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1. van Lochem EG, Wiegers YM, van den Beemd R, Hählen K, van Dongen JJ, Hooijkaas H: Regeneration pattern of precursor-B-cells in bone marrow of acute lymphoblastic leukemia patients depends on the type of preceding chemotherapy. Leukemia; 2000 Apr;14(4):688-95
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  • [Title] Regeneration pattern of precursor-B-cells in bone marrow of acute lymphoblastic leukemia patients depends on the type of preceding chemotherapy.
  • Over a period of 15 years, we studied the regeneration of CD10+, TdT+, and CD10+/TdT+ cells in BM of children with (CD10+) precursor-B-ALL during and after treatment according to three different treatment protocols of the Dutch Childhood Leukemia Study Group (DCLSG) which differed both in medication and time schedule.
  • At first sight this precursor-B-cell regeneration during treatment resembled the massive regeneration of the precursor-B-cell compartment after maintenance treatment, and appeared to be related to the post-induction or post-central nervous system (CNS) therapy stops in protocols VII and VIII.
  • However, careful evaluation of the distribution between the 'more mature' (CD10+/TdT-) and the 'immature' (CD10+/TdT+) precursor-B-cells revealed major differences between the post-induction/post-re-induction precursor-B-cell regeneration (low 'mature/immature' ratio: generally <1.0), the post-CNS treatment regeneration (moderate 'mature/immature' ratio: 1.2-2.8), and the post-maintenance regeneration (high 'mature/ immature' ratio: 5.7-7.6).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. B-Lymphocytes / drug effects. Hematopoiesis / drug effects. Hematopoietic Stem Cells / drug effects. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Asparaginase / administration & dosage. Asparaginase / pharmacology. Biomarkers, Tumor / analysis. Cell Differentiation. Cell Division / drug effects. Child. DNA Nucleotidylexotransferase / analysis. Dexamethasone / administration & dosage. Dexamethasone / pharmacology. Drug Evaluation. Female. Flow Cytometry. Humans. Immunophenotyping. Male. Microscopy. Neoplasm Proteins / analysis. Neoplasm, Residual. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Neprilysin / analysis. Vincristine / administration & dosage. Vincristine / pharmacology

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  • (PMID = 10764156.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 2.7.7.31 / DNA Nucleotidylexotransferase; EC 3.4.24.11 / Neprilysin; EC 3.5.1.1 / Asparaginase; ALL-VI protocol
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2. Ozkaynak MF, Sahdev I, Gross TG, Levine JE, Cheerva AC, Richards MK, Rozans MK, Shaw PJ, Kadota RP: A pilot study of addition of amifostine to melphalan, carboplatin, etoposide, and cyclophosphamide with autologous hematopoietic stem cell transplantation in pediatric solid tumors-A pediatric blood and marrow transplant consortium study. J Pediatr Hematol Oncol; 2008 Mar;30(3):204-9
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  • [Title] A pilot study of addition of amifostine to melphalan, carboplatin, etoposide, and cyclophosphamide with autologous hematopoietic stem cell transplantation in pediatric solid tumors-A pediatric blood and marrow transplant consortium study.
  • Limited information is available regarding the use of amifostine in pediatric hematopoietic stem cell transplant (HSCT) patients.
  • Melphalan, carboplatin, etoposide +/- cyclophosphamide is a commonly used preparatory regimen in pediatric solid tumor HSCT.
  • Therefore, we decided to determine the feasibility of the addition of amifostine (750 mg/m b.i.d. x 4 d) to melphalan (200 mg/m), carboplatin (1200 mg/m), and etoposide (800 mg/m) (level 1) and escalating doses of cyclophosphamide (3000 mg/m and 3800 mg/m, levels 2 and 3, respectively) followed by autologous HSCT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Amifostine / administration & dosage. Amifostine / adverse effects. Bone Marrow Transplantation. Bone Neoplasms / diagnosis. Bone Neoplasms / therapy. Carboplatin / administration & dosage. Central Nervous System Neoplasms / diagnosis. Central Nervous System Neoplasms / therapy. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug-Related Side Effects and Adverse Reactions. Etoposide / administration & dosage. Feasibility Studies. Hodgkin Disease / diagnosis. Hodgkin Disease / therapy. Humans. Hypocalcemia / chemically induced. Hypocalcemia / pathology. Kidney Neoplasms / diagnosis. Kidney Neoplasms / therapy. Melphalan / administration & dosage. Neuroblastoma / diagnosis. Neuroblastoma / therapy. Pilot Projects. Recurrence. Risk Factors. Sarcoma / diagnosis. Sarcoma / therapy. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome. Wilms Tumor / diagnosis. Wilms Tumor / therapy

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  • (PMID = 18376282.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; M487QF2F4V / Amifostine; Q41OR9510P / Melphalan
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3. Gardner SL: Application of stem cell transplant for brain tumors. Pediatr Transplant; 2004 Jun;8 Suppl 5:28-32
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  • Brain tumors are the second most common malignancy in children and the most common solid tumor.
  • This approach has been most successful in chemosensitive tumors including medulloblastoma, supratentorial primitive neuroectodermal tumors (SPNET) and central nervous system germ cell tumors (CNS GCT).
  • Future studies will most likely include the use of new agents as part of the cytoreduction.
  • Several possibilities include the use of anti-angiogenesis agents, monoclonal antibodies and biologic response modifiers.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Hematopoietic Stem Cell Transplantation

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  • (PMID = 15125703.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 25
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4. Han Y, Wang J, He T, Ransohoff RM: TNF-alpha down-regulates CXCR4 expression in primary murine astrocytes. Brain Res; 2001 Jan 5;888(1):1-10
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  • The physiological roles of CXCR4 in developmental patterning of the nervous and hematopoietic system; gastrointestinal angiogenesis; and cardiac organogenesis were established by studies in gene-targeted mice.
  • Studies on CXCR4 expression and regulation in neuroepithelial cells are fundamental for understanding its physiopathologic roles in the central nervous system (CNS).
  • We show here that CXCR4 expression by primary mouse astrocytes is suppressed by exposure to tumor necrosis factor-alpha (TNF-alpha).
  • These results suggest that TNF-alpha could modulate HIV and brain tumor pathogenesis and immune-mediated inflammation in the central nervous system (CNS) by regulation of CXCR4 expression.
  • [MeSH-major] Astrocytes / enzymology. Astrocytes / immunology. Receptors, CXCR4 / genetics. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] AIDS Dementia Complex / immunology. AIDS Dementia Complex / metabolism. Animals. Brain Neoplasms / immunology. Brain Neoplasms / metabolism. Cells, Cultured. Chemokine CXCL12. Chemokines, CXC / metabolism. Down-Regulation / drug effects. Down-Regulation / physiology. Encephalitis / immunology. Encephalitis / metabolism. Enzyme Activation / drug effects. Enzyme Activation / immunology. Female. Gene Expression / drug effects. Gene Expression / immunology. Humans. Male. Mice. Mice, Inbred Strains. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. RNA, Messenger / metabolism. Transcription, Genetic / drug effects. Transcription, Genetic / immunology

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  • (PMID = 11146046.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA 62220; United States / NINDS NIH HHS / NS / R01-NS 32151
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, CXCR4; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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5. Kawakami M, Kawakami K, Puri RK: Interleukin-4-Pseudomonas exotoxin chimeric fusion protein for malignant glioma therapy. J Neurooncol; 2003 Oct;65(1):15-25
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  • Human malignant glioma cell lines, primary cell cultures, and tumor specimens derived from surgical samples have been shown to overexpress high-affinity receptors (R) for interleukin-4 (IL-4) in vitro and in situ.
  • However, IL-4 has been reported to mediate functional effects in several solid tumor cell lines.
  • To target IL-4Rs on tumor cells, we have produced a chimeric recombinant fusion protein consisting of a binding ligand, circularly permuted IL-4 and a mutated form of Pseudomonas exotoxin.
  • Recombinant cpIL4-PE is highly and specifically cytotoxic to glioma cell lines in vitro, while it is not cytotoxic or less cytotoxic to hematopoietic and normal brain cells.
  • Encouraging preclinical efficacy, safety, and tolerability studies lead to testing of this agent in patients with recurrent glioblastoma.
  • The central nervous system toxicities observed were attributed to the volume of infusion and/or nonspecific toxicity.
  • [MeSH-major] Brain Neoplasms / drug therapy. Glioma / drug therapy. Immunotoxins / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials as Topic. Drug Evaluation, Preclinical. Humans. Interleukin-4. Receptors, Interleukin-4 / metabolism. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 14649882.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunotoxins; 0 / Receptors, Interleukin-4; 0 / Recombinant Fusion Proteins; 0 / interleukin 4 (38-37)-PE38KDEL; 207137-56-2 / Interleukin-4
  • [Number-of-references] 51
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6. Nagai A, Nakagawa E, Choi HB, Hatori K, Kobayashi S, Kim SU: Erythropoietin and erythropoietin receptors in human CNS neurons, astrocytes, microglia, and oligodendrocytes grown in culture. J Neuropathol Exp Neurol; 2001 Apr;60(4):386-92
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  • [Title] Erythropoietin and erythropoietin receptors in human CNS neurons, astrocytes, microglia, and oligodendrocytes grown in culture.
  • Erythropoietin (EPO) is a hematopoietic growth factor that stimulates proliferation and differentiation of erythroid precursor cells and is also known to exert neurotrophic activity in the central nervous system (CNS).
  • However, little is known about expression of EPO and EPO receptor (EPOR) in human CNS tissues.
  • These results suggest that proinflammatory cytokines regulate expression of EPO and EPOR in human neurons, astrocytes, and microglia and further facilitate interactions among different cell types in the human CNS.
  • [MeSH-minor] Cells, Cultured. Central Nervous System / cytology. Central Nervous System / embryology. Central Nervous System / metabolism. Cytokines / pharmacology. Enzyme-Linked Immunosorbent Assay. Gene Expression / drug effects. Humans. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 11305874.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Receptors, Erythropoietin; 0 / Tumor Necrosis Factor-alpha; 11096-26-7 / Erythropoietin
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7. Landen JW, Hau V, Wang M, Davis T, Ciliax B, Wainer BH, Van Meir EG, Glass JD, Joshi HC, Archer DR: Noscapine crosses the blood-brain barrier and inhibits glioblastoma growth. Clin Cancer Res; 2004 Aug 1;10(15):5187-201
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  • The opium alkaloid noscapine is a commonly used antitussive agent available in Europe, Asia, and South America.
  • Although the mechanism by which it suppresses coughing is currently unknown, it is presumed to involve the central nervous system.
  • In this study, we show that noscapine inhibits the proliferation of rat C6 glioma cells in vitro (IC(50) = 100 microm) and effectively crosses the blood-brain barrier at rates similar to the ones found for agents such as morphine and [Met]enkephalin that have potent central nervous system activity (P < or = 0.05).
  • Daily oral noscapine treatment (300 mg/kg) administered to immunodeficient mice having stereotactically implanted rat C6 glioblasoma into the striatum revealed a significant reduction of tumor volume (P < or = 0.05).
  • This was achieved with no identifiable toxicity to the duodenum, spleen, liver, or hematopoietic cells as determined by pathological microscopic examination of these tissues and flow cytometry.
  • Furthermore, noscapine treatment resulted in little evidence of toxicity to dorsal root ganglia cultures as measured by inhibition of neurite outgrowth and yielded no evidence of peripheral neuropathy in animals.
  • These unique properties of noscapine, including its ability to cross the blood-brain barrier, interfere with microtubule dynamics, arrest tumor cell division, reduce tumor growth, and minimally affect other dividing tissues and peripheral nerves, warrant additional investigation of its therapeutic potential.
  • [MeSH-major] Antitussive Agents / pharmacology. Blood-Brain Barrier / drug effects. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Noscapine / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Brain / metabolism. Brain / pathology. Bromodeoxyuridine / pharmacology. Cattle. Cell Count. Cell Line, Tumor. Cell Proliferation / drug effects. Chromatography, High Pressure Liquid. Coloring Agents / pharmacology. DNA / metabolism. Dose-Response Relationship, Drug. Endothelium, Vascular / pathology. Female. Flow Cytometry. Humans. Image Processing, Computer-Assisted. Inhibitory Concentration 50. Mice. Mice, Nude. Mice, SCID. Microcirculation / metabolism. Microtubules / drug effects. Mitosis. Models, Biological. Neoplasm Transplantation. Neuroglia / metabolism. Rats. S Phase. Time Factors. Tubulin / chemistry


8. de Oliveira DM, Pitanga BP, Grangeiro MS, Lima RM, Costa MF, Costa SL, Clarêncio J, El-Bachá RS: Catechol cytotoxicity in vitro: induction of glioblastoma cell death by apoptosis. Hum Exp Toxicol; 2010 Mar;29(3):199-212
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  • The exposure to benzene is a public health problem.
  • Although the most well-known effect of benzene is hematopoietic toxicity, there is little information about the benzene and its metabolites effects on the central nervous system (CNS).
  • GL-15 cell cultures were used as a model to provide more information about the toxic effects of aromatic compounds to the CNS.
  • [MeSH-major] Apoptosis / drug effects. Brain Neoplasms / pathology. Catechols / toxicity. Environmental Pollutants / toxicity. Glioblastoma / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Shape / drug effects. Cell Survival / drug effects. Chromatin Assembly and Disassembly / drug effects. Comet Assay. DNA Damage. Dose-Response Relationship, Drug. Glutathione / metabolism. Humans. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. bcl-2-Associated X Protein / metabolism

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  • (PMID = 20097727.001).
  • [ISSN] 1477-0903
  • [Journal-full-title] Human & experimental toxicology
  • [ISO-abbreviation] Hum Exp Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Catechols; 0 / Environmental Pollutants; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; GAN16C9B8O / Glutathione; LF3AJ089DQ / catechol
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9. Kushner BH, Cheung NK, Kramer K, Dunkel IJ, Calleja E, Boulad F: Topotecan combined with myeloablative doses of thiotepa and carboplatin for neuroblastoma, brain tumors, and other poor-risk solid tumors in children and young adults. Bone Marrow Transplant; 2001 Sep;28(6):551-6
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  • Topotecan appears to be relatively unaffected by the most common multidrug resistance mechanisms, may potentiate cytotoxicity of alkylators, has good penetration into the central nervous system, is active against a variety of neoplasms, and has myelosuppression as its paramount toxicity.
  • The patients were 1 to 29 (median 4) years old; 18 were in complete remission (CR) and three in partial remission (PR).
  • Post-transplant treatment included radiotherapy alone (four patients) or plus biological agents (11 patients with neuroblastoma).
  • With a follow-up of 6+ to 32+ (median 11+) months, event-free survivors include 10/11 neuroblastoma patients (first CR), 4/5 brain tumor patients (second PR or CR), 1/3 patients with metastatic Ewing's sarcoma (first or second CR), and a patient transplanted for multiply recurrent immature ovarian teratoma; a patient with desmoplastic small round-cell tumor (second PR) had progressive disease at 8 months.
  • Favorable results for disease control, manageable toxicity, and the antitumor profiles of topotecan, thiotepa, and carboplatin, support use of this three-drug regimen in the treatment of neuroblastoma and brain tumors; applicability to other tumors is still uncertain.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Carboplatin / administration & dosage. Neuroblastoma / drug therapy. Thiotepa / administration & dosage. Topotecan / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Female. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Radiotherapy, Adjuvant. Remission Induction. Treatment Outcome

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  • (PMID = 11607767.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA61017; United States / NCI NIH HHS / CA / CA72868
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Clinical Trial, Phase III; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 7M7YKX2N15 / Topotecan; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin
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10. Lewis LD: Preclinical and clinical studies: a preview of potential future applications of erythropoietic agents. Semin Hematol; 2004 Oct;41(4 Suppl 7):17-25
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  • [Title] Preclinical and clinical studies: a preview of potential future applications of erythropoietic agents.
  • Understanding the tissue distribution of erythropoietin receptors and cellular actions of erythropoietic agents may facilitate the development of wider applications for these compounds.
  • Erythropoietin receptors have been identified in the central nervous system (CNS), retina, heart, vascular endothelium, kidney, lung, liver, gastrointestinal and reproductive tracts, and erythroid bone marrow precursors.
  • Potential benefits of erythropoietic agents in several therapeutic areas may result from actions other than hematopoiesis stimulation.
  • Their hematopoietic effects may also have broader applications in treating anemia of the elderly and non-chemotherapy (CT)-related anemia in patients with cancer.
  • Furthermore, because hypoxic tumor cells tend to be more resistant to radiation therapy (RT) and some forms of CT, and more aggressive than normoxic cells, increased oxygenation resulting from anemia correction may increase RT and CT sensitivity, possibly impacting treatment outcomes.
  • Preliminary evidence suggests erythropoietin has CNS neuroprotective effects, including potential clinical benefits in ischemic stroke.
  • Thus, accumulating evidence suggests that erythropoietic agents may have clinical utility outside CT-related anemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic / trends. Drug Evaluation, Preclinical / trends. Erythropoietin / therapeutic use
  • [MeSH-minor] Anemia / chemically induced. Anemia / drug therapy. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Humans. Models, Biological

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  • (PMID = 15768475.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 11096-26-7 / Erythropoietin
  • [Number-of-references] 64
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11. Hagemeister FB: Treatment of relapsed aggressive lymphomas: regimens with and without high-dose therapy and stem cell rescue. Cancer Chemother Pharmacol; 2002 May;49 Suppl 1:S13-20
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  • [Title] Treatment of relapsed aggressive lymphomas: regimens with and without high-dose therapy and stem cell rescue.
  • For example, the International Prognostic Factor Index system, now in common usage, delineates four different groups of patients with differing complete remission, freedom from progression, and overall survival rates.
  • The Tumor Score System, developed at MDACC, delineates only two groups with very different survival rates, and may be a better scoring system for patients with diffuse large cell lymphomas, primarily because of its inclusion of the serum beta(2)-microglobulin level prior to treatment, an important predictor of relapse.
  • For the patient with relapse or progressive disease following induction with CHOP or a similar regimen, the type of response to initial therapy plays an important role in determining potential response to salvage therapy, including high-dose therapy followed by stem cell rescue.
  • Other limitations for SCT protocols include age greater than 60 or 65 years, significant chronic obstructive pulmonary, renal, or cardiac disease, a poor performance status, and central nervous system or marrow involvement.
  • Three broad groups of relapse therapy for aggressive lymphoma have been described, based upon the drugs contained within these regimens.
  • Results with these programs vary widely and are likely different because of tumor-related features prior to relapse therapy, including size of mass, beta(2)-microglobulin level, LDH level, and type of response to initial therapy.
  • Other features, such as dose of therapy, specific drugs utilized, and number of prior treatments also play important roles in determining results with relapse therapy.
  • Results varied according to type of response achieved with initial therapy, and serum LDH and beta(2)-microglobulin levels prior to treatment with MINE-ESHAP.
  • Using more intensive doses of ifosfamide and etoposide, we have described therapy for 36 patients with relapsed aggressive lymphomas, prior to pheresis and SCT.
  • This regimen has been extensively studied in patients with relapsed aggressive lymphomas and Hodgkin's disease, followed by SCT.
  • In patients with relapsed lymphomas, ICE has achieved a 66% complete response rate, with 89% undergoing transplant.
  • Finally, we have recently studied paclitaxel in combination with topotecan for relapsed and refractory aggressive lymphomas.
  • These and newer combinations should be further developed to treat patients in relapse of aggressive lymphomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / therapeutic use. Etoposide / therapeutic use. Ifosfamide / therapeutic use. Lymphoma / drug therapy
  • [MeSH-minor] Aged. Antineoplastic Agents, Alkylating / therapeutic use. Cyclophosphamide. Doxorubicin. Drug Administration Schedule. Hematopoietic Stem Cell Transplantation. Humans. Middle Aged. Prednisone. Prognosis. Randomized Controlled Trials as Topic. Recurrence. Vincristine

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  • (PMID = 12042984.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; UM20QQM95Y / Ifosfamide; VB0R961HZT / Prednisone; CHOP protocol; ICE protocol 3
  • [Number-of-references] 38
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12. Heath JA, Broxson EH Jr, Dole MG, Filippa DA, George D, Lyden D, Dunkel IJ: Epstein-Barr virus-associated lymphoma in a child undergoing an autologous stem cell rescue. J Pediatr Hematol Oncol; 2002 Feb;24(2):160-3
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  • In this article, a patient with EBV-lymphoma after autologous stem cell rescue for treatment of a nonhematologic solid tumor is described.
  • The child, a 4-year-old boy, had unilateral retinoblastoma with metastatic spread to the central nervous system.
  • He had previously received both local tumor bed and craniospinal radiation therapy together with intensive myeloablative alkylator chemotherapy before autologous stem cell rescue.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Eye Neoplasms / pathology. Hematopoietic Stem Cell Transplantation. Herpesvirus 4, Human / isolation & purification. Lymphoma, Large B-Cell, Diffuse / etiology. Neoplasms, Second Primary / etiology. Retinoblastoma / secondary
  • [MeSH-minor] Acyclovir / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents, Phytogenic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiviral Agents / therapeutic use. Carboplatin / administration & dosage. Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / radiotherapy. Central Nervous System Neoplasms / secondary. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Disease Progression. Etoposide / administration & dosage. Eye Enucleation. Fatal Outcome. Humans. Immunocompromised Host. Immunoglobulins, Intravenous / therapeutic use. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Immunotherapy. Male. Meningeal Neoplasms / drug therapy. Meningeal Neoplasms / radiotherapy. Meningeal Neoplasms / secondary. Meningeal Neoplasms / therapy. Methylprednisolone / therapeutic use. Neoplasm Recurrence, Local. Optic Nerve Neoplasms / radiotherapy. Optic Nerve Neoplasms / secondary. Radiotherapy, Adjuvant. Rituximab. Thiotepa / therapeutic use. Vincristine / therapeutic use

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  • (PMID = 11998794.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents, Phytogenic; 0 / Antiviral Agents; 0 / Immunoglobulins, Intravenous; 0 / Immunosuppressive Agents; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; X4HES1O11F / Acyclovir; X4W7ZR7023 / Methylprednisolone
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13. Aboody KS, Najbauer J, Schmidt NO, Yang W, Wu JK, Zhuge Y, Przylecki W, Carroll R, Black PM, Perides G: Targeting of melanoma brain metastases using engineered neural stem/progenitor cells. Neuro Oncol; 2006 Apr;8(2):119-26
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  • Brain metastases are an increasingly frequent and serious clinical problem for cancer patients, especially those with advanced melanoma.
  • Given the extensive tropism of neural stem/progenitor cells (NSPCs) for pathological areas in the central nervous system, we expanded investigations to determine whether NSPCs could also target multiple sites of brain metastases in a syngeneic experimental melanoma model.
  • Using cytosine deaminase-expressing NSPCs (CD-NSPCs) and systemic 5-fluorocytosine (5-FC) pro-drug administration, we explored their potential as a cell-based targeted drug delivery system to disseminated brain metastases.
  • Furthermore, in our therapeutic paradigm, animals with established melanoma brain metastasis received intracranial implantation of CD-NSPCs followed by systemic 5-FC treatment, resulting in a significant (71%) reduction in tumor burden.
  • These data provide proof of principle for the use of NSPCs for targeted delivery of therapeutic gene products to melanoma brain metastases.
  • [MeSH-major] Brain Neoplasms / secondary. Brain Neoplasms / therapy. Melanoma, Experimental / secondary. Melanoma, Experimental / therapy. Neurons / transplantation. Stem Cell Transplantation
  • [MeSH-minor] Animals. Cell Line, Tumor. Immunohistochemistry. Mice. Neoplasm Transplantation

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  • (PMID = 16524944.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1871940
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14. Gardner SL, Asgharzadeh S, Green A, Horn B, McCowage G, Finlay J: Intensive induction chemotherapy followed by high dose chemotherapy with autologous hematopoietic progenitor cell rescue in young children newly diagnosed with central nervous system atypical teratoid rhabdoid tumors. Pediatr Blood Cancer; 2008 Aug;51(2):235-40
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  • [Title] Intensive induction chemotherapy followed by high dose chemotherapy with autologous hematopoietic progenitor cell rescue in young children newly diagnosed with central nervous system atypical teratoid rhabdoid tumors.
  • BACKGROUND: Central nervous system (CNS) atypical teratoid rhabdoid tumors (AT/RT) are rare tumors of childhood with a dismal prognosis.
  • METHODS: Thirteen children newly diagnosed with CNS AT/RT were treated with either the "Head Start I" (HS I) or "Head Start II" (HS II) regimens.
  • Consolidation for both regimens included carboplatin, thiotepa, and etoposide with autologous hematopoietic progenitor cell rescue (AHPCR).
  • CONCLUSION: Three of seven children with CNS AT/RT treated on HS II have experienced long term remissions.
  • Long term survival can be achieved in a subset of young children with CNS AT/RT following resection with the use of multi-drug chemotherapy including high dose methotrexate and myeloablative chemotherapy without radiation therapy (RT).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Hematopoietic Stem Cell Transplantation. Rhabdoid Tumor / therapy. Teratoma / therapy

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  • (PMID = 18381756.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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15. Hwang JJ, Kim YS, Kim MJ, Jang S, Lee JH, Choi J, Ro S, Hyun YL, Lee JS, Kim CS: A novel histone deacetylase inhibitor, CG0006, induces cell death through both extrinsic and intrinsic apoptotic pathways. Anticancer Drugs; 2009 Oct;20(9):815-21
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  • Histone deacetylase inhibitors (HDACIs) are potent anticancer drugs, and suberoylanilide hydroxamic acid is used for the treatment of cutaneous T-cell lymphoma patients.
  • Micromolar levels of CG0006 induced cell death in several breast, central nervous system, colon, hematopoietic, lung, melanoma, ovarian, prostatic, renal, and stomach cancer cell lines.
  • The HDACI CG0006 may be a potent anticancer drug for solid tumors and leukemia.
  • [MeSH-major] Cell Death / drug effects. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors / metabolism. Hydroxamic Acids / pharmacology. Piperidines / pharmacology
  • [MeSH-minor] Acetylation / drug effects. Caspases / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Gene Expression / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Histones / metabolism. Humans. Sulfonamides. Tubulin / metabolism. bcl-X Protein / genetics. bcl-X Protein / metabolism

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  • (PMID = 19644355.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CG 0006; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Piperidines; 0 / Sulfonamides; 0 / Tubulin; 0 / bcl-X Protein; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 58IFB293JI / vorinostat; EC 3.4.22.- / Caspases; F4H96P17NZ / belinostat
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16. Sun ZK, Yang HQ, Pan J, Zhen H, Wang ZQ, Chen SD, Ding JQ: Protective effects of erythropoietin on tau phosphorylation induced by beta-amyloid. J Neurosci Res; 2008 Oct;86(13):3018-27
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  • The hematopoietic cytokine erythropoietin (Epo) is now considered as a viable agent with regard to central nervous system injury in a variety of cellular systems.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Erythropoietin / pharmacology. Neurons / drug effects. Neuroprotective Agents / pharmacology. tau Proteins / drug effects
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Humans. Phosphorylation. Signal Transduction

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18512763.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Neuroprotective Agents; 0 / tau Proteins; 11096-26-7 / Erythropoietin
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17. Turbyville TJ, Gürsel DB, Tuskan RG, Walrath JC, Lipschultz CA, Lockett SJ, Wiemer DF, Beutler JA, Reilly KM: Schweinfurthin A selectively inhibits proliferation and Rho signaling in glioma and neurofibromatosis type 1 tumor cells in a NF1-GRD-dependent manner. Mol Cancer Ther; 2010 May;9(5):1234-43
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  • [Title] Schweinfurthin A selectively inhibits proliferation and Rho signaling in glioma and neurofibromatosis type 1 tumor cells in a NF1-GRD-dependent manner.
  • Neurofibromatosis type 1 (NF1) is the most common genetic disease affecting the nervous system.
  • Natural products represent an opportunity to develop new therapies, as they have been evolutionarily selected to play targeted roles in organisms.
  • Schweinfurthin A is a prenylated stilbene natural product that has previously shown specific inhibitory activity against brain and hematopoietic tumor lines.
  • We show that patient-derived GBM and NF1 malignant peripheral nerve sheath tumor (MPNST) lines, as well as tumor lines derived from the Nf1-/+;Trp53-/+ (NPcis) mouse model of astrocytoma and MPNST are highly sensitive to inhibition by schweinfurthin A and its synthetic analogs.
  • In contrast, primary mouse astrocytes are resistant to the growth inhibitory effects of schweinfurthin A, suggesting that schweinfurthin A may act specifically on tumor cells.
  • In summary, we have identified a class of small molecules that specifically inhibit growth of cells from both central and peripheral nervous system tumors and seem to act on NF1-deficient cells through cytoskeletal reorganization correlating to changes in Rho signaling.

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  • (PMID = 20442305.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / Intramural NIH HHS / / Z01 BC010541-06; United States / PHS HHS / / HHSN261200800001E
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / Stilbenes; 0 / schweinfurthin A; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS187633; NLM/ PMC3268685
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18. Polanczyk M, Yellayi S, Zamora A, Subramanian S, Tovey M, Vandenbark AA, Offner H, Zachary JF, Fillmore PD, Blankenhorn EP, Gustafsson JA, Teuscher C: Estrogen receptor-1 (Esr1) and -2 (Esr2) regulate the severity of clinical experimental allergic encephalomyelitis in male mice. Am J Pathol; 2004 Jun;164(6):1915-24
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  • Estrogens and estrogen-receptor signaling function in establishing and regulating the female immune system and it is becoming increasingly evident that they may play a similar role in males.
  • We report that B10.PL/SnJ male mice with a disrupted estrogen receptor-1 (alpha) gene (Esr1(-/-)) develop less severe clinical experimental allergic encephalomyelitis (EAE) compared to either Esr1(+/-) or wild-type (Esr1(+/+)) controls when immunized with myelin basic protein peptide Ac1-11 (MBP(Ac1-11)).
  • In contrast, the disease course in B10.PL/SnJ male mice with a disrupted estrogen receptor-2 (beta) gene (Esr2(-/-)) does not differ from that of wild-type (Esr2(+/+)) mice.
  • No significant differences in central nervous system histopathology or MBP(Ac1-11)-specific T-cell responses as assessed by proliferation and interleukin-2 production were observed as a function of either Esr1 or Esr2 genotype.
  • Interferon-gamma secretion was found to be negatively regulated by Esr1 whereas interleukin-6 and tumor necrosis factor-alpha secretion exhibited classical Esr2 gene dose responses.
  • The contribution of the hematopoietic and nonhematopoietic cellular compartments associated with the heterotic effect at Esr2 in regulating the severity of clinical EAE was identified using reciprocal hematopoietic radiation bone marrow chimeras generated between male wild-type and Esr2(+/-) mice.
  • Wild-type --> Esr2(+/-) mice exhibited EAE equivalent in severity to that seen in Esr2(+/-) --> Esr2(+/-) control constructs; both of which were more severe than the clinical signs observed in Esr2(+/-) --> wild-type and wild-type --> wild-type mice.

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  • (PMID = 15161628.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI4515; United States / NINDS NIH HHS / NS / R01 NS023444; United States / NINDS NIH HHS / NS / R01 NS036526; United States / NINDS NIH HHS / NS / NS36526; United States / NIAID NIH HHS / AI / AI41747; United States / NIAID NIH HHS / AI / AI2376; United States / NIAID NIH HHS / AI / R01 AI041747; United States / NINDS NIH HHS / NS / NS23444
  • [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 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Receptors, Estrogen
  • [Other-IDs] NLM/ PMC1615766
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