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1. Gow KW, Lensing S, Hill DA, Krasin MJ, McCarville MB, Rai SN, Zacher M, Spunt SL, Strickland DK, Hudson MM: Thyroid carcinoma presenting in childhood or after treatment of childhood malignancies: An institutional experience and review of the literature. J Pediatr Surg; 2003 Nov;38(11):1574-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid carcinoma presenting in childhood or after treatment of childhood malignancies: An institutional experience and review of the literature.
  • METHODS: The authors reviewed the medical records of 8 children with PTM and 17 children with STM referred to St Jude Children's Research Hospital between February 1962 and February 2002 for evaluation and treatment of malignant thyroid carcinoma.
  • Seventeen patients had thyroid carcinoma as a second malignant neoplasm after treatment for acute lymphoblastic leukemia (n = 6), Hodgkin's disease (n = 5), central nervous system tumor (n = 2), Wilms' tumor (n = 1), retinoblastoma (n = 1), non-Hodgkin's lymphoma (n = 1), or neuroblastoma (n = 1).
  • CONCLUSIONS: Pediatric thyroid carcinoma is uncommon and responds well to current therapy.
  • Given the limited period of follow-up of our cohort of secondary malignant thyroid tumors that arise after childhood cancer, these lesions appear to have similar presentations and outcomes when compared with primary carcinomas and can therefore be managed in the same manner.
  • [MeSH-major] Adenocarcinoma, Follicular / epidemiology. Carcinoma, Papillary / epidemiology. Neoplasms, Second Primary / epidemiology. Thyroid Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Child. Cohort Studies. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / therapeutic use. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Neoplasms / drug therapy. Neoplasms / radiotherapy. Neoplasms, Radiation-Induced / epidemiology. Retrospective Studies. Tennessee / epidemiology. Thyroidectomy. Treatment Outcome

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  • (PMID = 14614703.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
  • [Number-of-references] 49
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2. Cavazos CM, Keir ST, Yoshinari T, Bigner DD, Friedman HS: Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts. Cancer Chemother Pharmacol; 2001 Sep;48(3):250-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts.
  • PURPOSE: The in vivo antitumor activity of a novel topoisomerase I inhibitor, J-107088, was tested in athymic nude mice bearing subcutaneous or intracranial pediatric and adult malignant CNS tumor-derived xenografts.
  • METHODS: J-107088 was administered to animals on days 1-5 and 8-12 via intraperitoneal injection at a dose of 54 mg/kg (162 mg/m2) per day in 10% dimethyl sulfoxide in 0.9% saline.
  • The xenografts evaluated were derived from a childhood glioblastoma multiforme (D-456 MG), a childhood medulloblastoma (D-341 MED), an adult anaplastic astrocytoma (D-54 MG), an adult glioblastoma multiforme (D-245 MG), and a procarbazine-resistant subline of D-245 MG [D-245 MG (PR)].
  • CONCLUSION: These results indicate that J-107088 may be active in the treatment of childhood and adult malignant brain tumors and provide the rationale for initiation of clinical trials with this agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Carbazoles / therapeutic use. Enzyme Inhibitors / therapeutic use. Glioma / drug therapy. Glucosides / therapeutic use. Indoles. Topoisomerase I Inhibitors
  • [MeSH-minor] Adult. Animals. Child. Female. Humans. Injections, Intraperitoneal. Injections, Subcutaneous. Male. Mice. Mice, Nude. Neoplasm Transplantation. Survival Rate. Transplantation, Heterologous. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 11592348.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 2RO1-NS30245-12; United States / NINDS NIH HHS / NS / 5P50-NS-20023-17; United States / NCI NIH HHS / CA / CA11898; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / Glucosides; 0 / Indoles; 0 / Topoisomerase I Inhibitors; 1V8X590XDP / edotecarin
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3. Khalili K: Human neurotropic JC virus and its association with brain tumors. Dis Markers; 2001;17(3):143-7
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  • [Title] Human neurotropic JC virus and its association with brain tumors.
  • JC virus (JCV) is a human polyomavirus known as the causative agent of the fatal demyelinating disease, Progressive Multifocal Leukoencephalopathy (PML).
  • Further, in experimental animals this virus causes a broad range of tumors of central nervous system origin.
  • Recent studies have suggested the association of JCV with several human tumors most notably malignant brain tumors of childhood, medulloblastoma.
  • The development of tumors by JCV is most likely through mechanisms involving inactivation of tumor suppressors and de-regulation of signaling pathways such as Wnt by the viral early protein, T-antigen.
  • The neurotropic nature of JCV along with the overwhelming evidence for its oncogenic potential in laboratory animals and its detection in significant numbers of human medulloblastomas invite the re-evaluation of the role for JCV in the development of human brain tumors.
  • [MeSH-major] Brain Neoplasms / virology. Leukoencephalopathy, Progressive Multifocal / complications
  • [MeSH-minor] Animals. Humans. Nervous System / pathology. Nervous System / virology

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  • (PMID = 11790878.001).
  • [ISSN] 0278-0240
  • [Journal-full-title] Disease markers
  • [ISO-abbreviation] Dis. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 28
  • [Other-IDs] NLM/ PMC3851256
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4. Daly BP, Brown RT: Scholarly literature review: management of neurocognitive late effects with stimulant medication. J Pediatr Psychol; 2007 Oct;32(9):1111-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scholarly literature review: management of neurocognitive late effects with stimulant medication.
  • OBJECTIVE: To examine the extant literature on stimulant drug therapy for survivors of childhood cancer during the late-effects period.
  • METHODS: A review of literature is provided on the mechanism of and cognitive toxicities for children and adolescents treated for acute lymphoblastic leukemia (ALL) and malignant brain tumors (BT) as well as the pharmacotherapy of stimulant medications, with a specific review of literature on the efficacy and safety of the stimulants for children with ALL and BT.
  • RESULTS: Only four studies were found that have examined the effects of stimulant medication on the cognitive toxicities of childhood survivors of cancer during the late-effects period and only two of these investigations were controlled clinical trials.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / psychology. Central Nervous System Stimulants / pharmacology. Central Nervous System Stimulants / therapeutic use. Cognition / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology

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  • (PMID = 17442692.001).
  • [ISSN] 0146-8693
  • [Journal-full-title] Journal of pediatric psychology
  • [ISO-abbreviation] J Pediatr Psychol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants
  • [Number-of-references] 150
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5. Löning L, Zimmermann M, Reiter A, Kaatsch P, Henze G, Riehm H, Schrappe M: Secondary neoplasms subsequent to Berlin-Frankfurt-Münster therapy of acute lymphoblastic leukemia in childhood: significantly lower risk without cranial radiotherapy. Blood; 2000 May 1;95(9):2770-5
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  • [Title] Secondary neoplasms subsequent to Berlin-Frankfurt-Münster therapy of acute lymphoblastic leukemia in childhood: significantly lower risk without cranial radiotherapy.
  • Secondary neoplasms (SNs) represent serious late complications after successful treatment of malignant diseases.
  • To evaluate the rate and type of SNs after Berlin-Frankfurt-Münster (BFM) treatment in children with acute lymphoblastic leukemia (ALL), we analyzed the data from the BFM database and the German Childhood Cancer Registry (GCCR).
  • By December 1997, 52 SNs were documented, including 16 acute myeloid leukemias (AMLs), 13 neoplasms of the central nervous system (CNS), and 23 other neoplasms.
  • Compared with the expected numbers estimated from incidence rates derived from the GCCR, this represented a 14-fold increase for all cancers and a 19-fold increase for CNS tumors.
  • The development of secondary AML was not associated with the use of any specific cytotoxic agent.
  • Considering the high-survival rate of this large unselected ALL cohort, the risk of SN is relatively low, though higher, especially after cranial irradiation, than in the general population.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Brain Neoplasms / prevention & control. Brain Neoplasms / secondary. Child. Child, Preschool. Combined Modality Therapy. Databases as Topic. Disease-Free Survival. Female. Follow-Up Studies. Germany. Humans. Infant. Infant, Newborn. Male. Registries. Retrospective Studies. Risk Factors. Survival Analysis


6. Badruddoja MA, Keir ST, King I, Zeidner J, Vredenburgh JJ, Muhlbaier LH, Bigner DD, Friedman HS: Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice. Neuro Oncol; 2007 Jul;9(3):240-4
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  • [Title] Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice.
  • VNP40101M, or 1,2-bis(methylsulfonyl)-1-(2-choloroethyl)-2-(methylamino)carbonylhydrazine (Cloretazine), is a bifunctional prodrug that belongs to a class of DNA-modifying agents-the sulfonylhydrazines-that has been synthesized and been shown to have activity against a wide spectrum of xenografts.
  • The current study was designed to assess the activity of VNP40101M administered at a dose of 18 mg/kg daily for five days against a panel of human adult and pediatric CNS tumors growing subcutaneously or intracranially in athymic nude mice.
  • The results demonstrated statistically significant (p < 0.05) growth delays of 15.0, 8.3, 51.0, 60+, 60+, and 60+ days in subcutaneous xenografts derived from childhood glioblastoma multiforme (D-456 MG), childhood ependymoma (D-528 EP and D-612 EP), childhood medulloblastoma (D-425 MED), and adult malignant glioma (D-245 MG and D-54 MG), respectively, with corresponding tumor regressions in 10 of 10, 4 of 10, 8 of 10, 9 of 10, 9 of 10, and 10 of 10 treated mice, respectively.
  • Delayed toxicity was seen more than 60 days after treatment, with 23 deaths in 100 treated animals, despite a median weight loss of only 0.06%.
  • Additional experiments conducted against subcutaneous D-245 MG xenografts by using reduced doses of 13.5 or 9.0 mg/kg daily for five days demonstrated tumor growth delays of 82.2 and 53.5 days, with corresponding tumor regressions in 8 of 9 and 9 of 10 treated mice, respectively (all values, p < 0.001), with one toxic death.
  • These findings suggest that VNP40101M is active in the treatment of a wide range of human central nervous system tumors and warrants translation to the clinic.

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  • (PMID = 17522334.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / 5P50-NS20023-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Prodrugs; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
  • [Other-IDs] NLM/ PMC1907418
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7. Rodini CO, Suzuki DE, Nakahata AM, Pereira MC, Janjoppi L, Toledo SR, Okamoto OK: Aberrant signaling pathways in medulloblastomas: a stem cell connection. Arq Neuropsiquiatr; 2010 Dec;68(6):947-52
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  • Medulloblastoma is a highly malignant primary tumor of the central nervous system.
  • It represents the most frequent type of solid tumor and the leading cause of death related to cancer in early childhood.
  • Current treatment includes surgery, chemotherapy and radiotherapy which may lead to severe cognitive impairment and secondary brain tumors.
  • From the clinical viewpoint, modulation of signaling pathways such as TGFβ, regulating neural stem cell proliferation and tumor development, might be attempted as an alternative strategy for future drug development aiming at more efficient therapies and improved clinical outcome of patients with pediatric brain cancers.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Neural Stem Cells / pathology. Signal Transduction. Transforming Growth Factor beta

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  • (PMID = 21243257.001).
  • [ISSN] 1678-4227
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta
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8. Zimmerman MA, Goumnerova LC, Proctor M, Scott RM, Marcus K, Pomeroy SL, Turner CD, Chi SN, Chordas C, Kieran MW: Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor. J Neurooncol; 2005 Mar;72(1):77-84
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  • [Title] Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor.
  • Atypical teratoid/rhabdoid tumors (AT/RT) are highly malignant lesions of childhood that carry a very poor prognosis.
  • AT/RT can occur in the central nervous system (CNS AT/RT) and disease in this location carries an even worse prognosis with a median survival of 7 months.
  • In spite of multiple treatment regimens consisting of maximal surgical resection (including second look surgery), radiation therapy (focal and craniospinal), and multi-agent intravenous, oral and intrathecal chemotherapy, with or without high-dose therapy and stem cell rescue, only seven long-term survivors of CNS AT/RT have been reported, all in patients with newly diagnosed disease.
  • We now report on four children, two with newly diagnosed CNS AT/RT and two with progressive disease after multi-agent chemotherapy who are long term survivors (median follow-up of 37 months) using a combination of surgery, radiation therapy, and intensive chemotherapy.
  • The chemotherapy component was modified from the Intergroup Rhabdomyosarcoma Study Group (IRS III) parameningeal protocol as three of the seven reported survivors in the literature were treated using this type of therapy.
  • More importantly, we report on the first two survivors after relapse with multi-agent intravenous and intrathecal chemotherapy treated with this modified regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Neoplasm Recurrence, Local / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy

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  • (PMID = 15803379.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 37
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9. Marchetti D, Mrak RE, Paulsen DD, Sinnappah-Kang ND: Neurotrophin receptors and heparanase: a functional axis in human medulloblastoma invasion. J Exp Clin Cancer Res; 2007 Mar;26(1):5-23
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  • Medulloblastoma (MB) is the most common malignant brain tumor of childhood.
  • Neurotrophins (NT) comprise a family of structurally and functionally related neurotrophic factors that are critical for central nervous system (CNS) development with nerve growth factor (NGF) being the prototypic NT.
  • NT acts through two groups of structurally unrelated neurotrophin receptors (NTR): a family of receptor tyrosine kinases (Trks, mainly TrkA, TrkB, and TrkC) and a tumor necrosis factor receptor (TNFR)-like molecule called p75NTR TrkC expression is a good prognostic indicator for MB.
  • Importantly, little is known about the biological functions of p75 in primitive neuroectodermal tumors such as MB.
  • In contrast, NT-regulated heparanase (HPSE) is a unique extracellular matrix-degrading enzyme known to be associated with tumor progression in a wide variety of cancers.
  • Taken together, our data provide evidence that HPSE functionality, in a context linked to TrkC and p75NTR activation, may play critical roles in medulloblastoma tumor invasion and progression.
  • [MeSH-major] Cerebellar Neoplasms / metabolism. Glucuronidase / metabolism. Medulloblastoma / metabolism. Meningeal Neoplasms / metabolism. Receptors, Nerve Growth Factor / metabolism
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Infant. Male. NF-kappa B / metabolism. Neoplasm Invasiveness. Nerve Tissue Proteins / metabolism. Neurotrophin 3 / metabolism. Neurotrophin 3 / pharmacology. Phosphorylation. Prognosis. Receptor, trkC / metabolism

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  • (PMID = 17550129.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA086832; United States / NCI NIH HHS / CA / CA103955
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / NGFR protein, human; 0 / Nerve Tissue Proteins; 0 / Neurotrophin 3; 0 / Receptors, Nerve Growth Factor; EC 2.7.10.1 / Receptor, trkC; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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10. Keir ST, Hausheer F, Lawless AA, Bigner DD, Friedman HS: Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice. Cancer Chemother Pharmacol; 2001 Jul;48(1):83-7
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  • [Title] Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice.
  • PURPOSE: Camptothecins have emerged as an important new class of antitumor drugs.
  • This study was designed to test the efficacy of karenitecin, a novel highly lipophilic camptothecin derivative, against a panel of human tumor xenografts derived from adult and pediatric central nervous system malignancies growing in athymic nude mice.
  • METHODS: Xenografts evaluated were derived from childhood high-grade gliomas (D-212 MG, D-456 MG), adult high-grade gliomas (D-54 MG, D-245 MG), medulloblastomas (D-341 MED, D-487 MED), and ependymomas (D-528 EP, D-612 EP), as well as sublines with demonstrated resistance to procarbazine (D-245 MG (PR)) and busulfan (D-456 (BR)).
  • In replicate experiments, karenitecin was given at 1.0 mg/kg per dose via intraperitoneal injection for a period of 10 consecutive days, which is the dosage lethal to 10% of treated animals.
  • Karenitecin also produced statistically significant (P < or = 0.001) increases in survival of animals bearing D-341 MED intracranial xenografts (69% increase) and those bearing D-456 MG xenografts (62% increase).
  • CONCLUSION: These preclinical studies confirm that karenitecin is active against human central nervous system xenografts and should undergo clinical evaluation in patients with malignant central nervous system tumors.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Camptothecin / therapeutic use. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 11488529.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 24R60NVC41 / cositecan; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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11. Mulhern RK, Khan RB, Kaplan S, Helton S, Christensen R, Bonner M, Brown R, Xiong X, Wu S, Gururangan S, Reddick WE: Short-term efficacy of methylphenidate: a randomized, double-blind, placebo-controlled trial among survivors of childhood cancer. J Clin Oncol; 2004 Dec 1;22(23):4795-803
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  • [Title] Short-term efficacy of methylphenidate: a randomized, double-blind, placebo-controlled trial among survivors of childhood cancer.
  • PURPOSE: Children surviving acute lymphoblastic leukemia (ALL) and malignant brain tumors (BTs) have a higher incidence of attention and learning problems in school than do their healthy peers.
  • PATIENTS AND METHODS: We report on 83 long-term survivors of ALL and BT identified as having attentional deficits on behavioral testing and parent or teacher report, and problems with academic achievement.
  • The primary end points were weekly teacher and parent reports on the Conners' Rating Scales and Social Skills Rating System.
  • RESULTS: Compared to placebo, significant improvement with MPH was reported by teachers and parents on the Conners' Rating Scales and by teachers on the Social Skills Rating System.
  • CONCLUSION: Treatment with MPH can at least temporarily reduce some attentional and social deficits among survivors of childhood ALL and BT.
  • [MeSH-major] Attention Deficit Disorder with Hyperactivity / drug therapy. Brain Neoplasms / complications. Central Nervous System Stimulants / administration & dosage. Cognition Disorders / drug therapy. Methylphenidate / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Child. Cross-Over Studies. Dose-Response Relationship, Drug. Double-Blind Method. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Probability. Reference Values. Risk Assessment. Severity of Illness Index. Survivors. Treatment Outcome

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  • [ErratumIn] J Clin Oncol. 2005 Jan 1;23(1):248
  • (PMID = 15570081.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765; United States / NCI NIH HHS / CA / R01 CA78957; United States / NCI NIH HHS / CA / U01 CA81445
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 207ZZ9QZ49 / Methylphenidate
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12. Hurwitz CA, Strauss LC, Kepner J, Kretschmar C, Harris MB, Friedman H, Kun L, Kadota R: Paclitaxel for the treatment of progressive or recurrent childhood brain tumors: a pediatric oncology phase II study. J Pediatr Hematol Oncol; 2001 Jun-Jul;23(5):277-81
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  • [Title] Paclitaxel for the treatment of progressive or recurrent childhood brain tumors: a pediatric oncology phase II study.
  • PURPOSE: To assess the efficacy and define the toxicity of paclitaxel given at a dosage of 350 mg/m2 every 3 weeks as a 24-hour continuous infusion to children with recurrent or progressive primary brain tumors.
  • PATIENTS AND METHODS: Seventy-three eligible patients, ages 4 months to 19 years, with progressive or recurrent primary brain tumors were treated according to a Pediatric Oncology Group (POG) phase II protocol with paclitaxel (POG 9330).
  • Tumor histologic strata included: astrocytoma (n = 4), malignant glioma (n = 13), medulloblastoma (n = 16), brain stem glioma (n = 15), ependymoma (n = 13), and miscellaneous histologies (n = 12).
  • All patients had previous histologic confirmation of a primary intracranial or spinal cord tumor with magnetic resonance imaging or computed tomography documentation of unequivocally measurable progressive or recurrent disease.
  • Toxicities included mild nausea, central nervous system toxicity, myelosuppression, and febrile neutropenia, including one septic death.
  • CONCLUSION: Paclitaxel is well tolerated in children with recurrent or progressive brain tumors at this dosage and schedule and may result in short-term disease stabilization in this patient population.
  • The lack of a significant number of patients with measurable disease regression, however, precludes it from being identified as an active agent when administered as a single agent by 24-hour continuous infusion.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy. Paclitaxel / therapeutic use
  • [MeSH-minor] Adolescent. Astrocytoma / drug therapy. Astrocytoma / pathology. Child. Child, Preschool. Dexamethasone / therapeutic use. Disease Progression. Drug Hypersensitivity / prevention & control. Ependymoma / drug therapy. Ependymoma / pathology. Female. Glioma / drug therapy. Glioma / pathology. Humans. Immunosuppressive Agents / therapeutic use. Infant. Infratentorial Neoplasms / drug therapy. Infratentorial Neoplasms / pathology. Infusions, Intravenous. Male. Medulloblastoma / drug therapy. Medulloblastoma / pathology. Nausea / chemically induced. Neoplasm Recurrence, Local. Neutropenia / chemically induced. Remission Induction. Salvage Therapy. Treatment Failure

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  • (PMID = 11464982.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA03161; United States / NCI NIH HHS / CA / CA07431; United States / NCI NIH HHS / CA / CA15525; etc
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Immunosuppressive Agents; 7S5I7G3JQL / Dexamethasone; P88XT4IS4D / Paclitaxel
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13. Hambardzumyan D, Amankulor NM, Helmy KY, Becher OJ, Holland EC: Modeling Adult Gliomas Using RCAS/t-va Technology. Transl Oncol; 2009 May;2(2):89-95
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  • Malignant gliomas remain the most devastating childhood and adult tumors of the central nervous system.
  • Although adult and pediatric gliomas are histologically indistinguishable, they differ in location, behavior, and molecular characteristics.
  • This implies that the molecular pathways and pathophysiology of malignant gliomagenesis in these two populations are distinct.
  • Such differences between adult and pediatric gliomas may predict different therapeutic responses.
  • Therefore, accurate genetically engineered models of adult and pediatric gliomas may help understand the biology of these tumors and evaluate therapeutic agents in preclinical studies.

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  • (PMID = 19412424.001).
  • [ISSN] 1936-5233
  • [Journal-full-title] Translational oncology
  • [ISO-abbreviation] Transl Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA141502
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2670576
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