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1. Tang JL, Lipkowski AW, Specter S: Molecular assessment of the potential combination therapy of cytokines with biphalin and AZT for Friend leukemia virus infection in vitro. Pharmacol Rep; 2008 Mar-Apr;60(2):190-8
Hazardous Substances Data Bank. ZIDOVUDINE .

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  • [Title] Molecular assessment of the potential combination therapy of cytokines with biphalin and AZT for Friend leukemia virus infection in vitro.
  • Biphalin, a dimeric enkephalin analog, is under investigation as a potential, long-lasting medication of pain associated with chronic diseases, like cancer or AIDS.
  • The role of cytokines, and splenocytes in anti-Friend leukemia virus (FLV) activity of biphalin, a synthetic opioid, and AZT was investigated in vitro.
  • In addition, cloned RT from Moloney murine leukemia virus (MMLV) was directly sensitive to inhibition by biphalin.
  • This antiviral activity of splenocytes or cytokines combined with chemotherapy, biphalin, and/or AZT, could be used as a complementary therapy to current approaches for retroviral infection and benefit acquired immunodeficiency syndrome (AIDS) patients.
  • In conclusion, biphalin applied primarily as a new medicine for chronic pain treatment in AIDS patients may play a significant beneficial role as a component of antiviral HIV multidrug therapies.
  • [MeSH-major] Analgesics / therapeutic use. Anti-HIV Agents / therapeutic use. Cytokines / therapeutic use. Enkephalins / therapeutic use. Friend murine leukemia virus. Retroviridae Infections / drug therapy. Zidovudine / therapeutic use
  • [MeSH-minor] Animals. Cells, Cultured. Cloning, Molecular. Drug Combinations. HIV Reverse Transcriptase / antagonists & inhibitors. Interferon-gamma / pharmacology. Interleukin-2 / biosynthesis. Interleukin-2 / genetics. Interleukin-4 / biosynthesis. Interleukin-4 / genetics. Mice. Mice, Inbred BALB C. Spleen / cytology. Spleen / drug effects

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  • (PMID = 18443380.001).
  • [ISSN] 1734-1140
  • [Journal-full-title] Pharmacological reports : PR
  • [ISO-abbreviation] Pharmacol Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Analgesics; 0 / Anti-HIV Agents; 0 / Cytokines; 0 / Drug Combinations; 0 / Enkephalins; 0 / Interleukin-2; 207137-56-2 / Interleukin-4; 4B9XT59T7S / Zidovudine; 82115-62-6 / Interferon-gamma; 83916-01-2 / biphalin; EC 2.7.7.49 / HIV Reverse Transcriptase
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2. Asano Y, Bujor AM, Trojanowska M: The impact of Fli1 deficiency on the pathogenesis of systemic sclerosis. J Dermatol Sci; 2010 Sep;59(3):153-62
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  • A growing body of evidence suggests that deficiency of the transcription factor Fli1 (Friend leukemia integration-1) has a pivotal role in the pathogenesis of SSc.
  • In this article, we review the impact of Fli1 deficiency on the pathogenesis of SSc and discuss a new therapeutic strategy for SSc by targeting the transcription factor Fli1.
  • [MeSH-major] Proto-Oncogene Protein c-fli-1 / metabolism. Scleroderma, Systemic / drug therapy. Scleroderma, Systemic / enzymology
  • [MeSH-minor] Acetylation / drug effects. Animals. Autoimmune Diseases / drug therapy. B-Lymphocytes / drug effects. Benzamides. Collagen Type I / antagonists & inhibitors. Down-Regulation. Drug Therapy, Combination. Epigenesis, Genetic. Extracellular Matrix / drug effects. Fibroblasts / drug effects. Gene Expression / drug effects. Hematopoiesis / drug effects. Humans. Imatinib Mesylate. Macrolides / pharmacology. Mice. Phosphorylation / drug effects. Piperazines / pharmacology. Piperazines / therapeutic use. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Protein Processing, Post-Translational / drug effects. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. T-Lymphocytes / drug effects

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  • [Copyright] Copyright 2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
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  • (PMID = 20663647.001).
  • [ISSN] 1873-569X
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR042334
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzamides; 0 / Collagen Type I; 0 / FLI1 protein, human; 0 / Macrolides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Protein c-fli-1; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS525829; NLM/ PMC3826615
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3. Elkareh J, Periyasamy SM, Shidyak A, Vetteth S, Schroeder J, Raju V, Hariri IM, El-Okdi N, Gupta S, Fedorova L, Liu J, Fedorova OV, Kahaleh MB, Xie Z, Malhotra D, Watson DK, Bagrov AY, Shapiro JI: Marinobufagenin induces increases in procollagen expression in a process involving protein kinase C and Fli-1: implications for uremic cardiomyopathy. Am J Physiol Renal Physiol; 2009 May;296(5):F1219-26
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  • We examined whether the transcription factor Friend leukemia integration-1 (Fli-1) might be involved in this process.
  • Fli-1-knockdown mice demonstrated greater cardiac collagen-1 expression and fibrosis compared with wild-type mice; both developed increased cardiac collagen expression and fibrosis after 5/6 nephrectomy.
  • This translocation was prevented by pharmacological inhibition of phospholipase C, and MBG-induced increases in procollagen-1 expression were prevented with a PKCdelta- but not a PKCalpha-specific inhibitor.
  • Should these findings be confirmed, we speculate that this pathway may represent a therapeutic target for uremic cardiomyopathy as well as other conditions associated with excessive fibrosis.

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  • (PMID = 19261738.001).
  • [ISSN] 1931-857X
  • [Journal-full-title] American journal of physiology. Renal physiology
  • [ISO-abbreviation] Am. J. Physiol. Renal Physiol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000609-17; United States / NCI NIH HHS / CA / P01-CA-78582; United States / NHLBI NIH HHS / HL / R01-HL-67963
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bufanolides; 0 / Enzyme Inhibitors; 0 / Fli1 protein, mouse; 0 / Procollagen; 0 / Proto-Oncogene Protein c-fli-1; 470-42-8 / marinobufagenin; EC 2.7.11.13 / Protein Kinase C-delta
  • [Other-IDs] NLM/ PMC2681369
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4. Banovic T, MacDonald KP, Morris ES, Rowe V, Kuns R, Don A, Kelly J, Ledbetter S, Clouston AD, Hill GR: TGF-beta in allogeneic stem cell transplantation: friend or foe? Blood; 2005 Sep 15;106(6):2206-14
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  • [Title] TGF-beta in allogeneic stem cell transplantation: friend or foe?
  • Donor treatment with granulocyte-colony-stimulating factor (G-CSF) attenuates the ability of donor T cells to induce acute graft-versus-host disease (aGVHD) but increases the severity of chronic GVHD (cGVHD).
  • Although the neutralization of TGF-beta augmented the proliferation and expansion of donor T cells after SCT, it paradoxically impaired cellular cytotoxicity to host antigens and associated graft-versus-leukemia (GVL) effects.
  • These data have important implications for the timing of therapeutic TGF-beta neutralization to prevent cGVHD after allogeneic SCT.
  • [MeSH-minor] Acute Disease. Animals. Chronic Disease. Disease Models, Animal. Graft vs Leukemia Effect / drug effects. Mice. Mice, Inbred Strains. Neoplasms, Experimental / complications. Neoplasms, Experimental / therapy. T-Lymphocytes / secretion. Time Factors. Transplantation, Homologous

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  • (PMID = 15941908.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta
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5. Gostout BS, Lindor NM, DiMarco CS, Peethambaram PP, Clayton AC: Pelvic primitive neuroectodermal tumor associated with a cluster of small round cell tumors: case report and review of current literature. Gynecol Oncol; 2003 Oct;91(1):247-53
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  • BACKGROUND: Peripheral primitive neuroectodermal tumor (pPNET) is aggressive and rare, comprising 1% of soft tissue sarcomas.
  • Chemotherapy with vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide and etoposide with mesna yielded complete response.
  • CONCLUSIONS: Genetic recombination resulting in a chimeric transcript of the Ewing sarcoma gene and the Friend leukemia virus integration site is characteristic of these tumors.
  • Surgical resection and multiagent chemotherapy may enhance survival.
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans

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  • (PMID = 14529689.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 25
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6. Gibbert K, Dietze KK, Zelinskyy G, Lang KS, Barchet W, Kirschning CJ, Dittmer U: Polyinosinic-polycytidylic acid treatment of Friend retrovirus-infected mice improves functional properties of virus-specific T cells and prevents virus-induced disease. J Immunol; 2010 Nov 15;185(10):6179-89
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  • [Title] Polyinosinic-polycytidylic acid treatment of Friend retrovirus-infected mice improves functional properties of virus-specific T cells and prevents virus-induced disease.
  • The induction of type I IFN is the most immediate host response to viral infections.
  • Type I IFN has a direct antiviral activity mediated by antiviral enzymes, but it also modulates the function of cells of the adaptive immune system.
  • Many viruses can suppress type I IFN production, and in retroviral infections, the initial type I IFN is weak.
  • Thus, one strategy of immunotherapy in viral infection is the exogenous induction of type I IFN during acute viral infection by TLR ligands.
  • However, the immunological mechanisms underlying this successful therapy have not been defined until now.
  • In this study, the Friend retrovirus (FV) mouse model was used to investigate the mode of action of poly(I:C) in antiretroviral immunotherapy.
  • Postexposure, poly(I:C) treatment of FV-infected mice resulted in a significant reduction in viral loads and protection from virus-induced leukemia.
  • This effect was IFN dependent because type I IFN receptor-deficient mice could not be protected by poly(I:C).
  • The results demonstrate a direct antiviral and immunomodulatory effect of poly(I:C) and, therefore, suggests its potential for clinical treatment of retroviral infections.
  • [MeSH-major] Antiviral Agents / pharmacology. Interferon Type I / biosynthesis. Poly I-C / pharmacology. Retroviridae Infections / drug therapy. T-Lymphocytes / drug effects. Tumor Virus Infections / drug therapy
  • [MeSH-minor] Animals. Female. Friend murine leukemia virus. Lymphocyte Activation / drug effects. Mice. Mice, Inbred C57BL. Reverse Transcriptase Polymerase Chain Reaction. Viral Load / drug effects


7. Cervi D, Klement G, Stempak D, Baruchel S, Koki A, Ben-David Y: Targeting cyclooxygenase-2 reduces overt toxicity toward low-dose vinblastine and extends survival of juvenile mice with Friend disease. Clin Cancer Res; 2005 Jan 15;11(2 Pt 1):712-9
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  • [Title] Targeting cyclooxygenase-2 reduces overt toxicity toward low-dose vinblastine and extends survival of juvenile mice with Friend disease.
  • PURPOSE: To test the efficacy of selective therapy against cyclooxygenase-2 in combination with a low-dose regimen of a cytotoxic agent in the treatment of juvenile hematopoietic malignancies in the experimental model, Friend disease.
  • EXPERIMENTAL DESIGN: Juvenile erythroleukemic mice (n = 8) received no treatment, celecoxib (1600 mg/kg/d), vinblastine (0.5 microg/g twice weekly), vehicle controls, or celecoxib + vinblastine combination (n = 9) over a 6-month period from time of tumor induction.
  • RESULTS: Among randomly selected mice from celecoxib treatment groups, plasma concentrations ranged from 2 to 6 micromol/L.
  • Coadministration of these two drugs alleviated the overt toxicity associated with vinblastine and resulted in a significant increase in survival (P < 0.05).
  • Despite similar degree of splenomegaly, histologic analysis revealed preserved splenic mantle architecture from mice given combination therapy compared with those sampled from mice on all other monotherapies, exhibiting a more diffuse burden of blasts and destruction of germinal centers.
  • CONCLUSION: We propose that addition of a selective cyclooxygenase-2 inhibitor to a modified low-dose conventional chemotherapeutic regimen protects juvenile mice with Friend disease from succumbing to low-dose cytotoxicity, in part, by neutralizing acute inflammatory responses.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Experimental / drug therapy. Prostaglandin-Endoperoxide Synthases / chemistry. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use. Vinblastine / therapeutic use
  • [MeSH-minor] Animals. Cardiovascular Diseases / chemically induced. Celecoxib. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Friend murine leukemia virus / genetics. Mice. Mice, Inbred BALB C. Survival Rate. Treatment Outcome

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  • (PMID = 15701860.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 5V9KLZ54CY / Vinblastine; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib
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8. Stromnes IM, Dittmer U, Schumacher TN, Schepers K, Messer RJ, Evans LH, Peterson KE, Race B, Hasenkrug KJ: Temporal effects of gamma interferon deficiency on the course of Friend retrovirus infection in mice. J Virol; 2002 Mar;76(5):2225-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temporal effects of gamma interferon deficiency on the course of Friend retrovirus infection in mice.
  • The current studies demonstrate complex and seemingly contradictory effects by gamma interferon (IFN-gamma) on Friend virus (FV) infection.
  • Both temporal and tissue-specific effects were observed.
  • During the first week of infection, IFN-gamma-deficiency caused increased levels of FV infection in multiple tissues.
  • Surprisingly, however, by 2 weeks postinfection, IFN-gamma-deficient mice had significantly lower levels of infection in both the spleen and bone marrow compared to wild-type mice.
  • The rapid reduction of virus in the IFN-gamma-deficient mice correlated with a more rapid virus-neutralizing antibody response than was observed in the wild-type mice.
  • Furthermore, the virus-neutralizing antibody response in wild-type mice could be accelerated by ablation of their IFN-gamma response.
  • Although the IFN-gamma-deficient mice developed an accelerated virus-neutralizing antibody response, they did not class-switch to immunoglobulin G class immunoglobulins nor could they maintain long-term virus-neutralizing antibody titers.
  • Eventually, all of the IFN-gamma-deficient mice failed to keep persistent virus in check and developed fatal FV-induced erythroleukemia.
  • [MeSH-major] Friend murine leukemia virus / pathogenicity. Interferon-gamma / deficiency. Leukemia, Experimental / physiopathology. Retroviridae Infections / physiopathology. Tumor Virus Infections / physiopathology
  • [MeSH-minor] Animals. Antibodies, Viral / blood. Antiviral Agents / therapeutic use. CD8-Positive T-Lymphocytes / immunology. DNA, Viral / blood. Flow Cytometry. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / virology. Mice. Mice, Inbred C57BL. Mice, Knockout. Neutralization Tests. Polymerase Chain Reaction. RNA, Viral / blood. Recombinant Proteins. Spleen / virology

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  • (PMID = 11836400.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Antiviral Agents; 0 / DNA, Viral; 0 / RNA, Viral; 0 / Recombinant Proteins; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC153801
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9. Hasegawa M, Kurata M, Yamamoto K, Yoshida K, Aizawa S, Kitagawa M: A novel role for acinus and MCM2 as host-specific signaling enhancers of DNA-damage-induced apoptosis in association with viral protein gp70. Leuk Res; 2009 Aug;33(8):1100-7
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  • We previously demonstrated that infection with Friend leukemia virus (FLV) radiosensitizes murine hematopoietic cells via a p53-dependent apoptotic pathway in C3H hosts.
  • Here, we show that the transduction of the env-gene (gp70) of Friend murine leukemia virus (F-MuLV) sensitized C3H-derived myeloid leukemia cells to DNA-damage (ionizing radiation as well as doxorubicin)-induced apoptosis through the activation of DNA-dependent protein kinase (DNA-PK) and P53.
  • The mechanisms involved in the ability of a viral protein to regulate cellular gene expression could provide invaluable insight into the manipulation of cellular pro-apoptotic signaling and the development of novel therapeutic strategies.
  • [MeSH-major] Apoptosis. DNA Damage. Friend murine leukemia virus / metabolism. Gene Products, env / biosynthesis. Leukemia, Experimental / metabolism. Nuclear Proteins / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / adverse effects. Antibiotics, Antineoplastic / pharmacology. DNA-Activated Protein Kinase / genetics. DNA-Activated Protein Kinase / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Doxorubicin / adverse effects. Doxorubicin / pharmacology. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / genetics. Gene Expression Regulation, Leukemic / radiation effects. Genetic Therapy. Mice. Mice, Inbred C3H. Minichromosome Maintenance Complex Component 2. Phosphorylation / drug effects. Phosphorylation / genetics. Phosphorylation / radiation effects. Radiation, Ionizing. Retroviridae Infections / genetics. Retroviridae Infections / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Signal Transduction / radiation effects. Transduction, Genetic. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Tumor Virus Infections / genetics. Tumor Virus Infections / metabolism

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  • (PMID = 19058849.001).
  • [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 / Antibiotics, Antineoplastic; 0 / DNA-Binding Proteins; 0 / Gene Products, env; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / Prkdc protein, mouse; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
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10. Catalina F, Milewich L, Kumar V, Bennett M: Dietary dehydroepiandrosterone inhibits bone marrow and leukemia cell transplants: role of food restriction. Exp Biol Med (Maywood); 2003 Dec;228(11):1303-20
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  • [Title] Dietary dehydroepiandrosterone inhibits bone marrow and leukemia cell transplants: role of food restriction.
  • (ii) stem cell stimulation by erythropoietin, growth hormone, interleukin-2, Friend leukemia virus, or cyclophosphamide failed to reverse suppression;.
  • Neither procedure affected the ability of food restriction or DHEA feeding to inhibit hematopoiesis;.
  • (viii) growth of GR-3 NM pre-B leukemia cells in unirradiated mice was also suppressed by DHEA or food restriction.
  • We conclude that DHEA, by reducing food intake in mice, inhibits bone marrow and leukemia cell growth.
  • The precise mechanism(s) by which reduced food intake per se inhibits hematopoiesis is not known, but may involve an increased rate of cellular apoptosis.
  • [MeSH-major] Bone Marrow Transplantation. Dehydroepiandrosterone / pharmacology. Hematopoiesis / drug effects
  • [MeSH-minor] Animals. Apoptosis / drug effects. Body Temperature / drug effects. Complement System Proteins / metabolism. Diet. Female. Glucosephosphate Dehydrogenase / metabolism. Immunosuppressive Agents / pharmacology. Leukemia, Experimental / diet therapy. Leukemia, Experimental / immunology. Leukemia, Experimental / pathology. Male. Mice. Mice, Inbred Strains. Mice, SCID. Neoplasm Transplantation / immunology. Steroids / physiology. Transplantation, Homologous. Transplantation, Isogeneic

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  • (PMID = 14681546.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / 5T32 GM08013; United States / NIAID NIH HHS / AI / AI 20451; United States / NIAID NIH HHS / AI / AI 38939; United States / NCI NIH HHS / CA / CA 36922; United States / NCI NIH HHS / CA / CA43311
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Steroids; 459AG36T1B / Dehydroepiandrosterone; 9007-36-7 / Complement System Proteins; EC 1.1.1.49 / Glucosephosphate Dehydrogenase
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11. Uren A, Toretsky JA: Ewing's sarcoma oncoprotein EWS-FLI1: the perfect target without a therapeutic agent. Future Oncol; 2005 Aug;1(4):521-8
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  • [Title] Ewing's sarcoma oncoprotein EWS-FLI1: the perfect target without a therapeutic agent.
  • This translocation joins the Ewing's sarcoma gene (EWS) located on chromosome 22 to an ets family gene; either friend leukemia insertion (FLI)1 located on chromosome 11, t(11;22), or ets-related gene (ERG) located on chromosome 21, t(21;22).
  • ESFT presents a clinical challenge, especially in patients with metastatic disease in which dose-intensifying chemotherapy with bone-marrow transplantation does not improve survival.
  • Therefore, ESFT contains a unique protein generated by a tumor-specific translocation that has great potential as a molecular target for therapy.
  • However, therapeutic applications directed towards eliminating or inactivating EWS-FLI1 have not reached the clinic.

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  • (PMID = 16556028.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA088004-08; United States / NCI NIH HHS / CA / R01 CA088004; United States / NCI NIH HHS / CA / R01 CA088004-08
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EWS-FLI fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Protein c-fli-1; 0 / RNA-Binding Protein EWS
  • [Number-of-references] 48
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12. Harikumar KB, Kuttan G, Kuttan R: Inhibition of progression of erythroleukemia induced by Friend virus in BALB/c mice by natural products--berberine, curcumin and picroliv. J Exp Ther Oncol; 2008;7(4):275-84
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  • [Title] Inhibition of progression of erythroleukemia induced by Friend virus in BALB/c mice by natural products--berberine, curcumin and picroliv.
  • The infection with Friend murine leukemia virus (FMuLv) is being used as a retrovirus infection model for searching the potential anti-viral medicinal preparations or establishing new treatment strategies.
  • To understand the effect of these compounds in the initiation and progression of leukemia we did a series of analysis, which include hematological and biochemical parameters, histopathological evaluations of the liver and the spleen and expression analysis of selected genes such as Bcl-2, p53, p45NFE2, Raf-1, Erk-1, IFNgamma receptor and erythropoietin in spleen.
  • The treatment with berberine, curcumin or picroliv were found to (a) elevate the life span of leukemia harboring animals by more than 60 days;.
  • Overall, our results suggest that berberine, curcumin and picroliv were able to suppress the progression of leukemia induced by FMuLv and further support their chemopreventive potential against virally induced cancers.
  • [MeSH-major] Berberine / pharmacology. Cinnamates / pharmacology. Curcumin / pharmacology. Friend murine leukemia virus / metabolism. Glycosides / pharmacology. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / virology. Vanillic Acid / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Biological Products / pharmacology. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia, Experimental / drug therapy. Leukemia, Experimental / genetics. Mice. Mice, Inbred BALB C. Uric Acid / blood

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  • (PMID = 19227007.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biological Products; 0 / Cinnamates; 0 / Glycosides; 0I8Y3P32UF / Berberine; 12708-05-3 / kutkin; 268B43MJ25 / Uric Acid; GM8Q3JM2Y8 / Vanillic Acid; IT942ZTH98 / Curcumin
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13. Breems-de Ridder MC, Löwenberg B, Jansen JH: Retinoic acid receptor fusion proteins: friend or foe. Mol Cell Endocrinol; 2000 Jul 25;165(1-2):1-6
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  • [Title] Retinoic acid receptor fusion proteins: friend or foe.
  • Acute promyelocytic leukemia (APL) is characterized by a block in differentiation of hematopoietic cells at the promyelocytic stage of development.
  • This disease is uniquely sensitive to treatment with pharmacological doses of all-trans retinoic acid (ATRA), and the combination of ATRA with chemotherapy has improved the durable disease-free survival in these patients to up to 80%.
  • Most RARalpha fusion proteins can still be induced to transactivate genes, but only at very high doses of ligand, explaining why pharmacological doses of ATRA are necessary to obtain a therapeutic effect in these patients.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism
  • [MeSH-minor] Hematopoiesis / drug effects. Hematopoiesis / genetics. Humans. Mutation. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transcriptional Activation. Tretinoin / therapeutic use

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  • (PMID = 10940477.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / Recombinant Fusion Proteins; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
  • [Number-of-references] 48
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14. Cataldi A, Di Pietro R, Centurione L, Rapino M, Santavenere E, Garaci F, Cocco L, Giuliani-Piccari G, Rana R: Engagement of PI-3-kinase mediated protein kinase C zeta activation in protecting Friend cells from ionizing radiation-induced apoptosis. Int J Oncol; 2003 Jan;22(1):129-35
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  • [Title] Engagement of PI-3-kinase mediated protein kinase C zeta activation in protecting Friend cells from ionizing radiation-induced apoptosis.
  • Murine erythroleukemia cells (Friend) respond to ionizing radiation with the activation and nuclear translocation of p85alpha subunit of phosphatidylinositol-3-kinase (PI-3-kinase) which mediates the downstream activation and nuclear translocation of atypical Protein kinase C zeta (PKC zeta).
  • This event occurs mainly upon high dose of ionizing radiation (15 Gy) and is concomitant to an increase in BrdU incorporation, which probably accounts for a predominant repair DNA synthesis.
  • Following treatment with wortmannin, a relatively specific inhibitor of PI-3-kinase, both an increased number of apoptotic cells and the inhibition of protein kinase C zeta translocation were detected.
  • Altogether the evidence suggests a potential role of the PI-3-kinase/PKC zeta pathway in protecting Friend cells from ionizing radiation-induced apoptosis offering PKC zeta for consideration as possible target of pharmacological treatments.
  • [MeSH-major] Apoptosis / radiation effects. Friend murine leukemia virus. Leukemia, Erythroblastic, Acute / radiotherapy. Phosphatidylinositol 3-Kinases / physiology. Protein Kinase C / physiology

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  • (PMID = 12469195.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 9007-49-2 / DNA; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C
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15. Cataldi A, Centurione L, Di Pietro R, Rapino M, Bosco D, Grifone G, Garaci F, Rana R: Protein kinase C zeta nuclear translocation mediates the occurrence of radioresistance in friend erythroleukemia cells. J Cell Biochem; 2003 Jan 1;88(1):144-51

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  • [Title] Protein kinase C zeta nuclear translocation mediates the occurrence of radioresistance in friend erythroleukemia cells.
  • Friend erythroleukemia cells require high doses (15 Gy) of ionizing radiation to display a reduced rate of proliferation and an increased number of dead cells.
  • Our results show an early and dose-dependent increased activity of zeta and epsilon isoforms, although PKC zeta is the only isoform significantly active and translocated into the nuclear compartment upon low (1.5 Gy) and high (15 Gy) radiation doses.
  • Our results point at the involvement of the PKC pathway in the survival response to ionizing radiation of this peculiar cell line, offering PKC zeta for consideration as a possible target of pharmacological treatments aimed at amplifying the effect of such a genotoxic agent.
  • [MeSH-major] Active Transport, Cell Nucleus. Leukemia, Erythroblastic, Acute / radiotherapy. Protein Kinase C / metabolism. Radiation Tolerance
  • [MeSH-minor] Animals. Blotting, Western. In Situ Nick-End Labeling. Mice. Microscopy, Electron. Microscopy, Immunoelectron. Protein Isoforms. Subcellular Fractions / metabolism. Time Factors. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12461784.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C
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16. Onishi H, Kamijo A, Onose M, Yamada T, Mizuno Y, Ito M, Saito H, Maruta I: Conversion disorder with convulsion and motor deficit mimicking the adverse effects of high-dose Ara-C treatment in a posttransplant acute myeloid leukemia patient: a case report and review of the literature. Palliat Support Care; 2004 Mar;2(1):79-82
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  • [Title] Conversion disorder with convulsion and motor deficit mimicking the adverse effects of high-dose Ara-C treatment in a posttransplant acute myeloid leukemia patient: a case report and review of the literature.
  • In this communication, we report an acute leukemia patient who developed conversion disorder mimicking the adverse effects of high-dose cytosine arabinoside (Ara-C) treatment after the patient received high-dose Ara-C treatment.
  • A 21-year-old woman, with acute recurrent leukemia after bone marrow transplantation, received high-dose Ara-C treatment and 10 days later was referred for psychiatric consultation because of an abrupt onset of convulsion.
  • She had no history of psychiatric illness or drug or alcohol abuse.
  • The patient explained that she knew about the recurrence of her own leukemia and the news of the death of a close friend due to leukemia at the same time, which was a shocking event for her, focusing her attention on her own fears of dying from the same disease.
  • Conversion disorder in cancer patients is not common; however, appropriate diagnosis is very important to avoid inappropriate examinations and treatments.
  • In leukemia patients receiving chemotherapy, various kinds of signs and symptoms may develop due to the adverse effects of chemotherapy and/or infection.
  • Therefore, conversion disorder might be overlooked and inappropriate treatment and examinations might be performed.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Conversion Disorder / diagnosis. Cytarabine / adverse effects. Leukemia, Myeloid / psychology. Neurotoxicity Syndromes / diagnosis

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  • (PMID = 16594237.001).
  • [ISSN] 1478-9515
  • [Journal-full-title] Palliative & supportive care
  • [ISO-abbreviation] Palliat Support Care
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
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17. Xiao X, Li BX, Mitton B, Ikeda A, Sakamoto KM: Targeting CREB for cancer therapy: friend or foe. Curr Cancer Drug Targets; 2010 Jun;10(4):384-91
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  • [Title] Targeting CREB for cancer therapy: friend or foe.
  • Overexpression and over-activation of CREB were observed in cancer tissues from patients with prostate cancer, breast cancer, non-small-cell lung cancer and acute leukemia while down-regulation of CREB in several distinct cancer cell lines resulted in inhibition of cell proliferation and induction of apoptosis, suggesting that CREB may be a promising target for cancer therapy.
  • These results suggest that CREB is a suitable transcription factor for drug targeting and therefore targeting CREB could represent a novel strategy for cancer therapy.

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  • (PMID = 20370681.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NIGMS NIH HHS / GM / R01 GM087305; United States / NHLBI NIH HHS / HL / HL83077; United States / NHLBI NIH HHS / HL / HL75826; United States / NHLBI NIH HHS / HL / R01 HL083077; United States / NICHD NIH HHS / HD / K12 HD034610; United States / NICHD NIH HHS / HD / HD034610-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein
  • [Other-IDs] NLM/ NIHMS635161; NLM/ PMC4206256
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18. Harikumar KB, Kuttan G, Kuttan R: Inhibition of viral carcinogenesis by Phyllanthus amarus. Integr Cancer Ther; 2009 Sep;8(3):254-60
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  • Friend murine leukemia virus (FMuLv) is an acutely oncogenic retrovirus, and its infection leads to erythroblastosis and leukemia in mice.
  • Injection of newborn mice with FMuLv resulted in leukemia and animals died due to splenomegaly.
  • Oral administration of P.amarus was found to enhance the life span of leukemia-harboring animals and decrease the incidence of anemia.
  • Treatment with P.amarus induced the expression of p53 and p45NFE2 and decreased the expression of Bcl-2 in the spleen of infected mice.
  • [MeSH-major] Friend murine leukemia virus. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Experimental / drug therapy. Phyllanthus / chemistry. Plant Extracts / therapeutic use. Retroviridae Infections / drug therapy. Tumor Virus Infections / drug therapy
  • [MeSH-minor] Anemia / blood. Anemia / drug therapy. Animals. Blood Cell Count. Body Weight / drug effects. Cell Transformation, Viral / drug effects. Disease Progression. Gene Expression / genetics. Hemoglobins / analysis. Hemoglobins / metabolism. Liver / drug effects. Liver / pathology. Mice. Mice, Inbred BALB C. NF-E2 Transcription Factor, p45 Subunit / genetics. Organ Size / drug effects. Proto-Oncogene Proteins c-bcl-2 / genetics. Spleen / drug effects. Spleen / metabolism. Spleen / pathology. Survival Analysis. Tumor Suppressor Protein p53 / genetics. Uric Acid / blood

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  • [ErratumIn] Integr Cancer Ther. 2010 Mar;9(1):122
  • (PMID = 19815595.001).
  • [ISSN] 1552-695X
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / 1K01AT004415-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / NF-E2 Transcription Factor, p45 Subunit; 0 / Nfe2 protein, mouse; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 268B43MJ25 / Uric Acid
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19. Olbrich AR, Schimmer S, Heeg K, Schepers K, Schumacher TN, Dittmer U: Effective postexposure treatment of retrovirus-induced disease with immunostimulatory DNA containing CpG motifs. J Virol; 2002 Nov;76(22):11397-404
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  • [Title] Effective postexposure treatment of retrovirus-induced disease with immunostimulatory DNA containing CpG motifs.
  • Therapeutic strategies for the treatment of acute retroviral infections have relied mainly on antiviral drugs.
  • In this study we used the Friend virus model system to demonstrate that enhancement of the immune system can also have dramatic therapeutic effects.
  • Since resistance to Friend virus-induced leukemia in mice is associated with T helper cell type 1 (Th1) immune responses, we enhanced these responses in susceptible mice by treatment with synthetic oligodeoxynucleotides containing unmethylated CpG motifs (CpG-ODN).
  • Treatments begun at 4 days postinfection increased recovery from 6% in the control group to 74% in the CpG-treated group.
  • The treatment promoted Th1-type cytokine production by splenocytes of Friend virus-infected mice and augmented Friend virus-specific cytotoxic T-cell responses, but no influence on the virus-specific neutralizing antibody response was observed.
  • Friend virus-specific CD8(+) T cells were critical for effective treatment with CpG-ODN, since in vivo depletion of these cells from treated mice prevented their recovery.
  • Our results demonstrate that CpG-ODN therapy can significantly enhance virus-specific cellular immune responses and prevent retrovirus-induced disease.
  • These findings may have implications for antiviral therapy in general.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Friend murine leukemia virus / physiology. Leukemia, Experimental / drug therapy. Oligodeoxyribonucleotides / therapeutic use. Retroviridae Infections / drug therapy. Tumor Virus Infections / drug therapy

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  • (PMID = 12388700.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / CPG-oligonucleotide; 0 / Cytokines; 0 / Oligodeoxyribonucleotides
  • [Other-IDs] NLM/ PMC136771
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20. Rappa G, Lorico A, Hildinger M, Fodstad Ø, Baum C: Novel bicistronic retroviral vector expressing gamma-glutamylcysteine synthetase and the multidrug resistance protein 1 (MRP1) protects cells from MRP1-effluxed drugs and alkylating agents. Hum Gene Ther; 2001 Sep 20;12(14):1785-96
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  • [Title] Novel bicistronic retroviral vector expressing gamma-glutamylcysteine synthetase and the multidrug resistance protein 1 (MRP1) protects cells from MRP1-effluxed drugs and alkylating agents.
  • We have utilized the hybrid FMEV (Friend mink cell focus-forming/murine embryonic stem cell virus) backbone, previously shown to be efficient in early hematopoietic cells, even when coexpressing two distinct genes.
  • Drug-resistant producer clones were subsequently selected with antimony potassium tartrate, a nonmutagenic MRP1 substrate.
  • Producer cells, 3T3 fibroblasts transduced with either SF91MRP or SF91GCS-MRP, and primary murine myeloid progenitor cells transduced with SF91GCS-MRP were resistant to MRP1-effluxed drugs.
  • The strategy of coexpressing gamma-GCS and MRP1 may help to design an effective in vivo selection for various clinical protocols of gene therapy.
  • [MeSH-minor] 3T3 Cells. Animals. Antimony / pharmacology. Blotting, Southern. Cells, Cultured. Chlorambucil / pharmacology. Cisplatin / pharmacology. Cloning, Molecular. DNA, Complementary / metabolism. Dose-Response Relationship, Drug. Doxorubicin / pharmacology. Etoposide / pharmacology. Fibroblasts / metabolism. Flow Cytometry. Friend murine leukemia virus / genetics. Genetic Therapy / methods. Genome, Viral. Glutathione / biosynthesis. Glutathione / metabolism. Hematopoietic Stem Cells / metabolism. Humans. Inhibitory Concentration 50. Male. Melphalan / pharmacology. Mice. Mice, Inbred BALB C. RNA / metabolism. RNA, Messenger / metabolism. Terminal Repeat Sequences. Transduction, Genetic. Viral Envelope Proteins / metabolism

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  • (PMID = 11560771.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / DNA, Complementary; 0 / G protein, vesicular stomatitis virus; 0 / Membrane Glycoproteins; 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Messenger; 0 / Viral Envelope Proteins; 0 / multidrug resistance-associated protein 1; 18D0SL7309 / Chlorambucil; 63231-63-0 / RNA; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 9IT35J3UV3 / Antimony; EC 6.3.2.2 / Glutamate-Cysteine Ligase; GAN16C9B8O / Glutathione; Q20Q21Q62J / Cisplatin; Q41OR9510P / Melphalan
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21. Miller SC, Delorme D, Shan JJ: CVT-E002 stimulates the immune system and extends the life span of mice bearing a tumor of viral origin. J Soc Integr Oncol; 2009;7(4):127-36

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The present study evaluated the dose-related effects of CVT-E002, a proprietary extract of Panax quinquefolius (CV Technologies Inc., Edmonton, AB), in the treatment of a tumor of viral origin, that is, erythroleukemia, in mice.
  • Three treatments including ingestion of 2, 40, and 120 mg/d were compared.
  • CVT-E002 treatment significantly elevated the absolute numbers of natural killer cells and monocytes and reduced the number of tumor cells in the bone marrow and spleen.
  • [MeSH-major] Friend murine leukemia virus. Killer Cells, Natural / drug effects. Leukemia, Erythroblastic, Acute / drug therapy. Monocytes, Activated Killer / drug effects. Plant Extracts / pharmacology
  • [MeSH-minor] Animals. Bone Marrow / drug effects. Bone Marrow / immunology. Bone Marrow Cells / drug effects. Bone Marrow Cells / immunology. Leukemia, Experimental. Male. Mice. Mice, Inbred DBA. Panax. Specific Pathogen-Free Organisms. Spleen / cytology. Spleen / drug effects. Spleen / immunology. Tumor Cells, Cultured

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  • (PMID = 19883528.001).
  • [ISSN] 1715-894X
  • [Journal-full-title] Journal of the Society for Integrative Oncology
  • [ISO-abbreviation] J Soc Integr Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / COLD-fX; 0 / Plant Extracts
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22. Campistol JM, Eris J, Oberbauer R, Friend P, Hutchison B, Morales JM, Claesson K, Stallone G, Russ G, Rostaing L, Kreis H, Burke JT, Brault Y, Scarola JA, Neylan JF: Sirolimus therapy after early cyclosporine withdrawal reduces the risk for cancer in adult renal transplantation. J Am Soc Nephrol; 2006 Feb;17(2):581-9
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  • [Title] Sirolimus therapy after early cyclosporine withdrawal reduces the risk for cancer in adult renal transplantation.
  • Median times to first skin and nonskin malignancies were compared between treatments using a survival analysis.
  • At 5 yr, the median time to a first skin carcinoma was delayed (491 versus 1126 d; log-rank test, P = 0.007), and the risk for an event was significantly lower with SRL-ST therapy (relative risk SRL-ST to SRL-CsA-ST 0.346; 95% confidence interval 0.227 to 0.526; P < 0.001, intention-to-treat analysis).
  • Nonskin cancers included those of the lung, larynx, oropharynx, kidney, gastrointestinal tract, prostate, breast, thyroid, and cervix as well as glioma, liposarcoma, astrocytoma, leukemia, lymphoma, and Kaposi's sarcoma.
  • Patients who received SRL-based, calcineurin inhibitor-free therapy after CsA withdrawal at month 3 had a reduced incidence of both skin and nonskin malignancies at 5 yr after renal transplantation compared with those who received SRL therapy combined with CsA.
  • [MeSH-minor] Adult. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Therapy, Combination. Follow-Up Studies. Humans. Incidence. Risk Assessment

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  • (PMID = 16434506.001).
  • [ISSN] 1046-6673
  • [Journal-full-title] Journal of the American Society of Nephrology : JASN
  • [ISO-abbreviation] J. Am. Soc. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; W36ZG6FT64 / Sirolimus
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23. Rhodes MM, Kopsombut P, Bondurant MC, Price JO, Koury MJ: Adherence to macrophages in erythroblastic islands enhances erythroblast proliferation and increases erythrocyte production by a different mechanism than erythropoietin. Blood; 2008 Feb 1;111(3):1700-8
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  • Erythroblasts adhere to central macrophages forming erythroblastic islands in hematopoietic tissues, but the function of these islands is not understood.
  • Direct contact with the macrophages was necessary for this enhanced erythroblast proliferation, which resulted from decreased transit time in the G(0)/G(1) phase of cell cycle.
  • These results suggest a mechanism for the development of anemias associated with abnormal macrophage function and for reduced responsiveness of those anemias to erythropoietin therapy.

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  • (PMID = 17993612.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK077056; United States / NHLBI NIH HHS / HL / T32 HL007751; United States / NIDDK NIH HHS / DK / K08DK077056; United States / NHLBI NIH HHS / HL / T32 HL07751
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 11096-26-7 / Erythropoietin
  • [Other-IDs] NLM/ PMC2214751
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24. Cervi D, Truong AH, Lee JS, Sukhai N, Li YJ, Koki A, Ben-David Y: Phosphorylation status of c-Kit and Epo receptors, and the presence of wild-type p53 confer in vitro resistance of murine erythroleukemic cells to Celecoxib. Oncogene; 2004 Mar 25;23(13):2305-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phosphorylation status of c-Kit and Epo receptors, and the presence of wild-type p53 confer in vitro resistance of murine erythroleukemic cells to Celecoxib.
  • By taking advantage of murine Friend Disease we have shown a strong antileukemic effect of celecoxib by determining novel in vitro targets.
  • Western blot analyses revealed the expression of COX-2 in a panel of Friend Virus-transformed, splenic-derived primary erythroleukemic blasts and established cell lines generated in our laboratory.
  • Our results also demonstrate that treatment of the established murine erythroleukemia cell line HB60-5 with celecoxib results in suppression of c-Kit and erythropoietin receptor (Epo-R) phosphorylation resulting in apoptosis, likely through decreased levels of survival factors.
  • Finally, since responsiveness of our murine erythroleukemia cell lines to celecoxib is above the reported physiologically achievable levels in vivo, we have provided in vitro evidence to suggest that reduced sensitivity of erythroleukemic cells to lower doses of celecoxib may be a consequence of the loss of wild-type p53.
  • [MeSH-major] Drug Resistance, Neoplasm / physiology. Leukemia, Erythroblastic, Acute / drug therapy. Proto-Oncogene Proteins c-kit / metabolism. Receptors, Erythropoietin / metabolism. Sulfonamides / pharmacology. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 14743207.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrazoles; 0 / Receptors, Erythropoietin; 0 / Sulfonamides; 0 / Tumor Suppressor Protein p53; EC 2.7.- / Phosphotransferases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; JCX84Q7J1L / Celecoxib
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25. García-Tojal J, Pizarro JL, García-Orad A, Pérez-Sanz AR, Ugalde M, Alvarez Díaz A, Serra JL, Arriortua MI, Rojo T: Biological activity of complexes derived from thiophene-2-carbaldehyde thiosemicarbazone. Crystal structure of [Ni(C(6)H(6)N(3)S(2))(2)]. J Inorg Biochem; 2001 Sep;86(2-3):627-33
Hazardous Substances Data Bank. NICKEL, ELEMENTAL .

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  • The observed order of cytotoxicity against melanoma B16F10 and Friend erythroleukemia cells is: 1< or =ligand<2<3.
  • [MeSH-minor] Animals. Crystallography, X-Ray. Leukemia, Erythroblastic, Acute / drug therapy. Ligands. Melanoma, Experimental / drug therapy. Mice. Molecular Structure. Nickel / chemistry. Spectroscopy, Fourier Transform Infrared. Tumor Cells, Cultured

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  • (PMID = 11566336.001).
  • [ISSN] 0162-0134
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Organometallic Compounds; 0 / Thiophenes; 0 / Thiosemicarbazones; 0 / bis(thiophene-2-carbaldehyde thiosemicarbazone)nickel(II); 7OV03QG267 / Nickel
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26. Beilharz MW, Sammels LM, Paun A, Shaw K, van Eeden P, Watson MW, Ashdown ML: Timed ablation of regulatory CD4+ T cells can prevent murine AIDS progression. J Immunol; 2004 Apr 15;172(8):4917-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We demonstrate that a single injection of the antimitotic drug vinblastine (Vb) given 14 days postinfection (p.i.) with LP-BM5 can prevent MAIDS progression.
  • Treatment with anti-CD4 mAb at 14 days p.i. is similarly able to prevent MAIDS.
  • Treatment at other time points with Vb or anti-CD4 mAb is ineffective.
  • MAIDS-infected mice also have CD4(+) T cells with significantly higher expression levels of CD38 and particularly CD69, which have been demonstrated to be regulator T cell markers in the Friend retroviral model.
  • These data define a new therapy for murine retroviral infection, which has potential for use in other diseases where T regulator cell-mediated immunosuppression plays a role in the disease process.
  • [MeSH-minor] Animals. Antibodies, Blocking / administration & dosage. Antigens, CD / biosynthesis. Antigens, Differentiation, T-Lymphocyte / biosynthesis. Antigens, Differentiation, T-Lymphocyte / immunology. Antigens, Differentiation, T-Lymphocyte / metabolism. Cell Cycle / drug effects. Cell Cycle / immunology. Disease Progression. Drug Administration Schedule. Female. Growth Inhibitors / administration & dosage. Growth Inhibitors / therapeutic use. Immunization Schedule. Immunization, Secondary. Injections, Intraperitoneal. Interleukin-10 / antagonists & inhibitors. Interleukin-10 / biosynthesis. Interleukin-4 / antagonists & inhibitors. Interleukin-4 / biosynthesis. Lectins, C-Type. Leukemia Virus, Murine / immunology. Mice. Mice, Inbred C57BL. Receptors, Interleukin-2 / biosynthesis. Spleen / immunology. Spleen / pathology. T-Lymphocyte Subsets / drug effects. T-Lymphocyte Subsets / immunology. T-Lymphocyte Subsets / metabolism. Vinblastine / administration & dosage. Vinblastine / therapeutic use. Viral Load

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  • (PMID = 15067071.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CD69 antigen; 0 / Growth Inhibitors; 0 / Lectins, C-Type; 0 / Receptors, Interleukin-2; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 5V9KLZ54CY / Vinblastine
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27. Bhojwani D, Pui CH: Intrathecal liposomal cytarabine: more friend than foe? Leuk Lymphoma; 2008 Aug;49(8):1427-30
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  • [Title] Intrathecal liposomal cytarabine: more friend than foe?

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  • (PMID = 18766957.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Carriers; 0 / Liposomes; 04079A1RDZ / Cytarabine
  • [Number-of-references] 14
  • [Other-IDs] NLM/ NIHMS162789; NLM/ PMC2803076
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28. Raĭkhlin NT, Andronova NV, Sedakova LA, Gadzhieva SSh, Smirnova EA, Treshchalina EM, Nebol'sin VE: [The effect of Dicarbamin on tumor hemopoietic cell differentiation in Friend's erythroblastoma (histologic and electron microscopic investigation)]. Vopr Onkol; 2004;50(2):228-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The effect of Dicarbamin on tumor hemopoietic cell differentiation in Friend's erythroblastoma (histologic and electron microscopic investigation)].
  • [Transliterated title] Deĭstvie preparata dikarbamin na differentsirovku opukholevykh gemopoéticheskikh kletok éritroblastoza Friend (gistologicheskoe i élektronno-mikroskopicheskoe issledovanie)
  • [MeSH-major] Antineoplastic Agents / pharmacology. Hematopoiesis / drug effects. Imidazoles / pharmacology. Leukemia, Erythroblastic, Acute / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Caproates. Cell Differentiation / drug effects. Humans. Mice. Mice, Inbred DBA. Microscopy, Electron. Necrosis. Neoplasm Transplantation

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  • (PMID = 15176228.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / 6-(2-(1H-imidazol-4-yl)ethylamino)-5-oxohexanoic acid; 0 / Antineoplastic Agents; 0 / Caproates; 0 / Imidazoles
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29. Bowden R, Soto S, Specter S: Modulation of fas/fasL in a murine retroviral infection by AZT and methionine enkephalin. Adv Exp Med Biol; 2001;493:143-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Antigens, CD95 / metabolism. Enkephalin, Methionine / pharmacology. Membrane Glycoproteins / metabolism. Retroviridae Infections / drug therapy. Retroviridae Infections / immunology. Zidovudine / pharmacology
  • [MeSH-minor] Animals. Antiviral Agents / administration & dosage. Antiviral Agents / pharmacology. Apoptosis / drug effects. Drug Therapy, Combination. Fas Ligand Protein. Female. Friend murine leukemia virus. Leukemia, Experimental / drug therapy. Leukemia, Experimental / immunology. Leukemia, Experimental / pathology. Lymphocytes / drug effects. Lymphocytes / immunology. Lymphocytes / pathology. Mice. Mice, Inbred BALB C. Tumor Virus Infections / drug therapy. Tumor Virus Infections / immunology. Tumor Virus Infections / pathology

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  • (PMID = 11727760.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antiviral Agents; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Membrane Glycoproteins; 4B9XT59T7S / Zidovudine; 58569-55-4 / Enkephalin, Methionine
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