):5363-9 [18593938.001]
  • [Cites] Mol Cancer Ther. 2008 Jul;7(7):2192-202 [18645028.001]
  • [CommentIn] Cancer Biol Ther. 2009 May;8(9):820-2 [19458484.001]
  • [CommentIn] NIH Guide Grants Contracts. 2015 Dec 18;:NOT-OD-16-040 [26693581.001]
  • [CommentIn] Fed Regist. 2015 Dec 10;80(237):76703-76704 [27737268.001]
  • (PMID = 19270531.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA130805-01A1; United States / NCI NIH HHS / CA / CA100866-06; United States / NCI NIH HHS / CA / CA093738-07; United States / NCI NIH HHS / CA / P50 CA130805-01A1; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA100866-06; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / R01 CA093738-07; United States / NCI NIH HHS / CA / CA 63753; United States / NCI NIH HHS / CA / CA 100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / 1P50 CA 130805; United States / NCI NIH HHS / CA / CA063753-14; United States / NCI NIH HHS / CA / R01 CA063753-14; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / CA 93738; United States / NCI NIH HHS / CA / R01 CA150214
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzopyrans; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / Protease Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; 69G8BD63PP / Bortezomib; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS209958; NLM/ PMC2902989
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24. Takahashi N, Tamagawa K, Shimizu K, Fukui T, Maitani Y: Effects on M5076-hepatic metastasis of retinoic acid and N-(4-hydroxyphenyl) retinamide, fenretinide entrapped in SG-liposomes. Biol Pharm Bull; 2003 Jul;26(7):1060-3
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  • Retinoic acid (RA), a potent inducer of cell differentiation, and N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide), a potent inducer of apoptosis, are well known as anticancer agents that are administered orally to patients for leukemia, breast and prostate cancer, respectively.
  • In mice implanted with M5076 cells, murine reticulum cell sarcoma survival times were prolonged by i.v. treatment of RA and 4-HPR entrapped in liposomes containing soybean-derived sterylglucoside mixture (SG), which accumulates in liver.
  • These results indicate that RA and 4-HPR in SG-liposomes exhibit anticancer efficacy on metastatic cancers, and may have great potential for clinical use in the treatment of various cancers.
  • [MeSH-major] Cholestenes / administration & dosage. Fenretinide / administration & dosage. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / secondary. Tretinoin / administration & dosage
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Evaluation, Preclinical / methods. Female. Liposomes. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Mice. Mice, Inbred C57BL. Xenograft Model Antitumor Assays / methods

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  • (PMID = 12843642.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cholestenes; 0 / Liposomes; 0 / soy derived sterylglucoside mixture; 187EJ7QEXL / Fenretinide; 5688UTC01R / Tretinoin
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25. Wang L, Woods KW, Li Q, Barr KJ, McCroskey RW, Hannick SM, Gherke L, Credo RB, Hui YH, Marsh K, Warner R, Lee JY, Zielinski-Mozng N, Frost D, Rosenberg SH, Sham HL: Potent, orally active heterocycle-based combretastatin A-4 analogues: synthesis, structure-activity relationship, pharmacokinetics, and in vivo antitumor activity evaluation. J Med Chem; 2002 Apr 11;45(8):1697-711
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  • Cytotoxicities of the heterocycle-based CA-4 analogues were evaluated against NCI-H460 and HCT-15 cancer cell lines.
  • Evaluation of 24h and 25f against murine M5076 reticulum sarcoma in mice revealed that both compounds were orally efficacious with an increase in life span of 38.5 and 40.5%, respectively.
  • [MeSH-minor] Administration, Oral. Animals. Biopolymers. Cell Division / drug effects. Dogs. Drug Screening Assays, Antitumor. Haplorhini. Humans. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Mice. Mice, Nude. Neoplasm Transplantation. Rats. Structure-Activity Relationship. Transplantation, Heterologous. Tubulin / chemistry. Tumor Cells, Cultured

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  • [ErratumIn] J Med Chem 2002 Oct 24;45(22):4946
  • (PMID = 11931625.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-methyl-4-(3,4,5-trimethoxyphenyl)-5-(3,4-bis(2-(methylamino)ethyl)phenyl)imidazole; 0 / 1-methyl-4-(3,4,5-trimethoxyphenyl)-5-(3-amino-4-methoxyphenyl)imidazole; 0 / Antineoplastic Agents; 0 / Biopolymers; 0 / Imidazoles; 0 / Stilbenes; 0 / Tubulin; I5590ES2QZ / fosbretabulin
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26. Okawa Y, Hideshima T, Ikeda H, Raje N, Vallet S, Kiziltepe T, Yasui H, Enatsu S, Pozzi S, Breitkreutz I, Cirstea D, Santo L, Richardson P, Anderson KC: Fatty acid synthase is a novel therapeutic target in multiple myeloma. Br J Haematol; 2008 May;141(5):659-71
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  • [Title] Fatty acid synthase is a novel therapeutic target in multiple myeloma.
  • Cerulenin triggered growth inhibition in both MM cell lines and MM patient cells, and overcame the survival and growth advantages conferred by interleukin-6, insulin-like growth factor-1, and bone marrow stromal cells.
  • It induced apoptosis in MM cell lines with only modest activation of caspase -8, -9, -3 and PARP; moreover, the pan-caspase inhibitor Z-VAD-FMK did not inhibit Cerulenin-induced apoptosis and cell death.
  • In addition, treatment of MM cells with Cerulenin primarily up-regulated apoptosis-inducing factor/endonuclease G, mediators of caspase-independent apoptosis.
  • Importantly, Cerulenin induced endoplasmic reticulum stress response via up-regulation of the Grp78/IRE1alpha/JNK pathway.
  • This report demonstrated that inhibition of FAS has anti-tumour activity against MM cells, suggesting that it represents a novel therapeutic target in MM.

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  • [Cites] Cancer Res. 2006 Jun 15;66(12):5977-80 [16778164.001]
  • [Cites] Immunol Cell Biol. 2006 Oct;84(5):448-54 [16942488.001]
  • [Cites] EMBO Rep. 2006 Sep;7(9):880-5 [16953201.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1262-9 [17283163.001]
  • [Cites] Cancer Res. 2007 Feb 15;67(4):1680-8 [17308109.001]
  • [Cites] Curr Opin Cell Biol. 2007 Apr;19(2):142-9 [17303404.001]
  • [Cites] Nat Rev Cancer. 2007 Aug;7(8):585-98 [17646864.001]
  • [Cites] Cell. 2000 Oct 13;103(2):239-52 [11057897.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):153-7 [11205903.001]
  • [Cites] Cell Death Differ. 2000 Dec;7(12):1244-52 [11175262.001]
  • [Cites] Prostate. 2001 May 1;47(2):102-10 [11340632.001]
  • [Cites] Curr Opin Cell Biol. 2006 Aug;18(4):444-52 [16781856.001]
  • [Cites] Oncogene. 2001 Apr 30;20(19):2365-77 [11402333.001]
  • [Cites] Oncogene. 2001 Apr 30;20(19):2401-12 [11402336.001]
  • [Cites] Oncogene. 2001 Sep 20;20(42):5991-6000 [11593406.001]
  • [Cites] Eur J Biochem. 2002 Jan;269(1):139-47 [11784307.001]
  • [Cites] J Biol Chem. 2002 Jan 18;277(3):1957-61 [11709549.001]
  • [Cites] J Cell Biol. 2002 Apr 29;157(3):455-68 [11980920.001]
  • [Cites] Cancer Res. 2007 Aug 1;67(15):7327-34 [17671202.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):763-77 [17882277.001]
  • [Cites] Science. 2000 Jan 28;287(5453):664-6 [10650002.001]
  • [Cites] Nutrition. 2000 Mar;16(3):202-8 [10705076.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3450-4 [10716717.001]
  • [Cites] FASEB J. 2000 Apr;14(5):729-39 [10744629.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5454-68 [10891486.001]
  • [Cites] Oncogene. 2000 Sep 7;19(38):4319-27 [10980607.001]
  • [Cites] Blood. 2000 Nov 1;96(9):2943-50 [11049970.001]
  • [Cites] Oncogene. 2002 Aug 22;21(37):5673-83 [12173037.001]
  • [Cites] Cell Death Differ. 2002 Sep;9(9):1017-25 [12181752.001]
  • [Cites] Mol Cancer Ther. 2002 Aug;1(10):851-60 [12492118.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Mar 21;302(4):898-903 [12646257.001]
  • [Cites] Nat Immunol. 2003 May;4(5):416-23 [12719731.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3799-804 [12839976.001]
  • [Cites] Eur J Neurosci. 2003 Aug;18(3):473-85 [12911744.001]
  • [Cites] Mol Cancer Res. 2003 Aug;1(10):707-15 [12939396.001]
  • [Cites] Mol Cancer Ther. 2003 Nov;2(11):1155-64 [14617789.001]
  • [Cites] J Cell Biochem. 2004 Jan 1;91(1):47-53 [14689581.001]
  • [Cites] J Biol Chem. 2004 Feb 13;279(7):5661-6 [14594800.001]
  • [Cites] Trends Biochem Sci. 2004 Mar;29(3):152-8 [15003273.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2070-5 [15026345.001]
  • [Cites] Cancer Cell. 2004 Mar;5(3):221-30 [15050914.001]
  • [Cites] Trends Cell Biol. 2004 Apr;14(4):184-93 [15066636.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2766-73 [15077140.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2785-96 [15077142.001]
  • [Cites] Curr Treat Options Oncol. 2004 Jun;5(3):227-38 [15115651.001]
  • [Cites] Cell Death Differ. 2004 Jun;11(6):591-5 [15017385.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1500-2 [15131264.001]
  • [Cites] Cancer Res. 2004 Jun 15;64(12):4286-93 [15205343.001]
  • [Cites] Semin Cancer Biol. 2004 Aug;14(4):283-94 [15219621.001]
  • [Cites] Curr Opin Pharmacol. 2004 Aug;4(4):333-9 [15251125.001]
  • [Cites] Blood. 2004 Aug 1;104(3):607-18 [15090448.001]
  • [Cites] Mol Cell. 2004 Sep 10;15(5):753-66 [15350219.001]
  • [Cites] J Cell Biol. 2004 Oct 11;167(1):35-41 [15466483.001]
  • [Cites] N Engl J Med. 2004 Oct 28;351(18):1860-73 [15509819.001]
  • [Cites] Biochem Biophys Res Commun. 1972 Aug 7;48(3):649-56 [4625866.001]
  • [Cites] Bacteriol Rev. 1976 Sep;40(3):681-97 [791237.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] Biochemistry. 1989 May 30;28(11):4523-30 [2669958.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):745-51 [8631008.001]
  • [Cites] Cancer Res. 1996 Jun 15;56(12):2745-7 [8665507.001]
  • [Cites] EMBO J. 1997 Apr 1;16(7):1695-709 [9130714.001]
  • [Cites] Mol Biol Cell. 1997 Sep;8(9):1805-14 [9307975.001]
  • [Cites] Clin Cancer Res. 1997 Nov;3(11):2115-20 [9815604.001]
  • [Cites] Blood. 1999 Mar 1;93(5):1658-67 [10029595.001]
  • [Cites] J Biol Chem. 1999 Mar 5;274(10):6031-4 [10037680.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4188-93 [15319277.001]
  • [Cites] J Biol Chem. 2004 Dec 10;279(50):52007-15 [15466475.001]
  • [Cites] Nat Struct Mol Biol. 2005 Mar;12(3):225-32 [15711565.001]
  • [Cites] Oncogene. 2005 Sep 1;24(38):5888-96 [15940263.001]
  • [Cites] J Clin Invest. 2005 Oct;115(10):2656-64 [16200199.001]
  • [Cites] Leuk Lymphoma. 2006 Mar;47(3):531-9 [16396777.001]
  • [Cites] J Biol Chem. 2006 Mar 17;281(11):7260-70 [16407291.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5934-40 [16740734.001]
  • [RetractionIn] Cotter F. Br J Haematol. 2008 May;141(5):659 [20712068.001]
  • (PMID = 18410446.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA078378; United States / NCI NIH HHS / CA / R01 CA050947
  • [Publication-type] Journal Article; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD95; 17397-89-6 / Cerulenin; EC 2.3.1.85 / Fatty Acid Synthases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ PMC2408665
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27. Zhang L, Littlejohn JE, Cui Y, Cao X, Peddaboina C, Smythe WR: Characterization of bortezomib-adapted I-45 mesothelioma cells. Mol Cancer; 2010;9:110
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  • BACKGROUND: Bortezomib, a proteasome-specific inhibitor, has emerged as a promising cancer therapeutic agent.
  • However, development of resistance to bortezomib may pose a challenge to effective anticancer therapy.
  • Therefore, characterization of cellular mechanisms involved in bortezomib resistance and development of effective strategies to overcome this resistance represent important steps in the advancement of bortezomib-mediated cancer therapy.
  • RESULTS: The present study reports the development of I-45-BTZ-R, a bortezomib-resistant cell line, from the bortezomib-sensitive mesothelioma cell line I-45.
  • I-45-BTZ-R cells showed no cross-resistance to the chemotherapeutic drugs cisplatin, 5-fluorouracil, and doxorubicin.
  • Further studies revealed that relatively low doses of bortezomib did not induce an unfolded protein response (UPR) in the bortezomib-adapted cells, while higher doses induced UPR with concomitant cell death, as evidenced by higher expression of the mitochondrial chaperone protein Bip and the endoplasmic reticulum (ER) stress-related pro-apoptotic protein CHOP.
  • CONCLUSION: These results suggest that UPR evasion, together with reduced pro-apoptotic gene induction, accounts for bortezomib resistance in the bortezomib-adapted mesothelioma cell line I-45-BTZ-R.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology. Drug Resistance, Neoplasm / genetics. Mesothelioma / metabolism. Pyrazines / pharmacology. Unfolded Protein Response / drug effects
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis Regulatory Proteins / drug effects. Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Bortezomib. Cell Line, Tumor. Cell Separation. Flow Cytometry. Gene Expression / drug effects. Humans. Oligopeptides / genetics. Oligopeptides / metabolism. Proteasome Endopeptidase Complex / drug effects. Proteasome Endopeptidase Complex / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Small Interfering. Transcription Factor CHOP / genetics. Transcription Factor CHOP / metabolism. Transfection

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  • [Cites] Cell Death Differ. 2006 Mar;13(3):363-73 [16397583.001]
  • [Cites] Leukemia. 2009 Jun;23(6):1098-105 [19225532.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4907-16 [16507771.001]
  • [Cites] Cancer Biol Ther. 2006 Jul;5(7):745-8 [16861900.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5942-51 [17908991.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3557-60 [17690257.001]
  • [Cites] J Cell Biochem. 2008 Jan 1;103(1):270-83 [17516511.001]
  • [Cites] Clin Cancer Res. 2008 Mar 15;14(6):1649-57 [18347166.001]
  • [Cites] Mol Cancer Ther. 2008 Jun;7(6):1647-55 [18566236.001]
  • [Cites] Clin Lymphoma Myeloma. 2008 Jun;8(3):140-5 [18650176.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2489-99 [18565852.001]
  • [Cites] Exp Hematol. 2008 Oct;36(10):1278-84 [18562081.001]
  • [Cites] Drug Resist Updat. 2008 Aug-Oct;11(4-5):164-79 [18818117.001]
  • [Cites] J Biol Chem. 2000 Aug 18;275(33):25255-61 [10837489.001]
  • [Cites] Nat Cell Biol. 2001 Mar;3(3):283-8 [11231578.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3071-6 [11306489.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):16639-47 [11872748.001]
  • [Cites] Gene Ther. 2002 Sep;9(18):1262-70 [12215894.001]
  • [Cites] N Engl J Med. 2003 Jun 26;348(26):2609-17 [12826635.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6174-7 [14559800.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7338-44 [14612532.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):349-60 [15122206.001]
  • [Cites] Cancer Cell. 2004 May;5(5):417-21 [15144949.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(22):9695-704 [15509775.001]
  • [Cites] Nature. 1998 Apr 9;392(6676):618-22 [9560160.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6282-93 [16024630.001]
  • [Cites] Nat Rev Drug Discov. 2006 Feb;5(2):107-14 [16518378.001]
  • (PMID = 20482802.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Bax-inhibiting peptide, BIP; 0 / Boronic Acids; 0 / DDIT3 protein, human; 0 / Oligopeptides; 0 / PMAIP1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / RNA, Small Interfering; 147336-12-7 / Transcription Factor CHOP; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2882347
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28. Schewe DM, Aguirre-Ghiso JA: Inhibition of eIF2alpha dephosphorylation maximizes bortezomib efficiency and eliminates quiescent multiple myeloma cells surviving proteasome inhibitor therapy. Cancer Res; 2009 Feb 15;69(4):1545-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of eIF2alpha dephosphorylation maximizes bortezomib efficiency and eliminates quiescent multiple myeloma cells surviving proteasome inhibitor therapy.
  • The proteasome inhibitor bortezomib (Velcade) effectively eradicates multiple myeloma (MM) cells, partly by activating endoplasmic reticulum (ER) stress apoptotic signaling.
  • Thus, we hypothesized that bortezomib therapy could induce quiescence and survival of residual MM cells, contributing to disease recurrence.
  • Here, we report that in MM cells, proteasome inhibition with MG-132 or bortezomib results in a surviving cell fraction that enters a prolonged quiescent state (G(0)-G(1) arrest).
  • The bortezomib-surviving quiescent fraction could be eradicated by a simultaneous or sequential combination therapy with salubrinal, an inhibitor of GADD34-PP1C phosphatase complex, and, in consequence, eIF2alpha dephosphorylation.
  • Our data indicate that bortezomib can induce growth arrest in therapy-surviving MM cells and that attenuation of eIF2alpha phosphorylation contributes to this survival.
  • Thus, strategies that maintain eIF2alpha in a hyperphosphorylated state may be a novel therapeutic approach to maximize bortezomib-induced apoptosis and reduce residual disease and recurrences in this type of cancer.

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  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12625-30 [11035797.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2489-99 [18565852.001]
  • [Cites] Cancer Res. 2003 Apr 1;63(7):1684-95 [12670923.001]
  • [Cites] J Clin Oncol. 2004 Jun 1;22(11):2108-21 [15169797.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(22):9695-704 [15509775.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8505-10 [10411905.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):344-54 [15531918.001]
  • [Cites] Science. 2005 Feb 11;307(5711):935-9 [15705855.001]
  • [Cites] Mol Cancer Ther. 2005 Apr;4(4):686-92 [15827343.001]
  • [Cites] Leuk Lymphoma. 2006 Mar;47(3):531-9 [16396777.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1702-11 [16452230.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1017-27 [16617327.001]
  • [Cites] J Biol Chem. 2000 Mar 31;275(13):9314-23 [10734073.001]
  • [Cites] Methods Cell Biol. 2001;63:375-98 [11060850.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4907-16 [16507771.001]
  • [Cites] J Biol Chem. 2007 Feb 9;282(6):3989-97 [17158450.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3496-9 [17440054.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1337-49 [17604722.001]
  • [Cites] PLoS One. 2007;2(7):e615 [17637831.001]
  • [Cites] FEBS Lett. 2007 Jul 31;581(19):3758-69 [17559840.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2641-9 [17525289.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9809-16 [17942911.001]
  • [Cites] Trends Biochem Sci. 2007 Oct;32(10):469-76 [17920280.001]
  • [Cites] Cancer Res. 2008 Jan 15;68(2):498-505 [18199545.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1654-64 [18006697.001]
  • [Cites] Int J Cancer. 2008 Jul 1;123(1):85-8 [18386815.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3260-8 [18451152.001]
  • [Cites] Methods Enzymol. 2008;442:395-419 [18662581.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jul 29;105(30):10519-24 [18650380.001]
  • [Cites] J Cell Biol. 2001 Mar 5;152(5):997-1006 [11238455.001]
  • (PMID = 19190324.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109182-02; United States / NCI NIH HHS / CA / R01 CA109182-01A1; United States / NCI NIH HHS / CA / CA109182; United States / NCI NIH HHS / CA / R01 CA109182-05; United States / NCI NIH HHS / CA / R01 CA109182; United States / NCI NIH HHS / CA / R01 CA109182-04; United States / NCI NIH HHS / CA / R01 CA109182-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Eukaryotic Initiation Factor-2; 0 / Leupeptins; 0 / Pyrazines; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 69G8BD63PP / Bortezomib
  • [Other-IDs] NLM/ NIHMS86032; NLM/ PMC2726651
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29. Hernández-Espinosa D, Miñano A, Martínez C, Pérez-Ceballos E, Heras I, Fuster JL, Vicente V, Corral J: L-asparaginase-induced antithrombin type I deficiency: implications for conformational diseases. Am J Pathol; 2006 Jul;169(1):142-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] L-asparaginase-induced antithrombin type I deficiency: implications for conformational diseases.
  • Interestingly, l-asparaginase treatment of acute lymphoblastic leukemia patients causes severe deficiency in the serpin antithrombin.
  • We studied the consequences of this drug on antithrombin levels, activity, conformation, and immunohistological and ultrastructural features in plasma from acute lymphoblastic leukemia patients, HepG2 cells, and plasma and livers from mice treated with this drug.
  • Additionally, we evaluated intracellular deposition of alpha1-antitrypsin. l-Asparaginase did not affect functional or conformational parameters of mature antithrombin; however, patients and mice displayed severe type I deficiency with no abnormal conformations of circulating antithrombin.
  • These effects were explained by the intracellular retention of antithrombin, forming aggregates within dilated endoplasmic reticulum cisterns.
  • This is the first report of a conformational drug-associated effect on serpins without genetic factors involved. l-Asparaginase treatment induces severe, acquired, and transient type I deficiency of antithrombin (and alpha1-antitrypsin) with intracellular accumulation of the nascent molecule, increasing the risk of thrombosis.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Asparaginase / adverse effects. Fibrin / chemistry. Fibrin / drug effects
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Line, Tumor. Electrophoresis, Polyacrylamide Gel. Factor Xa / drug effects. Factor Xa / metabolism. Humans. Liver / chemistry. Liver / metabolism. Male. Mice. Microscopy, Electron, Transmission. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Conformation. alpha 1-Antitrypsin / drug effects. alpha 1-Antitrypsin / metabolism

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  • [Cites] Haematologica. 2005 Feb;90(2):238-46 [15710578.001]
  • [Cites] Cancer. 1982 Aug 1;50(3):451-6 [7046902.001]
  • [Cites] J Thromb Haemost. 2005 Sep;3(9):1985-92 [16102104.001]
  • [Cites] Blood. 1999 Nov 15;94(10):3388-96 [10552948.001]
  • [Cites] Leuk Res. 2000 Jul;24(7):559-65 [10867129.001]
  • [Cites] J Clin Invest. 2000 Oct;106(7):873-8 [11018075.001]
  • [Cites] Genome Res. 2000 Dec;10(12):1845-64 [11116082.001]
  • [Cites] Thromb Haemost. 2001 Jul;86(1):14-22 [11487000.001]
  • [Cites] Exp Mol Pathol. 2001 Dec;71(3):241-6 [11733949.001]
  • [Cites] N Engl J Med. 2002 Jan 3;346(1):45-53 [11778003.001]
  • [Cites] Hepatology. 2002 May;35(5):1053-62 [11981755.001]
  • [Cites] Nat Rev Genet. 2002 Oct;3(10):759-68 [12360234.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2529-33 [12517808.001]
  • [Cites] J Biol Chem. 2003 Apr 25;278(17):15116-22 [12578831.001]
  • [Cites] J Neurochem. 2003 Jun;85(5):1117-25 [12753071.001]
  • [Cites] Clin Chem. 2003 Oct;49(10):1710-1 [14500607.001]
  • [Cites] Biochem Soc Symp. 2003;(70):163-78 [14587291.001]
  • [Cites] J Lab Clin Med. 2003 Nov;142(5):298-305 [14647033.001]
  • [Cites] Electrophoresis. 2003 Dec;24(24):4282-90 [14679575.001]
  • [Cites] Thromb Res. 1983 Feb 15;29(4):437-42 [6857592.001]
  • [Cites] Blood. 1994 Jan 15;83(2):386-91 [8286739.001]
  • [Cites] Blood Coagul Fibrinolysis. 1994 Jan;5 Suppl 1:S24-36; discussion S59-64 [8186353.001]
  • [Cites] J Clin Invest. 1994 Dec;94(6):2265-74 [7989582.001]
  • [Cites] Int J Clin Lab Res. 1995;25(3):146-8 [8562977.001]
  • [Cites] Biochem J. 1997 May 15;324 ( Pt 1):1-18 [9164834.001]
  • [Cites] Lancet. 1997 Jul 12;350(9071):134-8 [9228977.001]
  • [Cites] Mutat Res. 2005 Jan 6;569(1-2):29-63 [15603751.001]
  • [Cites] J Thromb Haemost. 2004 Dec;2(12):2170-7 [15613023.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):895-9 [14685250.001]
  • [Cites] Thromb Res. 2003;111(6):321-7 [14698648.001]
  • [Cites] Curr Med Chem. 2004 Feb;11(4):491-9 [14965229.001]
  • [Cites] J Gastroenterol. 2004;39(4):391-6 [15168253.001]
  • [Cites] J Bioenerg Biomembr. 2004 Aug;36(4):303-7 [15377862.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1973;39:185-248 [4583638.001]
  • [Cites] Lancet. 1980 Mar 22;1(8169):649-50 [6102647.001]
  • [Cites] Med Pediatr Oncol. 1979;7(4):335-40 [296786.001]
  • [Cites] Curr Protein Pept Sci. 2005 Apr;6(2):197-203 [15853655.001]
  • (PMID = 16816368.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha 1-Antitrypsin; 9001-31-4 / Fibrin; EC 3.4.21.6 / Factor Xa; EC 3.5.1.1 / Asparaginase
  • [Other-IDs] NLM/ PMC1698772
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30. Hertan LM, Koumenis C: Piling up the JNK: drug synergy through ER stress. Cancer Biol Ther; 2009 May;8(9):820-2
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Piling up the JNK: drug synergy through ER stress.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Benzopyrans / pharmacology. Boronic Acids / pharmacology. Endoplasmic Reticulum / enzymology. JNK Mitogen-Activated Protein Kinases / metabolism. Nitriles / pharmacology. Pyrazines / pharmacology
  • [MeSH-minor] Bortezomib. Drug Synergism. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / pharmacology. Humans. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Protease Inhibitors / administration & dosage. Protease Inhibitors / pharmacology. Signal Transduction

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  • [CommentOn] Cancer Biol Ther. 2009 May;8(9):808-19 [19270531.001]
  • (PMID = 19458484.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzopyrans; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / Protease Inhibitors; 0 / Pyrazines; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; 69G8BD63PP / Bortezomib; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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