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1. Hochberg F, Grossman SA, Mikkelsen T, Glantz M, Fisher JD, Piantadosi S: Lack of efficacy of 9-aminocamptothecin in adults with newly diagnosed glioblastoma multiforme and recurrent high-grade astrocytoma. NABTT CNS Consortium. Neuro Oncol; 2000 01;2(1):29-33
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  • [Title] Lack of efficacy of 9-aminocamptothecin in adults with newly diagnosed glioblastoma multiforme and recurrent high-grade astrocytoma. NABTT CNS Consortium.
  • 9-Aminocamptothecin (9-AC) was administered as a 72-h i.v. infusion every 2 weeks to a total of 99 adults with high-grade astrocytomas.
  • Fifty-one patients with newly diagnosed glioblastoma multiforme received 9-AC treatment prior to radiation therapy and 48 patients with high-grade astrocytomas were treated at the time of tumor recurrence.
  • The study specified that all apparent responders would have central review of their radiologic studies and histopathology.
  • The initial patients treated with 9-AC were also receiving anticonvulsants and were noted to have minimal myelosuppression with this chemotherapy.
  • Twenty-two patients with newly diagnosed glioblastoma multiforme received 9-AC at doses > or =1,776 microg/m2/24 h.
  • Of these, 18 had evaluable disease on central review, and 0 of 18 (0%) demonstrated a partial or complete response.
  • Twenty-one patients with recurrent high-grade astrocytomas were treated at 1,611 microg/m2/24 h; 20 had evaluable disease and 0 of 20 (0%) had a partial or complete response.
  • Evidence of drug failure was rapid with tumor progression in one-half of patients after 2 drug cycles.
  • 9-AC lacks evidence of substantial activity in patients with newly diagnosed or recurrent high-grade astrocytomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Camptothecin / analogs & derivatives. Camptothecin / therapeutic use. Glioblastoma / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Recurrence, Local. Retreatment. Treatment Failure

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  • (PMID = 11302251.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01CA6406-07
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5MB77ICE2Q / 9-aminocamptothecin; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC1920695
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2. Mikkelsen T, Lush R, Grossman SA, Carson KA, Fisher JD, Alavi JB, Rosenfeld S: Phase II clinical and pharmacologic study of radiation therapy and carboxyamido-triazole (CAI) in adults with newly diagnosed glioblastoma multiforme. Invest New Drugs; 2007 Jun;25(3):259-63
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  • [Title] Phase II clinical and pharmacologic study of radiation therapy and carboxyamido-triazole (CAI) in adults with newly diagnosed glioblastoma multiforme.
  • INTRODUCTION: Carboxyamido-triazole (CAI) is a synthetic inhibitor of non-voltage-gated calcium channels that reversibly inhibits angiogenesis, tumor cell proliferation, and metastatic potential.
  • This study examined the efficacy, safety and pharmacokinetics of oral CAI in the treatment of patients with newly diagnosed glioblastoma multiforme (GBM) in an open-label, single arm non-randomized phase 2 trial.
  • METHODS: Eligible patients with histologically confirmed GBM started CAI therapy (250 mg daily) on the first day of radiation (6000 cGy in 30 fractions) and continued until progression, unless side effects became intolerable.
  • The primary outcome was survival compared to historical controls within the NABTT CNS Consortium database.
  • The mean CAI plasma concentration for patients taking enzyme inducing antiepileptic drugs (EIAED) was 1.35 +/-1.22 compared to 4.06 +/- 1.50 (p < 0.001) for subjects not taking these agents.
  • Overall survival and grade > or = 3 toxicities were comparable by EIAED status.
  • CONCLUSIONS: This study demonstrated that (1) CAI can be administered safely with concomitant cranial irradiation, (2) the pharmacokinetics of CAI are significantly affected by co-administration of EIAED, and (3) the survival of patients with newly diagnosed GBM was not improved with this novel agent, despite achieving adequate drug levels.

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  • (PMID = 17080256.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / CA062475
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Calcium Channel Blockers; 0 / Triazoles; 99519-84-3 / carboxyamido-triazole
  • [Other-IDs] NLM/ NIHMS507872; NLM/ PMC3963813
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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice.
  • 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%.
  • In mice bearing intracranial D-245 MG xenografts, treatment with VNP40101M at a dose of 18 mg/kg daily for five days produced a 50% increase in median survival compared with controls.
  • 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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4. Khan MK, Hunter GK, Vogelbaum M, Suh JH, Chao ST: Evidence-based adjuvant therapy for gliomas: current concepts and newer developments. Indian J Cancer; 2009 Apr-Jun;46(2):96-107
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  • [Title] Evidence-based adjuvant therapy for gliomas: current concepts and newer developments.
  • Of the 18,820 new cases of primary central nervous system (CNS) tumors diagnosed annually in the United States, gliomas account for over 60% with 30-40% of them being glioblastoma multiforme (GBM), 10% being anaplastic astrocytoma (AA), and 10% being low grade gliomas (LGGs).
  • This is in contrast to one study from West Bengal, India, in which only 7.9% of the brain tumors were GBMs, while 46.8% were astrocytomas.
  • Of all adult primary CNS tumors, GBM is the most common and the most malignant with about 7,000 to 8,000 new cases annually in the United States.
  • Given poor outcomes, a number of treatment approaches have been investigated.
  • Common to these approaches is the use of adjuvant radiation therapy, even as surgery alone, with or without chemotherapy, may be the mainstay for some lower grade and low-risk gliomas.
  • Today, treatment typically involves external beam radiation, with concurrent and adjuvant chemotherapy for more aggressive histologies.
  • Specifically, the database is searched using the following keywords, with various combinations: glioma, low-grade, anaplastic, astrocytoma, oligodendroglioma, oligoastrocytoma, glioblastoma multiforme, chemotherapy, radiation, new concepts, phase III, MGMT, CDX-110 (Celldex), temozolomide, 1p/19q deletion, and bevacizumab.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Chemotherapy, Adjuvant. Evidence-Based Medicine. Glioma / therapy. Radiotherapy, Adjuvant
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Astrocytoma / therapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioblastoma / therapy. Humans

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  • (PMID = 19346643.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 64
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5. Hur H, Jung S, Jung TY, Kim IY: Cerebellar glioblastoma multiforme in an adult. J Korean Neurosurg Soc; 2008 Apr;43(4):194-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebellar glioblastoma multiforme in an adult.
  • Primary cerebellar glioblastoma multiforme (GBM) is a rare tumor in adults that accounts for just 1% of all cases of GBM.
  • After operation, glioblastoma was histologically confirmed.
  • Postoperative radiotherapy with concomitant and adjuvant temozolomide chemotherapy was subsequently followed.

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  • (PMID = 19096643.001).
  • [ISSN] 2005-3711
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2588262
  • [Keywords] NOTNLM ; Cerebellum / Differential diagnosis / Glioblastoma multiforme / Pathogenesis
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6. Perry SL, Bohlin C, Reardon DA, Desjardins A, Friedman AH, Friedman HS, Vredenburgh JJ: Tinzaparin prophylaxis against venous thromboembolic complications in brain tumor patients. J Neurooncol; 2009 Oct;95(1):129-134
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  • [Title] Tinzaparin prophylaxis against venous thromboembolic complications in brain tumor patients.
  • The purpose of this study was to determine the safety of tinzaparin for deep vein thrombosis prophylaxis in newly diagnosed grade III-IV malignant glioma patients.
  • During chemotherapy cycles, blood counts were monitored weekly and tinzaparin was held if the platelet count decreased to <50,000 and was re-initiated at a platelet count >100,000.
  • Forty patients were enrolled into the study, 35 with glioblastoma multiforme and 5 with anaplastic astrocytoma.
  • Possible attributable toxicity was limited to two patients who developed CNS hemorrhages (one grade 1 and one grade 2) and one patient with an increase in liver enzymes (grade 3).
  • There were no patients with a grade 4 or 5 CNS hemorrhages or systemic hemorrhages >or=grade 2.
  • The median time on prophylactic tinzaparin was 161 days (range of 5 to 601 days).
  • One patient developed a deep venous thrombosis while taking tinzaparin, and three patients developed thromboembolic complications while off tinzaparin.
  • Tinzaparin at a fixed prophylactic dose is safe and may decrease the incidence of thromboembolic complications in brain tumor patients.
  • [MeSH-major] Brain Neoplasms / complications. Fibrinolytic Agents / therapeutic use. Glioma / complications. Heparin, Low-Molecular-Weight / therapeutic use. Venous Thromboembolism / etiology. Venous Thromboembolism / prevention & control
  • [MeSH-minor] Adult. Aged. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Pulmonary Embolism / etiology. Pulmonary Embolism / prevention & control. Tomography, X-Ray Computed

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  • (PMID = 19415455.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K23 HL084233-02; United States / NHLBI NIH HHS / HL / K23 HL084233-03; United States / NHLBI NIH HHS / HL / K23 HL084233; United States / NHLBI NIH HHS / HL / K23 HL084233-01A1; United States / NHLBI NIH HHS / HL / K23-HL084233-02
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibrinolytic Agents; 0 / Heparin, Low-Molecular-Weight; 7UQ7X4Y489 / tinzaparin
  • [Other-IDs] NLM/ NIHMS180651; NLM/ PMC2837514
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7. Vredenburgh JJ, Desjardins A, Herndon JE 2nd, Marcello J, Reardon DA, Quinn JA, Rich JN, Sathornsumetee S, Gururangan S, Sampson J, Wagner M, Bailey L, Bigner DD, Friedman AH, Friedman HS: Bevacizumab plus irinotecan in recurrent glioblastoma multiforme. J Clin Oncol; 2007 Oct 20;25(30):4722-9
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  • [Title] Bevacizumab plus irinotecan in recurrent glioblastoma multiforme.
  • PURPOSE: The prognosis for patients with recurrent glioblastoma multiforme is poor, with a median survival of 3 to 6 months.
  • The dose of irinotecan was based on the patient's anticonvulsant: Patients taking enzyme-inducing antiepileptic drugs (EIAEDs) received 340 mg/m2, and patients not taking EIAEDs received 125 mg/m2.
  • After this regimen was deemed safe and effective, the irinotecan schedule was changed to an accepted brain tumor regimen of four doses in 6 weeks, in anticipation of a phase III randomized trial of irinotecan versus irinotecan and bevacizumab.
  • One patient developed a CNS hemorrhage, which occurred in his 10th cycle.
  • Four patients developed thromboembolic complications (deep venous thrombosis and/or pulmonary emboli).
  • CONCLUSION: Bevacizumab and irinotecan is an effective treatment for recurrent glioblastoma multiforme and has moderate toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • [CommentIn] Nat Clin Pract Oncol. 2008 Apr;5(4):186-7 [18285760.001]
  • [CommentIn] J Clin Oncol. 2007 Oct 20;25(30):4705-6 [17947716.001]
  • [CommentIn] J Clin Oncol. 2008 Nov 10;26(32):5304-5; author reply 5305 [18854564.001]
  • [CommentIn] Nat Clin Pract Neurol. 2008 May;4(5):242-3 [18212790.001]
  • [CommentIn] J Clin Oncol. 2008 Feb 20;26(6):1012-3; author reply 1013 [18281677.001]
  • (PMID = 17947719.001).
  • [ISSN] 1527-7755
  • [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 / 4 R37 CA11898; United States / NCI NIH HHS / CA / 5 P50 CA108786; United States / NINDS NIH HHS / NS / 5 P50 NS20023
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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8. 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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  • [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.
  • 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)].
  • Growth delays ranged from 7.6 days with D-245 MG to 62.1 days with D-456 MG (P < 0.001).
  • 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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9. Kleinberg L, Grossman SA, Carson K, Lesser G, O'Neill A, Pearlman J, Phillips P, Herman T, Gerber M: Survival of patients with newly diagnosed glioblastoma multiforme treated with RSR13 and radiotherapy: results of a phase II new approaches to brain tumor therapy CNS consortium safety and efficacy study. J Clin Oncol; 2002 Jul 15;20(14):3149-55
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  • [Title] Survival of patients with newly diagnosed glioblastoma multiforme treated with RSR13 and radiotherapy: results of a phase II new approaches to brain tumor therapy CNS consortium safety and efficacy study.
  • PURPOSE: The objectives of this phase II study were to determine survival, safety, pharmacokinetics (PK), and pharmacodynamics (PD) of 2,4-[[(3,5-dimethylanilino)carbonyl]methyl]phenoxy]-2-methylpropionic acid (RSR13, efaproxiral) 100 mg/kg per day administered with standard cranial radiotherapy (RT) for the treatment of glioblastoma multiforme (GBM).
  • RSR13, a synthetic allosteric modifier of hemoglobin, is a radiation-enhancing agent that noncovalently binds to hemoglobin, reduces oxygen-binding affinity, and increases oxygen unloading to hypoxic tissue.
  • Patients received daily RSR13 100 mg/kg intravenously infused for 30 minutes immediately before cranial RT (60 Gy in 30 fractions).
  • Supplemental oxygen was given during RSR13 infusion and continued until after the RT treatment was completed.
  • Twenty-four percent of patients had greater than grade 2 toxicity, which was generally transient and self-limited.
  • [MeSH-major] Aniline Compounds / therapeutic use. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Propionates / therapeutic use. Radiation-Sensitizing Agents / therapeutic use. Supratentorial Neoplasms / drug therapy. Supratentorial Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Confidence Intervals. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Radiotherapy, Adjuvant. Survival Analysis. Treatment Outcome. United States

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  • (PMID = 12118029.001).
  • [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 / CA62475
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / Propionates; 0 / Radiation-Sensitizing Agents; 131179-95-8 / efaproxiral
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10. Salmaggi A, Riva M, Silvani A, Merli R, Tomei G, Lorusso L, Russo A, Marchioni E, Imbesi F, Lombardia Neuro-oncology Group: A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy. Neurol Sci; 2005 Oct;26(4):227-34
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  • [Title] A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy.
  • The objective was to set the basis for a prospective, multicentre data collection on newly diagnosed adult glioblastoma patients diagnosed in Lombardia by means of a common database used by neurological and neurosurgical units of various hospitals, providing epidemiological, therapy and follow-up data.
  • All adult patients with a newly diagnosed glioblastoma in 9 Lombardia hospitals from 31 March 2003 to 31 March 2004 were followed prospectively by a form elaborated by the Lombardia Neuro-oncology Group.
  • Demographic data were recorded, as well as symptoms at onset, entity of tumour resection, post-surgical Karnofsky Performance Score, radio- and chemotherapy, presence/absence of venous thrombosis, type of antiepileptic treatment, time to tumour progression and survival time (ST).
  • One hundred and thirty-four newly diagnosed glioblastoma patients were enrolled during the first year of the study.
  • In 71 patients, the tumour involved 1 brain lobe at diagnosis.
  • At analysis of predictive value on ST, grossly total resection and chemotherapy were significantly associated with a longer ST.
  • A very high proportion of patients were treated with antiepileptic drugs, even in the absence of seizures.
  • Data in newly diagnosed glioblastoma patients in Lombardia are in line with other case series reported in other populations.
  • [MeSH-major] Brain Neoplasms / physiopathology. Glioblastoma / physiopathology
  • [MeSH-minor] Adult. Brain / pathology. Cohort Studies. Databases, Factual. Disease Progression. Female. Geography. Humans. Italy. Male. Middle Aged. Prospective Studies. Seizures / etiology. Survival Analysis

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  • (PMID = 16193249.001).
  • [ISSN] 1590-1874
  • [Journal-full-title] Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
  • [ISO-abbreviation] Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Italy
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11. Grossman SA, Alavi JB, Supko JG, Carson KA, Priet R, Dorr FA, Grundy JS, Holmlund JT: Efficacy and toxicity of the antisense oligonucleotide aprinocarsen directed against protein kinase C-alpha delivered as a 21-day continuous intravenous infusion in patients with recurrent high-grade astrocytomas. Neuro Oncol; 2005 Jan;7(1):32-40
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  • [Title] Efficacy and toxicity of the antisense oligonucleotide aprinocarsen directed against protein kinase C-alpha delivered as a 21-day continuous intravenous infusion in patients with recurrent high-grade astrocytomas.
  • Aprinocarsen is an antisense oligonucleotide against PKC-alpha that reduces PKC-alphain human cell lines and inhibits a human glioblastoma tumor cell line in athymic mice.
  • In this phase 2 study, aprinocarsen was administered to patients with recurrent high-grade gliomas by continuous intravenous infusion (2.0 mg/kg/day for 21 days per month).
  • Their median age was 46 years (range, 28-68 years), median Karnofsky performance status was 80 (range, 60-100), median tumor volume was 58 cm3 (range, 16-254 cm3), and histology included glioblastoma multiforme (n = 16), anaplastic oligodendroglioma (n = 4), and anaplastic astrocytoma (n = 1).
  • The number of prior chemotherapy regimens included none (n = 3), one (n = 10), and two (n = 8).
  • No tumor responses were observed.
  • Patients on this therapy rapidly developed symptoms of increased intracranial pressure with increased edema, enhancement, and mass effect on neuroimaging.
  • The median time to progression was 36 days, and median survival was 3.4 months.
  • The observed toxicities were mild, reversible, and uncommon (grade 3 thrombocytopenia [n = 3] and grade 4 AST [n = 1]), and no coagulopathy or CNS bleeding resulted from this therapy.
  • This is the first study to use an antisense oligonucleotide or a specific PKC-alpha inhibitor in patients with high-grade gliomas.
  • The rapid deterioration seen in these patients could result from tumor growth or an effect of aprinocarsen on bloodbrain barrier integrity.

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  • (PMID = 15701280.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / U01-CA-26406; United States / NCI NIH HHS / CA / UO1CA-62475
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Phosphorothioate Oligonucleotides; EC 2.7.11.13 / PRKCA protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-alpha; FMT95051CQ / aprinocarsen
  • [Other-IDs] NLM/ PMC1871621
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12. Lustig R, Mikkelsen T, Lesser G, Grossman S, Ye X, Desideri S, Fisher J, Wright J, New Approaches to Brain Tumor Therapy CNS Consortium: Phase II preradiation R115777 (tipifarnib) in newly diagnosed GBM with residual enhancing disease. Neuro Oncol; 2008 Dec;10(6):1004-9
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  • Glioblastoma multiforme (GBM) is a lethal primary malignant brain tumor in adults.
  • Following surgery, an MRI confirmed the presence of residual enhancing tumor.
  • Patients on enzyme-inducing antiseizure drugs (EIASDs) received 600 mg twice per day, and those not on EIASDs received 300 mg twice per day.
  • The primary end point was overall survival; secondary end points were tumor response rate and toxicity.
  • The overall median time of survival was 7.7 months.
  • There were no tumor responses.
  • A total of 24 patients (85%) were off study before the planned treatment schedule for radiation therapy.
  • R115777 administered prior to radiation therapy in patients with newly diagnosed GBM and residual enhancing disease did not result in any measurable responses or improvement in survival.
  • R115777 administered prior to radiation therapy is not recommended for patients with newly diagnosed GBM.

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  • (PMID = 18725460.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01-CA62475; United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / P30-CA0516; United States / NCI NIH HHS / CA / U01-CA105689; United States / NCI NIH HHS / CA / U01 CA105689
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib
  • [Other-IDs] NLM/ PMC2718997
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13. Grossman SA, Phuphanich S, Lesser G, Rozental J, Grochow LB, Fisher J, Piantadosi S, New Approaches to Brain Tumor Therapy CNS Consortium: Toxicity, efficacy, and pharmacology of suramin in adults with recurrent high-grade gliomas. J Clin Oncol; 2001 Jul 01;19(13):3260-6
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  • [Title] Toxicity, efficacy, and pharmacology of suramin in adults with recurrent high-grade gliomas.
  • PURPOSE: To determine the toxicity, efficacy, and pharmacology of suramin in patients with recurrent or progressive recurrent high-grade gliomas.
  • Ten patients had glioblastoma multiforme, and 11 had received prior nitrosoureas.
  • RESULTS: Drug-related toxicities were modest and reversible.
  • Three patients developed grade 3 to 4 neutropenia, constipation, diarrhea, or nausea.
  • No CNS bleeding was observed.
  • Median time to progression was 55 days (range, 17 to 242 days) and median survival was 191 days (range, 42 to 811 days).
  • One patient who "progressed" after 12 weeks of suramin had a subsequent marked reduction in tumor size and has maintained an excellent partial response for over 2 years without other therapy.
  • CONCLUSION: This study demonstrates that suramin is well tolerated by patients with recurrent high-grade gliomas and may have efficacy in this disease.
  • As a result of this data, suramin and radiation are now being administered concurrently to patients with newly diagnosed glioblastoma multiforme, with survival as the primary outcome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Central Nervous System Neoplasms / drug therapy. Glioma / drug therapy. Suramin / therapeutic use
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Survival Rate

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  • (PMID = 11432894.001).
  • [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 / U01-CA62475
  • [Publication-type] Clinical Trial; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 6032D45BEM / Suramin
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14. Phuphanich S, Carson KA, Grossman SA, Lesser G, Olson J, Mikkelsen T, Desideri S, Fisher JD, New Approaches to Brain Tumor Therapy (NABTT) CNS Consortium: Phase I safety study of escalating doses of atrasentan in adults with recurrent malignant glioma. Neuro Oncol; 2008 Aug;10(4):617-23
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  • Patients were evaluated for response every 8 weeks and remained on the study until the tumor progressed or toxicities occurred.
  • Twenty-two patients had glioblastoma multiforme (GBM), 2 had anaplastic astrocytoma, and 1 had an anaplastic oliogodendroglioma; 24 patients had received one prior chemo therapy regimen before being enrolled in the study.
  • The most common atrasentan-related toxicities were grade 1 or 2 rhinitis, fatigue, and edema.
  • One patient developed grade 3 hypoxia and peripheral edema at a dose of 90 mg/day.
  • Further study of atrasentan with radiation therapy and temozolomide in newly diagnosed GBM is warranted to evaluate the efficacy of this novel agent.

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  • (PMID = 18477765.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062406; United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / U01-CA62406; United States / NCI NIH HHS / CA / UO1 CA-62475
  • [Publication-type] Case Reports; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrrolidines; V6D7VK2215 / atrasentan
  • [Other-IDs] NLM/ PMC2666236
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15. Agnihotri S, Wolf A, Picard D, Hawkins C, Guha A: GATA4 is a regulator of astrocyte cell proliferation and apoptosis in the human and murine central nervous system. Oncogene; 2009 Aug 27;28(34):3033-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GATA4 is a regulator of astrocyte cell proliferation and apoptosis in the human and murine central nervous system.
  • The GATA transcription factors consist of six family members, which bind to the consensus DNA-binding element, W-GATA-R, and are poorly characterized in the central nervous system (CNS).
  • Using retroviral gene trapping on transgenic mouse glioma models, we identified GATA6 to be a novel tumor suppressor gene in glioblastoma multiforme.
  • We now show GATA4, a family member of GATA6, to be expressed in the neurons and glia of normal murine and human embryonic and adult CNS.
  • In contrast, knockdown of Gata4 in p53 null non-transformed murine astrocytes induced transformation, with increased proliferation and resistance to chemotherapy or radiation-induced apoptosis.
  • Furthermore, GATA4 expression was lost in a panel of human malignant astrocytoma cell lines.
  • Collectively, we show that GATA4 is expressed in the embryonic and adult CNS and acts as a negative regulator of astrocyte proliferation and growth.
  • [MeSH-major] Apoptosis. Astrocytes / physiology. Brain / cytology. GATA4 Transcription Factor / physiology
  • [MeSH-minor] Animals. Cell Cycle. Cell Proliferation. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Humans. Mice. Transforming Growth Factor beta / pharmacology. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 19543315.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / Gata4 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Protein p53
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16. Benesch M, Wagner S, Berthold F, Wolff JE: Primary dissemination of high-grade gliomas in children: experiences from four studies of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH). J Neurooncol; 2005 Apr;72(2):179-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary dissemination of high-grade gliomas in children: experiences from four studies of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH).
  • PURPOSE: Clinical data on central nervous system (CNS) dissemination of high-grade gliomas (HGG) at initial presentation in children are rare.
  • PATIENTS AND METHODS: We conducted a retrospective data analysis of all patients enrolled into four consecutive HGG protocols of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH) to determine the incidence of primary CNS dissemination of HGG and to describe clinical characteristics and outcome of children with HGG who were diagnosed with CNS dissemination at initial presentation.
  • Data concerning tumor dissemination are available from 324 patients.
  • RESULTS: A total of 10 patients (3.1%) (anaplastic astrocytoma: n=3, glioblastoma multiforme: n=6, diffuse intrinsic pontine glioma: n=1) had primary tumor dissemination.
  • The most frequent primary tumor sites were the cortex (n=4), followed by the ventricles (n=2), cerebellum (n=1), spinal cord (n=1), and pons (n=1).
  • Following surgery eight patients received local radiotherapy and eight additional chemotherapy.
  • Median progression-free and overall survival was 0.8 years (95% CI 0.2-1.4) and 1.5 years (95% CI 0.67-2.29) for patients with primary tumor dissemination, respectively, with no statistically significant differences between the group with and the group without primary tumor dissemination.
  • CONCLUSIONS: Initial diagnostic evaluation should include complete CNS imaging as well as cerebrospinal fluid examination in all patients with HGG.
  • As prognosis of children with HGG and primary CNS dissemination was not inferior to patients without dissemination in our population, these patients should be treated in the same way as patients without primary CNS dissemination.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / therapy. Glioma / pathology. Glioma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / analogs & derivatives. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Neoplasm Invasiveness. Radiotherapy. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 15925999.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; H64JRU6GJ0 / trofosfamide
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17. Chi AS, Sorensen AG, Jain RK, Batchelor TT: Angiogenesis as a therapeutic target in malignant gliomas. Oncologist; 2009 Jun;14(6):621-36
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  • [Title] Angiogenesis as a therapeutic target in malignant gliomas.
  • Currently, adult glioblastoma (GBM) patients have poor outcomes with conventional cytotoxic treatments.
  • Because GBMs are highly angiogenic tumors, inhibitors that target tumor vasculature are considered promising therapeutic agents in these patients.
  • Encouraging efficacy and tolerability in preliminary clinical trials suggest that targeting angiogenesis may be an effective therapeutic strategy in GBM patients.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Glioma / blood supply. Glioma / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Cell Movement / drug effects. Clinical Trials as Topic. Drug Resistance, Neoplasm. Edema / drug therapy. Endothelial Cells / drug effects. Humans. Protein Kinase Inhibitors / therapeutic use. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 19487335.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 175
  • [Other-IDs] NLM/ NIHMS765709; NLM/ PMC4790121
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18. Kunwar S, Prados MD, Chang SM, Berger MS, Lang FF, Piepmeier JM, Sampson JH, Ram Z, Gutin PH, Gibbons RD, Aldape KD, Croteau DJ, Sherman JW, Puri RK, Cintredekin Besudotox Intraparenchymal Study Group: Direct intracerebral delivery of cintredekin besudotox (IL13-PE38QQR) in recurrent malignant glioma: a report by the Cintredekin Besudotox Intraparenchymal Study Group. J Clin Oncol; 2007 Mar 1;25(7):837-44
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  • PURPOSE: Glioblastoma multiforme (GBM) is a devastating brain tumor with a median survival of 6 months after recurrence.
  • Convection-enhanced delivery (CED) is a locoregional-administration method leading to high-tissue concentrations with large volume of distributions.
  • PATIENTS AND METHODS: Three phase I clinical studies evaluated intracerebral CED of CB along with tumor resection.
  • The main objectives were to assess the tolerability of various concentrations and infusion durations; tissue distribution; and methods for optimizing delivery.
  • All patients underwent tumor resection followed by a single intraparenchymal infusion (in addition to the intraparenchymal one following resection), with a portion of patients who had a preresection intratumoral infusion.
  • The maximum tolerated intraparenchymal concentration was 0.5 microg/mL and tumor necrosis was observed at this concentration.
  • Postoperative catheter placement appears to be important for optimal drug distribution.
  • CB- and procedure-related adverse events were primarily limited to the CNS.
  • CED is a complex delivery method requiring catheter placement via a second procedure to achieve accurate catheter positioning, better drug distribution, and better outcome.
  • [MeSH-major] Drug Delivery Systems / methods. Exotoxins / administration & dosage. Glioma / drug therapy. Immunotoxins / administration & dosage. Interleukin-13 / administration & dosage. Supratentorial Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Catheterization. Convection. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Tissue Distribution

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  • (PMID = 17327604.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Exotoxins; 0 / IL13-PE38QQR; 0 / Immunotoxins; 0 / Interleukin-13
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19. Loh KC, Willert J, Meltzer H, Roberts W, Kerlin B, Kadota R, Levy M, White G, Geddis A, Schiff D, Martin L, Yu A, Kung F, Spear MA: Temozolomide and radiation for aggressive pediatric central nervous system malignancies. J Pediatr Hematol Oncol; 2005 May;27(5):254-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temozolomide and radiation for aggressive pediatric central nervous system malignancies.
  • This study describes the outcomes of children treated with combinations of temozolomide and radiation therapy for various aggressive central nervous system malignancies.
  • Patients with focal disease were treated with concomitant temozolomide (daily 75 mg/m) and three-dimensional conformal radiotherapy in a dose that ranged from 50 to 54 Gy, followed by temozolomide (200 mg/m/d x 5 days/month in three patients, 150 mg/m x 5 days/ month in one patient).
  • Patients with disseminated disease were treated with craniospinal radiation (39.6 Gy) before conformal boost.
  • Three patients achieved a partial response during treatment, with two of these patients dying of progressive disease after treatment.
  • Three patients achieved stable disease, with one of these patients dying of progressive disease after treatment.
  • Toxicities observed included low-grade neutropenia, thrombocytopenia, and lymphopenia.
  • The combination of temozolomide and radiotherapy appears to be well tolerated in a variety of treatment schemas for aggressive pediatric central nervous system malignancies.
  • This information is of particular use in designing future studies, given the recent positive results in a randomized study examining the use of temozolomide concomitant with radiation in the treatment of adult glioblastoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Fatal Outcome. Female. Humans. Infant. Magnetic Resonance Imaging. Male

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  • (PMID = 15891559.001).
  • [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 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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20. Bax DA, Gaspar N, Little SE, Marshall L, Perryman L, Regairaz M, Viana-Pereira M, Vuononvirta R, Sharp SY, Reis-Filho JS, Stávale JN, Al-Sarraj S, Reis RM, Vassal G, Pearson AD, Hargrave D, Ellison DW, Workman P, Jones C: EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines. Clin Cancer Res; 2009 Sep 15;15(18):5753-61
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  • [Title] EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines.
  • PURPOSE: The epidermal growth factor receptor (EGFR) is amplified and overexpressed in adult glioblastoma, with response to targeted inhibition dependent on the underlying biology of the disease.
  • We have sought to clarify the role of EGFR in pediatric high-grade glioma (HGG).
  • Pediatric glioblastoma cells transduced with wild-type or deletion mutant EGFRvIII were not rendered more sensitive to erlotinib despite expressing wild-type PTEN.
  • Phosphorylated receptor tyrosine kinase profiling showed a specific activation of platelet-derived growth factor receptor alpha/beta in EGFRvIII-transduced pediatric glioblastoma cells, and targeted coinhibition with erlotinib and imatinib leads to enhanced efficacy in this model.
  • [MeSH-major] Glioma / drug therapy. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Sequence Deletion
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Erlotinib Hydrochloride. Humans. Prognosis. Quinazolines / pharmacology. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Cells, Cultured

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  • [ErratumIn] Clin Cancer Res. 2009 Nov 15;15(22):7110
  • (PMID = 19737945.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C1178/A10294; United Kingdom / Cancer Research UK / / C309/A2187; United Kingdom / Cancer Research UK / / C309/A8274
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0 / epidermal growth factor receptor VIII; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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21. Dreyer ZE, Kadota RP, Stewart CF, Friedman HS, Mahoney DH, Kun LE, McCluggage CW, Burger PC, Kepner J, Heideman RL, Pediatric Oncology Group: Phase 2 study of idarubicin in pediatric brain tumors: Pediatric Oncology Group study POG 9237. Neuro Oncol; 2003 Oct;5(4):261-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase 2 study of idarubicin in pediatric brain tumors: Pediatric Oncology Group study POG 9237.
  • In previous reports, the alcohol metabolite of IDA, 4-demethoxydaunorubicinol (idarubicinol, or IDOL), had cytotoxic activity and the ability to penetrate the blood-brain barrier.
  • For this reason, the Pediatric Oncology Group conducted a Phase 2 trial of IDA for children with recurrent or progressive brain tumors.
  • Patients were stratified by tumor types into 6 categories: stratum 1, low-grade astrocytoma; stratum 2, malignant glioma (glioblastoma multiforme and anaplastic astrocytoma); stratum 3, medulloblastoma; stratum 4, brainstem glioma; stratum 5, ependymoma; and stratum 6, miscellaneous malignant tumors not included in the previous diagnoses.
  • Cycles were repeated at approximately 21-day intervals until patients developed progressive disease or had completed 6 cycles with stable or improved disease.
  • Most patients developed progressive disease; however, in 21 patients with medulloblastoma there was 1 partial response, and 6 patients had stable disease (SD) that in 4 patients lasted more than 20 weeks.
  • Only 1 patient developed reduced cardiac function.
  • The systemic clearance data for IDA and IDOL were nearly identical to those published on patients with leukemia, and the plasma elimination of the IDOL metabolite was substantially longer than that of the parent drug IDA.
  • We conclude from this data and from that in nonhuman primates that it is unlikely that IDA, daunomycin, or other related anthracyclines will be useful for treating primary CNS tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Idarubicin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 14565163.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] ZRP63D75JW / Idarubicin
  • [Other-IDs] NLM/ PMC1920677
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22. Sung T, Miller DC, Hayes RL, Alonso M, Yee H, Newcomb EW: Preferential inactivation of the p53 tumor suppressor pathway and lack of EGFR amplification distinguish de novo high grade pediatric astrocytomas from de novo adult astrocytomas. Brain Pathol; 2000 Apr;10(2):249-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preferential inactivation of the p53 tumor suppressor pathway and lack of EGFR amplification distinguish de novo high grade pediatric astrocytomas from de novo adult astrocytomas.
  • Classification of high grade astrocytomas of children into genetic subtypes similar to the adult remains to be defined.
  • Here we report an extensive characterization of 29 high grade pediatric astrocytomas, 7 WHO grade III and 22 WHO grade IV, for genetic alterations frequently observed in high grade adult astrocytomas occurring in either the p53/MDM2/p14ARF or Rb/CDK4/p16INK4a tumor suppressor pathways.
  • In addition, we have assessed the contribution of EGFR overexpression and amplification and LOH for chromosome 10, two genetic alterations commonly associated with the development of de novo adult glioblastoma for their roles in the development of de novo astrocytomas of childhood.
  • Our results suggest two major differences in the genetic pathway(s) leading to the formation of de novo high grade astrocytomas in children compared with those of the adult.
  • Our findings show preferential inactivation of the p53 tumor suppressor pathway in >95% of pediatric astrocytomas versus inactivation of the Rb tumor suppressor pathway in <25% of the same tumors.
  • In addition, de novo high grade pediatric astrocytomas lack amplification of the EGFR gene compared with EGFR amplification in one-third of adult glioblastomas.
  • Since drug treatments and gene therapy strategies exploit specific genetic alterations in tumor cells, our findings have important implications for the future development of treatments for high grade pediatric astrocytomas.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Gene Amplification. Gene Silencing. Genes, Tumor Suppressor / genetics. Glioblastoma / genetics. Nuclear Proteins. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins
  • [MeSH-minor] Adolescent. Adult. Carrier Proteins / genetics. Child. Child, Preschool. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p16. Diagnosis, Differential. Female. Gene Deletion. Gene Expression. Humans. Male. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-mdm2

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  • (PMID = 10764044.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16087
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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