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1. Stefanowicz J, Izycka-Swieszewska E, Drozyńska E, Pienczk J, Połczyńska K, Czauderna P, Sierota D, Bień E, Stachowicz-Stencel T, Kosiak W, Balcerska A: Neuroblastoma and opsoclonus-myoclonus-ataxia syndrome--clinical and pathological characteristics. Folia Neuropathol; 2008;46(3):176-85
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  • [Title] Neuroblastoma and opsoclonus-myoclonus-ataxia syndrome--clinical and pathological characteristics.
  • The group included two ganglioneuroblastomas, one ganglioneuroma and one differentiating neuroblastoma.
  • Immunohistochemical analysis of inflammatory infiltrations revealed mixed type populations of lymphocytes with prevalence of the cytotoxic type (CD8 and CD56-positive cells).
  • All patients were treated by surgery alone or with adjuvant chemotherapy with a positive outcome.
  • Children with OMA and neuroblastoma despite a good oncological prognosis often present permanent neurological and developmental deficits.


2. Rousseau R, Combaret V, Yvon E, Schell M, Philip I, Puisieux A, Frappaz D, Philip T, Bergeron C: [Immunotherapy of poor-prognosis neuroblastoma in children: from bench to bedside]. Bull Cancer; 2006 Feb;93(2):153-61
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  • [Title] [Immunotherapy of poor-prognosis neuroblastoma in children: from bench to bedside].
  • [Transliterated title] Immunothérapie des neuroblastomes de mauvais pronostic chez l'enfant: depuis les concepts fondamentaux jusqu'aux essais cliniques de phase I-II.
  • During the last two decades, improvements in the induction and consolidation treatment phases in patients with high-risk neuroblastoma have not translated into significant increases in survival rates.
  • Efforts to improve outcome have used high-dose chemotherapy with stem cell rescue and more recently, differentiating (retinoids) and antiangiogenic agents.
  • In parallel, immunotherapy has become an increasingly important part of the treatment of high-risk neuroblastoma.
  • [MeSH-major] Immunotherapy. Neuroblastoma / therapy

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  • (PMID = 16517413.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 60
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3. Izycka-Swieszewska E, Drozyńska E, Rzepko R, Dembowska B, Grajkowska W, Brozyna A, Perek D, Balcerska A, Jaśkiewicz K: Clinicopathological considerations on angiogenic potential in neuroblastoma Schwannian stroma - poor tumours. Folia Neuropathol; 2007;45(1):1-8
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  • [Title] Clinicopathological considerations on angiogenic potential in neuroblastoma Schwannian stroma - poor tumours.
  • The aim of the study was to determine microscopic angiogenic parameters of neuroblastoma (NB) Schwannian stroma-poor tumours.
  • Examined tissue samples from 62 NB came from 39 untreated and 23 chemotherapy pretreated tumours.
  • The clinicopathological data comprised: patients' age, gender, survival, tumour site and stage, tumour histology and MYCN status.The morphological analysis of the angiogenic potential concentrated on examination of vascular patterns - classical type or pathological angiogenesis with mural microvascular proliferation (MVP).
  • Pathologic angiogenesis with MVP, including simple and/or glomeruloid type, was encountered in 25 cases and was more frequent in differentiating histology subtype and extraadrenal tumours.
  • Pathologic type angiogenesis and lower VD were found to be associated with shorter survival.
  • This points toward heterogeneity of NB tumours in vascular aspects, possibly affecting tumours' reactivity to antiangiogenic therapy.

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  • (PMID = 17357004.001).
  • [ISSN] 1641-4640
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins
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4. Yu JH, Nakajima A, Nakajima H, Diller LR, Bloch KD, Bloch DB: Restoration of promyelocytic leukemia protein-nuclear bodies in neuroblastoma cells enhances retinoic acid responsiveness. Cancer Res; 2004 Feb 1;64(3):928-33
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  • [Title] Restoration of promyelocytic leukemia protein-nuclear bodies in neuroblastoma cells enhances retinoic acid responsiveness.
  • Neuroblastoma is the most common solid tumor of infancy and is believed to result from impaired differentiation of neuronal crest embryonal cells.
  • During the course of studies to examine the composition and function of PML-nuclear bodies, we observed that the human neuroblastoma cell line SH-SY5Y lacked these structures and that the absence of PML-nuclear bodies was a feature of N- and I-type, but not S-type, neuroblastoma cell lines.
  • Induction of neuroblastoma cell differentiation with 5-bromo-2'deoxyuridine, all-trans-retinoic acid, or IFN-gamma induced PML-nuclear body formation.
  • PML-nuclear bodies were not detected in tissue sections prepared from undifferentiated neuroblastomas but were present in neuroblasts in differentiating tumors.
  • Expression of PML in neuroblastoma cells restored PML-nuclear bodies, enhanced responsiveness to all-trans-retinoic acid, and induced cellular differentiation.
  • Pharmacological therapies that increase PML expression may prove to be important components of combined modalities for the treatment of neuroblastoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Nucleus Structures / metabolism. Neoplasm Proteins / biosynthesis. Neuroblastoma / drug therapy. Neuroblastoma / metabolism. Nuclear Proteins. Transcription Factors / biosynthesis. Tretinoin / pharmacology
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Differentiation / physiology. Cell Line, Tumor. HL-60 Cells. Humans. Immunohistochemistry. Tumor Suppressor Proteins

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  • (PMID = 14871822.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-051179; United States / NIDDK NIH HHS / DK / DK-40561; United States / NHLBI NIH HHS / HL / HL-57172
  • [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 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; 5688UTC01R / Tretinoin
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5. Chen L, Malcolm AJ, Wood KM, Cole M, Variend S, Cullinane C, Pearson AD, Lunec J, Tweddle DA: p53 is nuclear and functional in both undifferentiated and differentiated neuroblastoma. Cell Cycle; 2007 Nov 1;6(21):2685-96
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  • [Title] p53 is nuclear and functional in both undifferentiated and differentiated neuroblastoma.
  • Aberrant cytoplasmic sequestration has been reported as an alternative mechanism of p53 inactivation to mutation in neuroblastoma.
  • We hypothesized that p53 localization and function in neuroblastoma is related to differentiation status.
  • Eighty-two untreated and 24 paired pre and post-chemotherapy neuroblastomas were studied by immunocytochemistry for p53, p21(WAF1), BAX, Bcl2 and Ki67.
  • Predominantly nuclear p53 was detected in undifferentiated neuroblastoma, and both nuclear and cytoplasmic p53 in differentiating neuroblastoma.
  • There was a significant reduction in p53, p21(WAF1) and Ki67 LI after chemotherapy (p < 0.01), an increase in BAX (p <0.05), but no change in Bcl2. p53 localization and function were examined in two p53 wild-type undifferentiated and 9-cis retinoic acid differentiated neuroblastoma cell lines.
  • Following irradiation, there was upregulation of p53, p21(WAF1) and MDM2, but less induced PARP and caspase 3 cleavage in differentiated cells, suggesting intact p53 transcriptional function, but resistance to apoptosis. p53 function in undifferentiated and differentiated cells was confirmed by upregulation of p21(WAF1) and MDM2 following Nutlin-3 treatment.
  • In conclusion, p53 is predominantly nuclear and functional in neuroblastoma regardless of differentiation status.
  • [MeSH-major] Cell Differentiation / physiology. Cell Nucleus / physiology. Neuroblastoma / metabolism. Neuroblastoma / pathology. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 17912039.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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6. Murata H, Tajima N, Nagashima Y, Yao M, Baba M, Goto M, Kawamoto S, Yamamoto I, Okuda K, Kanno H: Von Hippel-Lindau tumor suppressor protein transforms human neuroblastoma cells into functional neuron-like cells. Cancer Res; 2002 Dec 1;62(23):7004-11
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  • [Title] Von Hippel-Lindau tumor suppressor protein transforms human neuroblastoma cells into functional neuron-like cells.
  • To elucidate the neuronal differentiating potential of VHL protein in neuroblastoma cells, we overexpressed or inhibited VHL protein in human neuroblastoma cells (SY-SH5Y), and examined the morphological change, expressions of neuronal markers, and electrophysiological functions.
  • Also, by treatment with retinoic acid, they rapidly underwent cell death related to apoptosis.
  • In conclusion, VHL protein has a neuronal differentiating potential to transform neuroblastoma cells into functional neuron-like cells.
  • Our finding of the neuronal differentiation of neuroblastoma cells under the control of the VHL gene may contribute to the development of clinical techniques for neuronal regeneration in the case of intractable neuronal diseases and for differentiation therapy against neuroblastomas.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Ligases / physiology. Neuroblastoma / pathology. Neurons / cytology. Tumor Suppressor Proteins. Ubiquitin-Protein Ligases
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. Cell Differentiation / genetics. Down-Regulation. Ether-A-Go-Go Potassium Channels. Genetic Therapy. Humans. Ion Channel Gating / physiology. Neurofilament Proteins / biosynthesis. Neurofilament Proteins / genetics. Neurofilament Proteins / metabolism. Neuropeptide Y / biosynthesis. Neuropeptide Y / genetics. Neuropeptide Y / secretion. Potassium Channels / biosynthesis. Potassium Channels / genetics. Potassium Channels / physiology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Sodium Channels / physiology. Transfection. Tretinoin / pharmacology. Tumor Cells, Cultured. Von Hippel-Lindau Tumor Suppressor Protein

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  • (PMID = 12460920.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ether-A-Go-Go Potassium Channels; 0 / Neurofilament Proteins; 0 / Neuropeptide Y; 0 / Potassium Channels; 0 / RNA, Messenger; 0 / Sodium Channels; 0 / Tumor Suppressor Proteins; 108688-71-7 / neurofilament protein H; 5688UTC01R / Tretinoin; EC 6.- / Ligases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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7. Messi E, Florian MC, Caccia C, Zanisi M, Maggi R: Retinoic acid reduces human neuroblastoma cell migration and invasiveness: effects on DCX, LIS1, neurofilaments-68 and vimentin expression. BMC Cancer; 2008;8:30
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  • [Title] Retinoic acid reduces human neuroblastoma cell migration and invasiveness: effects on DCX, LIS1, neurofilaments-68 and vimentin expression.
  • BACKGROUND: Neuroblastoma is a severe pediatric tumor, histologically characterised by a variety of cellular phenotypes.
  • One of the pharmacological approaches to neuroblastoma is the treatment with retinoic acid.
  • The mechanism of action of retinoic acid is still unclear, and the development of resistance to this differentiating agent is a great therapy problem.Doublecortin, a microtubule-associated protein involved in neuronal migration, has recently been proposed as a molecular marker for the detection of minimal residual disease in human neuroblastoma.
  • Nevertheless, no information is available on the expression of doublecortin in the different cell-types composing human neuroblastoma, its correlation with neuroblastoma cell motility and invasiveness, and the possible modulations exerted by retinoic acid treatment.
  • METHODS: We analysed by immunofluorescence and by Western blot analysis the presence of doublecortin, lissencephaly-1 (another protein involved in neuronal migration) and of two intermediate filaments proteins, vimentin and neurofilament-68, in SK-N-SH human neuroblastoma cell line both in control conditions and under retinoic acid treatment.
  • Treatment with retinoic acid reduces cell migration and invasiveness, down regulates doublecortin and lissencephaly-1 expression and up regulates neurofilament-68 expression.
  • CONCLUSION: a) Doublecortin is expressed in human neuroblastoma cells that show high motility and invasiveness;b) Retinoic acid treatment reduces migration and invasiveness of the more aggressive cell components of SK-N-SH cells;c) The cells that after retinoic acid exposure show migration and invasive capability may be identified on the basis of doublecortin expression.
  • [MeSH-major] 1-Alkyl-2-acetylglycerophosphocholine Esterase / biosynthesis. Cell Movement / drug effects. Microtubule-Associated Proteins / biosynthesis. Neuroblastoma / metabolism. Neurofilament Proteins / biosynthesis. Neuropeptides / biosynthesis. Tretinoin / pharmacology. Vimentin / biosynthesis

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  • (PMID = 18230156.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Microtubule-Associated Proteins; 0 / Neurofilament Proteins; 0 / Neuropeptides; 0 / Vimentin; 0 / doublecortin protein; 0 / neurofilament protein NF 68; 5688UTC01R / Tretinoin; EC 3.1.1.47 / 1-Alkyl-2-acetylglycerophosphocholine Esterase; EC 3.1.1.47 / PAFAH1B1 protein, human
  • [Other-IDs] NLM/ PMC2254429
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8. Lam WA, Cao L, Umesh V, Keung AJ, Sen S, Kumar S: Extracellular matrix rigidity modulates neuroblastoma cell differentiation and N-myc expression. Mol Cancer; 2010 Feb 10;9:35
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  • [Title] Extracellular matrix rigidity modulates neuroblastoma cell differentiation and N-myc expression.
  • Neuroblastoma is a pediatric malignancy characterized by tremendous clinical heterogeneity, in which some tumors are extremely aggressive while others spontaneously differentiate into benign forms.
  • Because the degree of differentiation correlates with prognosis, and because differentiating agents such as retinoic acid (RA) have proven to decrease mortality, much effort has been devoted to identifying critical regulators of neuroblastoma differentiation in the cellular microenvironment, including cues encoded in the extracellular matrix (ECM).
  • Given that RA-mediated neuroblastoma differentiation is accompanied by profound changes in cell morphology and neurite extension, both of which presumably rely upon mechanotransductive signaling systems, it occurred to us that mechanical cues from the ECM might also influence RA-mediated differentiation, which in turn might regulate clinically-relevant aspects of neuroblastoma biology.
  • In this study, we tested this hypothesis by subjecting a series of neuroblastoma culture models to ECM microenvironments of varying mechanical stiffness and examined the regulatory role of ECM stiffness in proliferation, differentiation, and expression of tumor markers.
  • Remarkably, increasing ECM stiffness also reduces expression of N-Myc, a transcription factor involved in multiple aspects of oncogenic proliferation that is used for evaluating prognosis and clinical grading of neuroblastoma.
  • Together, our data strongly support the notion that the mechanical signals from the cellular microenvironment influence neuroblastoma differentiation and do so synergistically with RA.
  • These observations support further investigation of the role of microenvironmental mechanical signals in neuroblastoma proliferation and differentiation and suggest that pharmacological agents that modulate the underlying mechanotransductive signaling pathways may have a role in neuroblastoma therapy.

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  • (PMID = 20144241.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / 1DP2OD004213; United States / NCI NIH HHS / CA / 1U54CA143836; United States / NHLBI NIH HHS / HL / F32HL078531
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC2831820
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9. Nakagawa-Yagi Y, Choi DK, Ogane N, Shimada S, Seya M, Momoi T, Ito T, Sakaki Y: Discovery of a novel compound: insight into mechanisms for acrylamide-induced axonopathy and colchicine-induced apoptotic neuronal cell death. Brain Res; 2001 Aug 3;909(1-2):8-19
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  • Here we show that acrylamide induces morphological changes and tyrosine phosphorylation of focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), a member of the FAK subfamily, in human differentiating neuroblastoma SH-SY5Y cells.
  • Our findings not only provide insight into FAK and Pyk2 functions in neuronal cells, but may also be important in the development of therapeutic agents for peripheral neuropathy and neurodegeneration.
  • [MeSH-major] Acrylamides / toxicity. Apoptosis / drug effects. Axons / drug effects. Benzimidazoles / pharmacology. Colchicine / toxicity. Cyclopentanes / pharmacology. Imidazoles / pharmacology. Nerve Degeneration / drug therapy. Neuroprotective Agents / pharmacology
  • [MeSH-minor] CELF Proteins. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Focal Adhesion Kinase 1. Focal Adhesion Kinase 2. Focal Adhesion Protein-Tyrosine Kinases. Humans. Movement Disorders / drug therapy. Movement Disorders / etiology. Movement Disorders / physiopathology. Nerve Tissue Proteins. Peripheral Nervous System Diseases / chemically induced. Peripheral Nervous System Diseases / drug therapy. Peripheral Nervous System Diseases / physiopathology. Phosphorylation / drug effects. Poly(ADP-ribose) Polymerases / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Protein-Tyrosine Kinases / drug effects. Protein-Tyrosine Kinases / metabolism. RNA, Messenger / drug effects. RNA, Messenger / metabolism. RNA-Binding Proteins / genetics. Signal Transduction / drug effects. Signal Transduction / physiology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Tumor Cells, Cultured / pathology

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  • (PMID = 11478917.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 2-cyclopentyl-5-(5-isoquinolylsulfonyl)-6-nitro-1H-benzo(D)imidazole; 0 / Acrylamides; 0 / Benzimidazoles; 0 / CELF Proteins; 0 / CELF2 protein, human; 0 / Cyclopentanes; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Nerve Tissue Proteins; 0 / Neuroprotective Agents; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; 7GBN705NH1 / imidazole; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / Focal Adhesion Kinase 2; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / PTK2 protein, human; SML2Y3J35T / Colchicine
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10. Reynolds CP: Differentiating agents in pediatric malignancies: retinoids in neuroblastoma. Curr Oncol Rep; 2000 Nov;2(6):511-8
Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differentiating agents in pediatric malignancies: retinoids in neuroblastoma.
  • High levels of either ATRA or 13-cis-RA can cause arrest of cell growth and morphologic differentiation of human neuroblastoma cell lines.
  • Phase I trials have shown that higher and more sustained drug levels were obtained with 13-cis-RA relative to ATRA.
  • A phase III randomized trial showed that high-dose pulse therapy with 13-cis-RA given after completion of intensive chemoradiotherapy (with or without autologous bone marrow transplantation) significantly improves event-free survival in high-risk neuroblastoma.
  • Because 4-HPR achieves multi-log cell kills in neuroblastoma cell lines that are resistant to ATRA and 13-cis-RA, a pediatric phase I trial is in progress to determine the maximum tolerated dose of 4-HPR, with a view toward giving 4-HPR after completion of myeloablative therapy and 13-cis-RA.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Fenretinide / pharmacology. Isotretinoin / pharmacology. Neuroblastoma / drug therapy. Tretinoin / pharmacology
  • [MeSH-minor] Child. Drug Administration Schedule. Humans. Randomized Controlled Trials as Topic. Receptors, Retinoic Acid / drug effects. Receptors, Retinoic Acid / physiology. Tumor Cells, Cultured

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  • (PMID = 11122886.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Retinoic Acid; 187EJ7QEXL / Fenretinide; 5688UTC01R / Tretinoin; EH28UP18IF / Isotretinoin
  • [Number-of-references] 50
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11. Messina E, Lupi F, Barile L, Giacomello A: Cyclic nucleotides and neuroblastoma differentiation. Nucleosides Nucleotides Nucleic Acids; 2004 Oct;23(8-9):1551-4
MedlinePlus Health Information. consumer health - Neuroblastoma.

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  • [Title] Cyclic nucleotides and neuroblastoma differentiation.
  • We have shown that intracellular cGMP levels increase during retinoic acid- and mycophenolic acid-induced neuroblastoma differentiation and that a 6 days treatment with 1 mM dbcGMP lead LAN5 cell to elaborate a network of neuritic processes suggesting an involvement of cGMP in neuroblastoma differentiation.
  • We have also investigated the effects of some specific inhibitors of phosphodiesterases (PDE1, PDE3, PDE4 and PDE5) on human neuroblastoma (LAN5 and SHEP) growth and differentiation.
  • After six days of incubation in the presence of each specific inhibitor at 10 x IC50 levels a cytostatic and differentiating effect was only observed with the PDE5 inhibitors Zaprinast and MY-5445.
  • [MeSH-major] Neuroblastoma / drug therapy. Neuroblastoma / pathology. Nucleotides, Cyclic / pharmacology
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclic AMP / metabolism. Cyclic GMP / metabolism. Dipyridamole / pharmacology. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Humans. Inhibitory Concentration 50. Phosphodiesterase Inhibitors / pharmacology. Phthalazines / pharmacology. Purinones / pharmacology. Time Factors

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  • (PMID = 15571296.001).
  • [ISSN] 1525-7770
  • [Journal-full-title] Nucleosides, nucleotides & nucleic acids
  • [ISO-abbreviation] Nucleosides Nucleotides Nucleic Acids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Nucleotides, Cyclic; 0 / Phosphodiesterase Inhibitors; 0 / Phthalazines; 0 / Purinones; 64ALC7F90C / Dipyridamole; 78351-75-4 / MY 5445; E0399OZS9N / Cyclic AMP; GXT25D5DS0 / zaprinast; H2D2X058MU / Cyclic GMP
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12. DeCou JM, Schlatter MG, Mitchell DS, Abrams RS: Primary thoracoscopic gross total resection of neuroblastoma. J Laparoendosc Adv Surg Tech A; 2005 Oct;15(5):470-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary thoracoscopic gross total resection of neuroblastoma.
  • PATIENTS AND METHODS: We reviewed the records of patients who underwent primary thoracoscopic resection of neuroblastoma (NB) between 1998 and 2002.
  • Data included demographics, symptoms, size, location, operative time, complications, hospital stay, histology, biologic markers, adjuvant therapy, and outcome.
  • Operative time ranged from 64 to 175 minutes.
  • Histology ranged from ganglioneuroma to differentiating NB, with a favorable classification in 4 of 5 cases.
  • Chemotherapy or radiation therapy was not indicated for any patient.
  • [MeSH-major] Neuroblastoma / surgery. Thoracic Neoplasms / surgery. Thoracoscopy

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  • (PMID = 16185118.001).
  • [ISSN] 1092-6429
  • [Journal-full-title] Journal of laparoendoscopic & advanced surgical techniques. Part A
  • [ISO-abbreviation] J Laparoendosc Adv Surg Tech A
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Deubzer HE, Ehemann V, Kulozik AE, Westermann F, Savelyeva L, Kopp-Schneider A, Riester D, Schwab M, Witt O: Anti-neuroblastoma activity of Helminthosporium carbonum (HC)-toxin is superior to that of other differentiating compounds in vitro. Cancer Lett; 2008 Jun 8;264(1):21-8
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  • [Title] Anti-neuroblastoma activity of Helminthosporium carbonum (HC)-toxin is superior to that of other differentiating compounds in vitro.
  • Treatment of high-risk neuroblastoma (NB) is difficult.
  • Novel therapeutics improving survival rates are urgently required.
  • We have previously shown that the histone deacetylase inhibitor (HDACI) Helminthosporium carbonum (HC)-toxin induces differentiation of neuroblastoma (NB) cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Helminthosporium. Mycotoxins / pharmacology. Neuroblastoma / drug therapy. Peptides, Cyclic / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Histone Deacetylase Inhibitors. Humans. Inhibitory Concentration 50. Phosphorylation / drug effects. Retinoblastoma Protein / drug effects. Retinoblastoma Protein / metabolism. Structure-Activity Relationship

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  • (PMID = 18262346.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / Mycotoxins; 0 / Peptides, Cyclic; 0 / Retinoblastoma Protein; 83209-65-8 / HC toxin
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14. Moon SB, Park KW, Jung SE, Youn WJ: Neuroblastoma: treatment outcome after incomplete resection of primary tumors. Pediatr Surg Int; 2009 Sep;25(9):789-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroblastoma: treatment outcome after incomplete resection of primary tumors.
  • PURPOSE: For International Neuroblastoma Staging System (INSS) stages III or IV neuroblastoma (intermediate or high risk), complete excision of the primary tumor is not always feasible.
  • Most current studies on the treatment outcome of these patients have reported on the complete excision status.
  • The aim of this study is to review the treatment outcome after the incomplete resection.
  • Incomplete resection was assessed by review of the operative notes and postoperative computerized tomography.
  • Age, gender, tumor location, INSS stage, N-myc gene copy number, pre- and postoperative therapy, and treatment outcome were reviewed.
  • The treatment outcome was evaluated according to the postoperative treatment protocol in the high-risk group.
  • RESULTS: Intermediate-risk patients were treated with conventional chemotherapy, isotretinoin (ITT) and interleukin-2 (IL-2).
  • Before the introduction of PBSCT, the high-risk patients were also treated with the conventional chemotherapy (N = 19).
  • For the high-risk patients (N = 32), 19 patients were treated with chemotherapy alone; 15 patients died of their disease while four patients currently have an NED status.
  • CONCLUSIONS: For intermediate risk, conventional chemotherapy appears to be acceptable treatment.
  • However, for high-risk patients, every effort should be made to control residual disease including the use of myeloablative chemotherapy, differentiating agents and immune-modulating agents.
  • [MeSH-major] Neuroblastoma / mortality. Neuroblastoma / therapy
  • [MeSH-minor] Adrenal Gland Neoplasms / mortality. Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / therapy. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Dermatologic Agents / therapeutic use. Female. Follow-Up Studies. Genes, myc. Humans. Infant. Interleukin-2 / therapeutic use. Isotretinoin / therapeutic use. Male. Mediastinal Neoplasms / mortality. Mediastinal Neoplasms / pathology. Mediastinal Neoplasms / therapy. Neoplasm, Residual. Pelvic Neoplasms / mortality. Pelvic Neoplasms / pathology. Pelvic Neoplasms / therapy. Peripheral Blood Stem Cell Transplantation. Radiotherapy, Adjuvant. Retroperitoneal Neoplasms / mortality. Retroperitoneal Neoplasms / pathology. Retroperitoneal Neoplasms / therapy. Retrospective Studies

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  • (PMID = 19629500.001).
  • [ISSN] 1437-9813
  • [Journal-full-title] Pediatric surgery international
  • [ISO-abbreviation] Pediatr. Surg. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dermatologic Agents; 0 / Interleukin-2; EH28UP18IF / Isotretinoin
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15. Cross SF, Dalla Pozza L, Munns CF: Hypercalcemia and osteoblastic lesions induced by 13-Cis-retinoic acid mimicking relapsed neuroblastoma. Pediatr Blood Cancer; 2009 Oct;53(4):666-8
Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .

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  • [Title] Hypercalcemia and osteoblastic lesions induced by 13-Cis-retinoic acid mimicking relapsed neuroblastoma.
  • A 6-year-old male diagnosed with extensive neuroblastoma was treated with chemotherapy, surgery, autotransplantation, and radiotherapy.
  • 13-cis-retinoic acid therapy caused severe bone pain and hypercalcemia.
  • Serum markers of bone turnover were increased and the patient required pamidronate therapy to treat persistent hypercalcemia.
  • MIBG scans can assist in differentiating from recurrent disease.
  • [MeSH-major] Hypercalcemia / chemically induced. Isotretinoin / adverse effects. Neuroblastoma / drug therapy. Osteoblasts / drug effects

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  • (PMID = 19492317.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 35MRW7B4AD / 3-Iodobenzylguanidine; EH28UP18IF / Isotretinoin
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16. Gutenberg A, Schulten HJ, Gunawan B, Ludwig HC, Brück W, Larsen J, Rohde V: CNS tumor 22 years after spinal neuroblastoma IV: diagnostic dilemma between recurrence and secondary malignancy. Pediatr Neurosurg; 2009;45(1):61-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CNS tumor 22 years after spinal neuroblastoma IV: diagnostic dilemma between recurrence and secondary malignancy.
  • We present the very unusual case of a young woman suffering from a brain tumor 22 years after a stage IV spinal neuroblastoma as an infant, demonstrating the difficulties of differentiating late neuroblastoma relapse from secondary supratentorial primitive neuroectodermal tumor (sPNET).
  • Lacking specific immunohistochemical features, the first cerebral tumor at the age of 21 was regarded as sPNET, and we pursued a therapeutic approach consisting of neurosurgical resection as well as irradiation and high-dose alkylator-based chemotherapy according to the HIT2000 protocol.
  • Moreover, the lack of PNET-specific translocations (EWS/FLI1 gene fusion) in both brain tumors as well as the development of hepatic metastases was more compatible with the diagnosis of a very late relapse 22 years after initial stage IV spinal neuroblastoma.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Neoplasms, Second Primary / pathology. Neuroblastoma / pathology. Spinal Neoplasms / pathology
  • [MeSH-minor] Adult. DNA, Neoplasm / genetics. Diagnosis, Differential. Female. Genetic Markers. Humans. Immunohistochemistry. Infant. Magnetic Resonance Imaging. Neoplasm Staging. Time Factors

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  • (PMID = 19258732.001).
  • [ISSN] 1423-0305
  • [Journal-full-title] Pediatric neurosurgery
  • [ISO-abbreviation] Pediatr Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Genetic Markers
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17. Di Bella G, Colori B: Complete objective response of neuroblastoma to biological treatment. Neuro Endocrinol Lett; 2009;30(4):437-49
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  • [Title] Complete objective response of neuroblastoma to biological treatment.
  • OBJECTIVES: The combined use (MDB) of Somatostatin, Melatonin, Retinoids, Vitamins E, C, and D3, with Calcium, Chondroitin sulfate, and microdoses of Cyclophosphamide in a seven-month old baby affected by a voluminous retroperitoneal neuroblastoma measuring 4 x 8 cm produced a 50% objective response in six months, an almost total response in one year and a complete response at 14 months, with cure and absence of disease for over ten years.
  • RESULTS: This paper discusses the rationale and the molecular mechanisms of action of the treatment which has a differentiating, apoptotic and antiproliferative effect, preserving and enhancing both the trophism and functionality of organs and tissues, and the neuroimmunoendocrine and antiblastic homeostasis.
  • CONCLUSIONS: We believe it is of use to report this case in order to invite greater interest in the oncological possibilities offered by the immunoneuroendocrine and biological-receptorial properties of the MDB treatment.
  • [MeSH-major] Melatonin / therapeutic use. Neuroblastoma / drug therapy. Retinoids / therapeutic use. Retroperitoneal Neoplasms / drug therapy. Somatostatin / therapeutic use. Vitamins / therapeutic use
  • [MeSH-minor] Antioxidants / therapeutic use. Drug Therapy, Combination. Humans. Infant. Magnetic Resonance Imaging. Male. Positron-Emission Tomography. Remission Induction

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  • (PMID = 20010503.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Retinoids; 0 / Vitamins; 51110-01-1 / Somatostatin; JL5DK93RCL / Melatonin
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18. Kim EK, Kang HJ, Park JA, Choi HS, Shin HY, Ahn HS: Retrospective analysis of peripheral blood stem cell transplantation for the treatment of high-risk neuroblastoma. J Korean Med Sci; 2007 Sep;22 Suppl:S66-72
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  • [Title] Retrospective analysis of peripheral blood stem cell transplantation for the treatment of high-risk neuroblastoma.
  • Disease relapse after autologous peripheral blood stem cell transplantation (APBSCT) is the main cause of treatment failure in high-risk neuroblastoma (NBL).
  • The patients were allocated to three groups according to the APBSCT type.
  • To improve long-term survival, various efforts should be made such as chemotherapy dose intensification, more effective tumor purging, and control of minimal residual disease via the use of differentiating and immune-modulating agents.
  • [MeSH-major] Neuroblastoma / therapy

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  • (PMID = 17923758.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Other-IDs] NLM/ PMC2694391
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19. Santos A, Calvet L, Terrier-Lacombe MJ, Larsen A, Bénard J, Pondarré C, Aubert G, Morizet J, Lavelle F, Vassal G: In vivo treatment with CPT-11 leads to differentiation of neuroblastoma xenografts and topoisomerase I alterations. Cancer Res; 2004 May 1;64(9):3223-9
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  • [Title] In vivo treatment with CPT-11 leads to differentiation of neuroblastoma xenografts and topoisomerase I alterations.
  • Topoisomerase I inhibitors, such as CPT-11, are potent anticancer drugs against neuroblastoma (NB).
  • Differentiating agents, such as retinoids, improve the survival of children with metastatic NB.
  • During treatment, tumors differentiated into ganglioneuroblastomas (GGNB), which reverted into an immature phenotype when treatment was discontinued.
  • The full-length Mr 100,000 topo I protein was present in both pre and post-treatment immature NB xenografts.
  • [MeSH-major] Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Enzyme Inhibitors / pharmacology. Neuroblastoma / drug therapy. Neuroblastoma / enzymology. Topoisomerase I Inhibitors
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / pharmacology. Cell Differentiation / drug effects. Cell Division / drug effects. Child. Child, Preschool. DNA Topoisomerases, Type I / metabolism. Female. Humans. Infant. Infant, Newborn. Male. Mice. Mice, Nude. Retinaldehyde / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 15126363.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] 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 / Enzyme Inhibitors; 0 / Topoisomerase I Inhibitors; 472-86-6 / 13-cis-retinal; 7673326042 / irinotecan; EC 5.99.1.2 / DNA Topoisomerases, Type I; RR725D715M / Retinaldehyde; XT3Z54Z28A / Camptothecin
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20. Garcia I, Mayol G, Rodríguez E, Suñol M, Gershon TR, Ríos J, Cheung NK, Kieran MW, George RE, Perez-Atayde AR, Casala C, Galván P, de Torres C, Mora J, Lavarino C: Expression of the neuron-specific protein CHD5 is an independent marker of outcome in neuroblastoma. Mol Cancer; 2010;9:277
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  • [Title] Expression of the neuron-specific protein CHD5 is an independent marker of outcome in neuroblastoma.
  • BACKGROUND: The chromodomain, helicase DNA-binding protein 5 (CHD5) is a potential tumor suppressor gene located on chromosome 1p36, a region recurrently deleted in high risk neuroblastoma (NB).
  • Previous data have shown that CHD5 mRNA is present in normal neural tissues and in low risk NB, nevertheless, the distribution of CHD5 protein has not been explored.
  • With this purpose, CHD5 protein expression was analyzed in normal neural tissues and neuroblastic tumors (NTs).
  • CHD5 gene and protein expression was reexamined after induction chemotherapy in a subset of high risk tumors to identify potential changes reflecting tumor response.
  • RESULTS: We provide evidence that CHD5 is a neuron-specific protein, absent in glial cells, with diverse expression amongst neuron types.
  • Within NTs, CHD5 immunoreactivity was found restricted to differentiating neuroblasts and ganglion-like cells, and absent in undifferentiated neuroblasts and stromal Schwann cells.
  • The prognostic value of CHD5 was confirmed in an independent, blinded set of 32 NB tumors (P < 0.001).Reactivation of CHD5 expression after induction chemotherapy was observed mainly in those high risk tumors with induced tumor cell differentiation features.
  • Re-establishment of CHD5 expression induced by chemotherapy could be a surrogate marker of treatment response.
  • [MeSH-major] DNA Helicases / metabolism. Gene Expression Regulation, Neoplastic. Nerve Tissue Proteins / metabolism. Neuroblastoma / metabolism

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  • (PMID = 20950435.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / CHD5 protein, human
  • [Other-IDs] NLM/ PMC2992029
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21. Cesi V, Vitali R, Tanno B, Giuffrida ML, Sesti F, Mancini C, Raschellà G: Insulin-like growth factor binding protein 5: contribution to growth and differentiation of neuroblastoma cells. Ann N Y Acad Sci; 2004 Dec;1028:59-68
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  • [Title] Insulin-like growth factor binding protein 5: contribution to growth and differentiation of neuroblastoma cells.
  • Neuroblastoma (NB) is a childhood tumor that depends on insulin-like growth factors (IGFs) for its growth and metastatic spread.
  • NB cell lines retain the ability to differentiate in vitro toward neuronal, schwann-like or melanocytic phenotypes upon treatment with retinoic acid (RA).
  • Retinoids are currently used in NB therapy to achieve a mature postmitotic phenotype.
  • Here, we present evidence that the expression of IGFBP-5 is a common feature of neuroblastoma cell lines and that IGFBP-5 acts in concert with IGF-2 in inducing cell proliferation.
  • Functional assays carried out in differentiating conditions demonstrate that IGFBP-5 transcription is sensitive to RA treatment.
  • Given the relevance of IGF-2 in determining the proliferative and metastatic behavior of NB, the role of IGFBP-5 as a modulator of the IGF signal transduction pathway should be studied further for potential therapeutic applications.
  • [MeSH-major] Insulin-Like Growth Factor Binding Protein 5 / genetics. Insulin-Like Growth Factor Binding Protein 5 / metabolism. Neuroblastoma / metabolism
  • [MeSH-minor] Blotting, Western. Cell Differentiation. Cell Line, Tumor. Cell Proliferation. DNA Primers / chemistry. Dose-Response Relationship, Drug. Humans. Insulin-Like Growth Factor II / metabolism. Luciferases / metabolism. Mitosis. Models, Genetic. Mutation. Phenotype. Plasmids / metabolism. Promoter Regions, Genetic. Recombinant Proteins / chemistry. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transfection. Tretinoin / metabolism. Tretinoin / pharmacology

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  • (PMID = 15650232.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Insulin-Like Growth Factor Binding Protein 5; 0 / Recombinant Proteins; 5688UTC01R / Tretinoin; 67763-97-7 / Insulin-Like Growth Factor II; EC 1.13.12.- / Luciferases
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22. Zage PE, Zeng L, Palla S, Fang W, Nilsson MB, Heymach JV, Zweidler-McKay PA: A novel therapeutic combination for neuroblastoma: the vascular endothelial growth factor receptor/epidermal growth factor receptor/rearranged during transfection inhibitor vandetanib with 13-cis-retinoic acid. Cancer; 2010 May 15;116(10):2465-75
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  • [Title] A novel therapeutic combination for neuroblastoma: the vascular endothelial growth factor receptor/epidermal growth factor receptor/rearranged during transfection inhibitor vandetanib with 13-cis-retinoic acid.
  • BACKGROUND: High-risk cases of neuroblastoma have poor survival rates, and novel therapies are needed.
  • Vandetanib (ZD6474, Zactima) is an inhibitor of the vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases, which have each been implicated in neuroblastoma pathogenesis.
  • The authors hypothesized that vandetanib combined with 13-cis-retinoic acid (CRA), a differentiating agent used in most current neuroblastoma treatment regimens, would be effective against neuroblastoma tumor models.
  • METHODS: The authors evaluated the effects of vandetanib with and without CRA on RET phosphorylation and on the proliferation and survival of human neuroblastoma cell lines in vitro.
  • Using a subcutaneous mouse xenograft model of human neuroblastoma, they analyzed tumors treated with CRA, vandetanib, and the combination of vandetanib plus CRA for growth, gross and histologic appearance, vascularity, and apoptosis.
  • RESULTS: Vandetanib treatment inhibited RET phosphorylation and resulted in induction of apoptosis in the majority of neuroblastoma cell lines in vitro, whereas CRA treatment induced morphologic differentiation and cell-cycle arrest.
  • Treatment with vandetanib plus CRA resulted in more significant reduction in neuroblastoma cell viability than either alone.
  • CONCLUSIONS: Vandetanib induces neuroblastoma tumor cell death in vitro and reduces tumor growth and vascularity in vivo.
  • The combination of vandetanib with CRA was more effective in reducing tumor growth than either treatment alone.
  • The antitumor effects of vandetanib plus CRA suggest a novel combination for use in neuroblastoma patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Isotretinoin / administration & dosage. Neuroblastoma / drug therapy. Piperidines / administration & dosage. Quinazolines / administration & dosage. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival. DNA-Binding Proteins / metabolism. Humans. Mice. Neovascularization, Pathologic / drug therapy. Phosphorylation. Tumor Suppressor Proteins / metabolism. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2010 American Cancer Society.
  • (PMID = 20225331.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Quinazolines; 0 / TRIM13 protein, human; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EH28UP18IF / Isotretinoin
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23. de Buys Roessingh AS, Rougemont AL, Wiesenauer C, Barrette S, Bouron-Dal Soglio D, Lallier M: Implication of unfavorable histology, MYCN amplification and diploidy for stage I and II neuroblastomas. Eur J Pediatr Surg; 2008 Dec;18(6):410-4
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  • BACKGROUND: Surgery is the first line treatment for low-grade neuroblastomas.
  • In stage I tumors, the presence of MYCN amplification is rarely detected and the Shimada histology is not always taken into consideration when deciding on the treatment.
  • Favorable histology was defined as stroma-poor tumors with more than 5 % differentiating neuroblasts and a mitosis karyorrhexis index (MKI) of less than 100/5000 cells.
  • Of these 30 patients, 27 underwent surgery alone and three received chemotherapy after surgery.
  • The combination of MYCN amplification, unfavorable histology and diploidy was noted in one patient who developed metastases within two months.
  • It seems that no single clinical or biological feature can be considered a significant factor in establishing a prognosis or determining whether additional treatment is required.
  • [MeSH-major] DNA, Neoplasm / metabolism. Diploidy. Gene Amplification. Genetic Markers. Neuroblastoma / pathology. Nuclear Proteins / genetics. Oncogene Proteins / genetics

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  • (PMID = 19012235.001).
  • [ISSN] 0939-7248
  • [Journal-full-title] European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift für Kinderchirurgie
  • [ISO-abbreviation] Eur J Pediatr Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Genetic Markers; 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins
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24. Barlow JW, Wiley JC, Mous M, Narendran A, Gee MF, Goldberg M, Sexsmith E, Malkin D: Differentiation of rhabdomyosarcoma cell lines using retinoic acid. Pediatr Blood Cancer; 2006 Nov;47(6):773-84
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  • BACKGROUND: Rhabdomyosarcoma (RMS) is the most frequent sporadic soft tissue sarcoma of childhood and adolescence.
  • The overall 5-year survival rate for patients with RMS is 70% with the use of surgery, radiation, and chemotherapy.
  • Novel therapeutic approaches are necessary to improve on these outcomes particularly among the more aggressive alveolar RMS (ARMS) and late stages of disease, where 5-year survival is less than 20%.
  • Retinoids have been successfully used in the treatment of acute promyelocytic leukemia (APML) and neuroblastoma.
  • PURPOSE: However, analysis of retinoids as a differentiating agent for RMS has been incomplete.
  • Following treatment with ATRA FACS analysis showed an altered cell cycle with the same pattern as the growth curves.
  • ATRA altered cellular morphology of two cell lines, Rh4 and Rh28, and induced Troponin T expression in these cells suggesting a differentiating effect.
  • CONCLUSIONS: These studies suggest that retinoids are effective inducers of growth arrest and differentiation in some RMS cell lines, and offer a basis for further in vivo testing in mice of ATRA as a potential approach to ARMS treatment.
  • [MeSH-major] Cell Differentiation / drug effects. Rhabdomyosarcoma / drug therapy. Tretinoin / pharmacology. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Ethanol / pharmacology. Flow Cytometry / methods. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Mutation. Sensitivity and Specificity. Troponin T / analysis. Tumor Cells, Cultured

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16283617.001).
  • [ISSN] 1545-5009
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / TP53 protein, human; 0 / Troponin T; 0 / Tumor Suppressor Protein p53; 3K9958V90M / Ethanol; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
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25. Miniati D, Gay AN, Parks KV, Naik-Mathuria BJ, Hicks J, Nuchtern JG, Cass DL, Olutoye OO: Imaging accuracy and incidence of Wilms' and non-Wilms' renal tumors in children. J Pediatr Surg; 2008 Jul;43(7):1301-7
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  • The nWT group included congenital mesoblastic nephroma (5), clear cell sarcoma (4), neuroblastoma (4), renal cell carcinoma (4), lymphoma (2), angiomyolipoma (2), teratoma (1), hemangioma (1), and renal epithelial tumor (1).
  • Sensitivity, specificity, positive predictive value, and negative predictive value for computed tomography (CT) determining a diagnosis of WT were 0.92, 0.55, 0.84, and 0.73, respectively.
  • Preoperative imaging is of limited value in differentiating these tumors.
  • These data have significant implications for parental counseling, surgical plan, and the choice of neoadjuvant chemotherapy and argue in favor of obtaining a tissue diagnosis before instituting therapy.

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  • (PMID = 18639686.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Ravindra S, Kini U: Cytomorphology and morphometry of small round-cell tumors in the region of the kidney. Diagn Cytopathol; 2005 Apr;32(4):211-6
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  • Small round-cell tumors (SRCTs), with malignant cell components measuring 10 m or less in diameter with scanty cytoplasm in alcohol-fixed smears, pose a diagnostic challenge at fine-needle aspiration cytology (FNAC), especially when they are situated in and around the kidney and need facilities such as electron microscopy, immunohistochemistry, tissue culture, and cytogenetics for their subtyping.
  • A precise cytodiagnosis of SRCTs is important because a definite diagnosis is mandatory in preoperative diagnostic workup for presurgical chemotherapy in these cases.
  • Twenty-one were diagnosed as Wilms' tumor (WT), 10 were diagnosed as neuroblastoma (NB), 3 were ganglioneuroblastoma (GNB), 1 was a cellular congenital mesoblastic nephroma (CMN), and 1 was an adrenocortical carcinoma (ACC).
  • Aspirates from CMN and ACC were considered as simulators/mimickers of SRCT because they had superficial resemblance to SRCT and their differentiating cytomorphological features observed at histology were too subtle to be noted at cytology.

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15754373.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Beltz LA: The 'other' telomerase inhibitors: non-G-quadruplex interactive agent, non-antisense, non-reverse transcriptase telomerase inhibitors. Curr Med Chem Anticancer Agents; 2002 Sep;2(5):589-603
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Between 80-95% of tumors are telomerase-positive, including ovarian carcinoma, hepatocellular carcinoma, neuroblastoma, leukemia/lymphoma, and cancers of the breast, prostate, lung, kidneys and bladder, as well as many immortalized cell lines.
  • While absent in most normal tissues, this enzyme is expressed at higher levels in germline tissues, bone marrow, and lymphocytes.
  • Due to the expression of telomerase in most tumor cells and its absence in most normal tissues, telomerase inhibitors are being investigated as possible anticancer agents.
  • These agents include: differentiating agents, kinases and phosphatases, cell cycle and apoptosis regulating agents, immunotherapeutic agents, antibiotics, steroids, bisindole derivatives, and a variety of other compounds.
  • These agents hold much promise for the future treatment of malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / therapeutic use. Telomerase / antagonists & inhibitors
  • [MeSH-minor] Animals. Heterocyclic Compounds / chemistry. Heterocyclic Compounds / pharmacology. Heterocyclic Compounds / therapeutic use. Humans. Hydrocarbons, Aromatic / chemistry. Hydrocarbons, Aromatic / pharmacology. Hydrocarbons, Aromatic / therapeutic use. Neoplasms / drug therapy. Neoplasms / pathology. Organic Chemicals / chemistry. Organic Chemicals / pharmacology. Organic Chemicals / therapeutic use. Structure-Activity Relationship

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  • (PMID = 12678726.001).
  • [ISSN] 1568-0118
  • [Journal-full-title] Current medicinal chemistry. Anti-cancer agents
  • [ISO-abbreviation] Curr Med Chem Anticancer Agents
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Heterocyclic Compounds; 0 / Hydrocarbons, Aromatic; 0 / Organic Chemicals; EC 2.7.7.49 / Telomerase
  • [Number-of-references] 131
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