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1. Lu A, Ran R, Parmentier-Batteur S, Nee A, Sharp FR: Geldanamycin induces heat shock proteins in brain and protects against focal cerebral ischemia. J Neurochem; 2002 Apr;81(2):355-64
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  • [Title] Geldanamycin induces heat shock proteins in brain and protects against focal cerebral ischemia.
  • Adult male Sprague-Dawley rats were subjected to 2-hour middle cerebral artery occlusions (MCAO) using the suture technique followed by 22-h reperfusions.
  • GA or vehicle was injected into the lateral cerebral ventricles (i.c.v) 24 h before ischemia.
  • Geldanamycin at 1 microg/kg decreased infarct volumes by 55.7% (p < 0.01) and TUNEL-positive cells by 30% in cerebral cortex.
  • Immunocytochemistry showed that GA induced Hsp70 in neurons and Hsp25 in glia and arteries in cortex, hippocampus, hypothalamus, and other brain regions.
  • GA reduced co-immunoprecipitation of HSF1 with Hsp90 in brain tissue homogenates, promoted HSE-binding of HSF in brain nuclear extracts using gel shift assays, and increased luciferase reporter gene transcription for the Hsp70 promoter in PC12 cells.
  • [MeSH-major] Brain / drug effects. Brain Ischemia / drug therapy. Heat-Shock Proteins / metabolism. Quinones / pharmacology
  • [MeSH-minor] Animals. Benzoquinones. Blotting, Western. DNA-Binding Proteins / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. HSP27 Heat-Shock Proteins. HSP70 Heat-Shock Proteins / metabolism. Immunohistochemistry. Injections, Intraventricular. Lactams, Macrocyclic. Male. Neoplasm Proteins / metabolism. Protein Binding / drug effects. Rats. Transcription Factors. Transcriptional Activation / drug effects

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  • (PMID = 12064483.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG19561; United States / NINDS NIH HHS / NS / NS28167; United States / NINDS NIH HHS / NS / NS38084
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / DNA-Binding Proteins; 0 / HSP27 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hspb1 protein, rat; 0 / Lactams, Macrocyclic; 0 / Neoplasm Proteins; 0 / Quinones; 0 / Transcription Factors; 0 / heat shock transcription factor; Z3K3VJ16KU / geldanamycin
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2. Mitchell DA, Fecci PE, Sampson JH: Immunotherapy of malignant brain tumors. Immunol Rev; 2008 Apr;222:70-100
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  • Despite aggressive multi-modality therapy including surgery, radiation, and chemotherapy, the prognosis for patients with malignant primary brain tumors remains very poor.
  • Moreover, the non-specific nature of conventional therapy for brain tumors often results in incapacitating damage to surrounding normal brain and systemic tissues.
  • Thus, there is an urgent need for the development of therapeutic strategies that precisely target tumor cells while minimizing collateral damage to neighboring eloquent cerebral cortex.
  • The rationale for using the immune system to target brain tumors is based on the premise that the inherent specificity of immunologic reactivity could meet the clear need for more specific and precise therapy.
  • Recent advances in our understanding of tumor-induced and host-mediated immunosuppressive mechanisms, the development of effective strategies to combat these suppressive effects, and a better understanding of how to deliver immunologic effector molecules more efficiently to CNS tumors have all facilitated significant progress toward the realization of true clinical benefit from immunotherapeutic treatment of malignant gliomas.
  • [MeSH-major] Antigens, Neoplasm / immunology. Brain Neoplasms / immunology. Immunotherapy / methods

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  • (PMID = 18363995.001).
  • [ISSN] 1600-065X
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Amyloid beta-Peptides; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Toll-Like Receptors
  • [Number-of-references] 401
  • [Other-IDs] NLM/ NIHMS396799; NLM/ PMC3418681
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3. Chen YY, Tiang XY, Li Z, Luo BN, Huang Q: Sporadic meningioangiomatosis-associated atypical meningioma mimicking parenchymal invasion of brain: a case report and review of the literature. Diagn Pathol; 2010;5:39
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • He had no stigmata of neurofibromatosis type 2.
  • The diagnosis of atypical meningioma associated with sporadic meningioangiomatosis was made.
  • The patient had been followed-up for 11 months without adjuvant radiotherapy or chemotherapy.
  • We suggest that postoperative radiotherapy or chemotherapy should be given careful consideration to avoid over-treatment due to erroneously interpret as malignant meningioma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Central Nervous System Vascular Malformations / diagnosis. Cerebral Cortex / pathology. Meningeal Neoplasms / diagnosis. Meningioma / diagnosis
  • [MeSH-minor] Adult. Biopsy. Diagnosis, Differential. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Treatment Outcome

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  • (PMID = 20565869.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2904739
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4. Reddy AT, Janss AJ, Phillips PC, Weiss HL, Packer RJ: Outcome for children with supratentorial primitive neuroectodermal tumors treated with surgery, radiation, and chemotherapy. Cancer; 2000 May 1;88(9):2189-93
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  • [Title] Outcome for children with supratentorial primitive neuroectodermal tumors treated with surgery, radiation, and chemotherapy.
  • Recently, 5-year progression free survival rates as high as 80% have been reported for children with MB treated with craniospinal radiation (CRT) and chemotherapy including cisplatin, lomustine (CCNU), and vincristine (VCR).
  • Five patients had disease dissemination at diagnosis.
  • All patients underwent surgery and staging, followed by CRT and chemotherapy with cisplatin, CCNU, and VCR.
  • RESULTS: Of the 22 patients, 13 had developed disease progression and 10 had died at the time of last follow-up.
  • CONCLUSIONS: The results of the current study demonstrate that the outcome for children with SPNET treated with radiation and chemotherapy appears worse than for children with MB treated with identical therapy.
  • This suggests that there may be biologic differences between supratentorial and infratentorial primitive neuroectodermal tumors, thus requiring refinements in treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neuroectodermal Tumors, Primitive / surgery. Supratentorial Neoplasms / surgery
  • [MeSH-minor] Adolescent. Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Cerebral Cortex / drug effects. Cerebral Cortex / radiation effects. Cerebral Cortex / surgery. Child. Child, Preschool. Cisplatin / administration & dosage. Disease Progression. Disease-Free Survival. Follow-Up Studies. Humans. Linear Models. Lomustine / administration & dosage. Neoplasm Staging. Pinealoma / drug therapy. Pinealoma / radiotherapy. Pinealoma / surgery. Retrospective Studies. Survival Rate. Thalamic Diseases / drug therapy. Thalamic Diseases / radiotherapy. Thalamic Diseases / surgery. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 10813733.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; Q20Q21Q62J / Cisplatin
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5. Sisodiya SM, Martinian L, Scheffer GL, van der Valk P, Cross JH, Scheper RJ, Harding BN, Thom M: Major vault protein, a marker of drug resistance, is upregulated in refractory epilepsy. Epilepsia; 2003 Nov;44(11):1388-96
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  • [Title] Major vault protein, a marker of drug resistance, is upregulated in refractory epilepsy.
  • PURPOSE: The molecular basis of drug resistance in epilepsy is being explored.
  • Two proteins associated with drug resistance in cancer, P-glycoprotein and multidrug resistance-associated protein 1, are upregulated in human epileptogenic pathologies.
  • Nonepileptogenic control and histologically normal brain adjacent to epileptogenic tissue were used for comparison.
  • CONCLUSIONS: These results show that more than one resistance protein may be upregulated in a given epileptogenic pathology and may contribute to drug resistance.
  • Determination of the types, amounts, and distribution of such proteins will be necessary for rational treatment for drug resistance in epilepsy.
  • [MeSH-major] Anticonvulsants / adverse effects. Drug Resistance, Multiple / genetics. Epilepsy / drug therapy. Epilepsy / genetics. Vault Ribonucleoprotein Particles / genetics
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / genetics. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Capillaries / pathology. Cerebral Cortex / abnormalities. Cerebral Cortex / pathology. Endothelium, Vascular / pathology. Hippocampus / pathology. Humans. Immunoenzyme Techniques. Neoplasm Proteins / genetics. Neoplasms, Neuroepithelial / genetics. Neoplasms, Neuroepithelial / pathology. Neurons / pathology. Phenotype. Reference Values. Sclerosis. Up-Regulation / genetics

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  • (PMID = 14636345.001).
  • [ISSN] 0013-9580
  • [Journal-full-title] Epilepsia
  • [ISO-abbreviation] Epilepsia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Anticonvulsants; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
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6. Guo M, Roman RJ, Fenstermacher JD, Brown SL, Falck JR, Arbab AS, Edwards PA, Scicli AG: 9L gliosarcoma cell proliferation and tumor growth in rats are suppressed by N-hydroxy-N'-(4-butyl-2-methylphenol) formamidine (HET0016), a selective inhibitor of CYP4A. J Pharmacol Exp Ther; 2006 Apr;317(1):97-108
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  • HET0016 treatment increased mean survival time of the animals from 17 to 22 days.
  • The normal surrounding brain tissue, however, avidly makes 20-HETE, and this activity is selectively inhibited by HET0016.
  • In vivo, it may act in part by inhibiting the formation of 20-HETE by the surrounding tissue.
  • [MeSH-major] Amidines / therapeutic use. Brain Neoplasms / drug therapy. Cell Proliferation / drug effects. Cytochrome P-450 CYP4A / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Gliosarcoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Arachidonic Acid / metabolism. Cell Line, Tumor. Cerebral Cortex / pathology. Male. Neoplasm Transplantation. Rats. Rats, Inbred F344

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  • (PMID = 16352703.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY014385; United States / NHLBI NIH HHS / HL / HL36279; United States / NIGMS NIH HHS / GM / GM31278; United States / NHLBI NIH HHS / HL / HL29587; United States / NHLBI NIH HHS / HL / R37 HL036279; United States / NHLBI NIH HHS / HL / HL059996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amidines; 0 / Enzyme Inhibitors; 0 / N-hydroxy-N'-(4-butyl-2-methylphenyl)formamidine; 27YG812J1I / Arachidonic Acid; EC 1.14.15.3 / Cytochrome P-450 CYP4A
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7. Tange Y, Miyazaki M, Iwata J, Aiko Y, Sakamoto S, Mori K: Novel antitumor effect of carboplatin delivered by intracerebral microinfusion in a rat malignant glioma model. Neurol Med Chir (Tokyo); 2009 Dec;49(12):572-9
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  • The high dose group showed significant longer survival time than the control and low dose groups.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Carboplatin / administration & dosage. Glioma / drug therapy. Infusion Pumps, Implantable. Microinjections / instrumentation
  • [MeSH-minor] Animals. Brain Edema / chemically induced. Brain Edema / diagnosis. Brain Edema / physiopathology. Cell Line, Tumor. Cerebral Cortex / drug effects. Cerebral Cortex / pathology. Disease Models, Animal. Dose-Response Relationship, Drug. Evans Blue. Injections, Intravenous. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness / pathology. Rats. Rats, Inbred F344. Survival Rate. Treatment Outcome

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  • (PMID = 20035131.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 45PG892GO1 / Evans Blue; BG3F62OND5 / Carboplatin
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8. Witwer BP, Moftakhar R, Hasan KM, Deshmukh P, Haughton V, Field A, Arfanakis K, Noyes J, Moritz CH, Meyerand ME, Rowley HA, Alexander AL, Badie B: Diffusion-tensor imaging of white matter tracts in patients with cerebral neoplasm. J Neurosurg; 2002 Sep;97(3):568-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffusion-tensor imaging of white matter tracts in patients with cerebral neoplasm.
  • OBJECT: Preserving vital cerebral function while maximizing tumor resection is a principal goal in surgical neurooncology.
  • Although functional magnetic resonance imaging has been useful in the localization of eloquent cerebral cortex, this method does not provide information about the white matter tracts that may be involved in invasive, intrinsic brain tumors.
  • Recently, diffusion-tensor (DT) imaging techniques have been used to map white matter tracts in the normal brain.
  • The aim of this study was to demonstrate the role of DT imaging in preoperative mapping of white matter tracts in relation to cerebral neoplasms.
  • METHODS: Nine patients with brain malignancies (one pilocytic astrocytoma, five oligodendrogliomas, one low-grade oligoastrocytoma, one Grade 4 astrocytoma, and one metastatic adenocarcinoma) underwent DT imaging examinations prior to tumor excision.
  • Depending on the tumor type and location, evidence of white matter tract edema (two patients), infiltration (two patients), displacement (five patients), and disruption (two patients) could be assessed with the aid of DT imaging in each case.
  • The authors' experience with DT imaging indicates that anatomically intact fibers may be present in abnormal-appearing areas of the brain.

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  • (PMID = 12296640.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH62015
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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9. Schmorl P, Heer-Sonderhoff A, Vosshenrich R, Conrad S: [Cerebral vasculitis associated with gemcitabine]. Urologe A; 2010 Feb;49(2):268-70
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  • [Title] [Cerebral vasculitis associated with gemcitabine].
  • Neoadjuvant chemotherapy consisting of cisplatin and gemcitabine was given to a 50-year-old woman suffering from transitional cell carcinoma of the bladder.
  • Magnetic resonance imaging of the brain was consistent with cerebral vasculitis.
  • Although recent reports have linked this drug with leukoencephalopathy and vasculitis in various localizations, this is the first case of cerebral vasculitis associated with gemcitabine.
  • [MeSH-major] Antimetabolites, Antineoplastic / toxicity. Antineoplastic Combined Chemotherapy Protocols / toxicity. Carcinoma, Transitional Cell / drug therapy. Deoxycytidine / analogs & derivatives. Neoadjuvant Therapy. Urinary Bladder Neoplasms / drug therapy. Vasculitis, Central Nervous System / chemically induced
  • [MeSH-minor] Cerebral Cortex / drug effects. Cerebral Cortex / pathology. Cisplatin / administration & dosage. Cisplatin / toxicity. Cognition Disorders / chemically induced. Cognition Disorders / diagnosis. Epilepsy, Tonic-Clonic / chemically induced. Epilepsy, Tonic-Clonic / diagnosis. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Neoplasm Staging

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  • [Cites] Arch Ophthalmol. 2000 May;118(5):726-7 [10815173.001]
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  • (PMID = 20213928.001).
  • [ISSN] 1433-0563
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin
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10. Wick W, Menn O, Meisner C, Steinbach J, Hermisson M, Tatagiba M, Weller M: Pharmacotherapy of epileptic seizures in glioma patients: who, when, why and how long? Onkologie; 2005 Aug;28(8-9):391-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacotherapy of epileptic seizures in glioma patients: who, when, why and how long?
  • BACKGROUND: The risk for patients with primary brain tumors of experiencing an epileptic seizure at least once in the course of disease probably exceeds 50%, depending on tumor location and tumor type.
  • Several aspects regarding the role of anticonvulsants in the treatment of brain tumor patients have remained controversial.
  • PATIENTS AND METHODS: We reviewed the seizure history in 107 patients undergoing a surgical procedure for glioma at our institution.
  • After surgery, postoperative chemo- or radiotherapy and anticonvulsive therapy one third of patients was seizure-free whereas one third showed frequent seizures despite this treatment.
  • Seizure frequency increased regardless of anticonvulsive treatment with progressive or recurrent tumor growth.
  • [MeSH-major] Anticonvulsants / administration & dosage. Brain Neoplasms / complications. Cerebral Cortex. Epilepsies, Partial / drug therapy. Glioma / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Chemotherapy, Adjuvant. Combined Modality Therapy. Disease Progression. Drug Interactions. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / complications. Neoplasm Recurrence, Local / diagnosis. Retrospective Studies

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  • (PMID = 16160401.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents
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11. Chinot OL: [Cerebral metastases]. Rev Prat; 2006 Oct 31;56(16):1799-804
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  • [Title] [Cerebral metastases].
  • Improvement of diagnosis techniques and cancer treatment efficacy explain in part the increasing incidence of brain metastasis, observed in 20 to 30 % of cancer patients.
  • New techniques of MRI improve its sensibility and guide therapeutic decision, in conjunction with prognostic factors including age, Karnovsky performance score and control of the general disease.
  • In other cases, whole brain radiation therapy remains the treatment of choice for brain metastasis, while no clear data support it use complementary to surgery.
  • Chemotherapy has no proven efficacy as part of first line treatment of patients with brain metastasis and still warren further research.
  • [MeSH-major] Brain Neoplasms / secondary. Brain Neoplasms / therapy
  • [MeSH-minor] Administration, Oral. Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / therapeutic use. Age Factors. Aged. Breast Neoplasms. Colonic Neoplasms. Combined Modality Therapy. Humans. Karnofsky Performance Status. Kidney Neoplasms. Lung Neoplasms. Lymphoma / diagnosis. Magnetic Resonance Imaging. Magnetic Resonance Spectroscopy. Middle Aged. Neoplasm Recurrence, Local. Positron-Emission Tomography. Prognosis. Radiosurgery. Research

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  • (PMID = 17315506.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
  • [Number-of-references] 13
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12. Beuthien-Baumann B, Hahn G, Winkler C, Heubner G: Differentiation between recurrent tumor and radiation necrosis in a child with anaplastic ependymoma after chemotherapy and radiation therapy. Strahlenther Onkol; 2003 Dec;179(12):819-22
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  • [Title] Differentiation between recurrent tumor and radiation necrosis in a child with anaplastic ependymoma after chemotherapy and radiation therapy.
  • BACKGROUND: In patients after treatment for malignant brain tumors, a clear distinction between tumor recurrence and radiation necrosis can be challenging.
  • This case report describes the diagnostic workup in a child with anaplastic ependymoma and inconclusive MRI (magnetic resonance imaging) and PET (positron emission tomography) findings.
  • CASE REPORT: 1.5 years after resection, hyperfractionated radiotherapy and chemotherapy of an anaplastic ependymoma in the right parietal region, the cranial MRI of an 11-year-old girl showed multiple small contrast-enhanced lesions in the frontal cortex.
  • In the following months, these lesions increased in number and size and neurologic symptoms developed.
  • A biopsy, performed 6 months later when the clinical appearance worsened, showed no tumor tissue.
  • CONCLUSION: The final interpretation of the lesions was multiple focal radiation necrosis based on perfusion abnormalities after chemotherapy and conformal hyperfractionated radiotherapy, probably due to an individually enhanced vulnerability of the cerebral vessels.
  • [MeSH-major] Brain Diseases / etiology. Brain Neoplasms / radiotherapy. Ependymoma / radiotherapy. Magnetic Resonance Imaging. Necrosis. Neoplasm Recurrence, Local / diagnosis. Radiation Injuries / diagnosis. Radiotherapy / adverse effects. Tomography, Emission-Computed
  • [MeSH-minor] Biopsy. Brain / pathology. Child. Combined Modality Therapy. Diagnosis, Differential. Dose Fractionation. Female. Follow-Up Studies. Humans. Radiotherapy Dosage. Radiotherapy, Conformal. Time Factors


13. Weber MA, Kroll A, Günther M, Delorme S, Debus J, Giesel FL, Essig M, Kauczor HU, Schad LR: [Noninvasive measurement of relative cerebral blood flow with the blood bolus MRI arterial spin labeling: basic physics and clinical applications]. Radiologe; 2004 Feb;44(2):164-73
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  • [Title] [Noninvasive measurement of relative cerebral blood flow with the blood bolus MRI arterial spin labeling: basic physics and clinical applications].
  • [Transliterated title] Nichtinvasive Messung des relativen zerebralen Blutflusses mit der MR-Blutbolusmarkierungstechnik (arterial-spin-labeling): Physikalische Grundlagen und klinische Anwendungen.
  • Knowledge of tumor blood flow is important for diagnosis and follow-up of brain tumors after therapy, especially to discriminate necrosis from tumor recurrence after radiation or chemotherapy.
  • The MRI-based arterial spin labeling technique (ASL) is a novel approach for measuring relative cerebral blood flow (rCBF) without using extrinsic contrast agents, by labeling spins of flowing arterial blood as intrinsic contrast agent.
  • This article describes physical basics of ASL and shows clinical examples in neuroimaging such as in meningeoma, glioblastoma, oligodendroglioma, and cerebral ischemia, using the Q2TIPS ASL technique.
  • Meningeoma and glioblastoma show elevated rCBF, whereas oligodendroglioma and cerebral ischemia have reduced rCBF values.
  • [MeSH-minor] Blood Flow Velocity / physiology. Brain Ischemia / diagnosis. Brain Ischemia / physiopathology. Cerebral Cortex / blood supply. Cerebral Cortex / pathology. Diagnosis, Differential. Follow-Up Studies. Glioblastoma / blood supply. Glioblastoma / diagnosis. Glioblastoma / therapy. Humans. Meningeal Neoplasms / blood supply. Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy. Meningioma / blood supply. Meningioma / diagnosis. Meningioma / therapy. Microcirculation / physiopathology. Necrosis. Neoplasm Recurrence, Local / blood supply. Neoplasm Recurrence, Local / diagnosis. Oligodendroglioma / blood supply. Oligodendroglioma / diagnosis. Oligodendroglioma / therapy. Reference Values. Regional Blood Flow / physiology. Stroke / diagnosis. Stroke / physiopathology

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  • (PMID = 14991136.001).
  • [ISSN] 0033-832X
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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14. Ducray F, Colin P, Cartalat-Carel S, Pelissou-Guyotat I, Mahla K, Audra P, Gaucherand P, Honnorat J, Trouillas P: [Management of malignant gliomas diagnosed during pregnancy]. Rev Neurol (Paris); 2006 Mar;162(3):322-9
Hazardous Substances Data Bank. Fotemustine .

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  • [Transliterated title] Prise en charge des gliomes malins découverts au cours d'une grossesse.
  • In post-partum additional treatment with chemotherapy was started.
  • In post-partum additional treatment with radiotherapy and chemotherapy was started.
  • Two weeks after surgery the patient's neurological condition worsened and in agreement with the patient a therapeutic abortion was decided.
  • Afterwards additional treatment with radiotherapy and chemotherapy was started.
  • The last patient received combined treatment with radiotherapy and chemotherapy for local recurrence of a mesencephalic high-grade glioma.
  • A posteriori it was discovered that the patient was at 4 months' gestation during this treatment.
  • Their pregnancy should not prevent them from receiving the best treatment for their glioma.
  • Treatment will depend upon clinico-radiological presentation, histology, gestational age and the patient's desires.
  • After delivery, if the delay between surgery and delivery is too long it is possible to begin cerebral radiotherapy during pregnancy.
  • After the first trimester of gestation this treatment can be given without any important risks for the child.
  • [MeSH-major] Case Management. Glioblastoma / therapy. Pregnancy Complications, Neoplastic / therapy. Supratentorial Neoplasms / therapy
  • [MeSH-minor] Abortion, Therapeutic. Adrenal Cortex Hormones / therapeutic use. Adult. Algorithms. Anesthesia, General. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carbamazepine / therapeutic use. Carmustine / administration & dosage. Cesarean Section. Chemotherapy, Adjuvant. Cranial Irradiation. Craniotomy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Frontal Lobe. Humans. Infant, Newborn. Intracranial Hypertension / etiology. Magnetic Resonance Imaging. Male. Neoplasm Recurrence, Local. Nitrosourea Compounds / administration & dosage. Nitrosourea Compounds / therapeutic use. Organophosphorus Compounds / administration & dosage. Organophosphorus Compounds / therapeutic use. Paresis / drug therapy. Paresis / etiology. Prednisolone / therapeutic use. Pregnancy. Prenatal Exposure Delayed Effects. Radiotherapy, Adjuvant. Remission Induction. Temporal Lobe

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  • [CommentIn] Rev Neurol (Paris). 2006 Mar;162(3):293-4 [16585883.001]
  • (PMID = 16585887.001).
  • [ISSN] 0035-3787
  • [Journal-full-title] Revue neurologique
  • [ISO-abbreviation] Rev. Neurol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 0 / Nitrosourea Compounds; 0 / Organophosphorus Compounds; 33CM23913M / Carbamazepine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9PHQ9Y1OLM / Prednisolone; GQ7JL9P5I2 / fotemustine; U68WG3173Y / Carmustine
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15. Lu J, Moochhala S, Shirhan M, Ng KC, Teo AL, Tan MH, Moore XL, Wong MC, Ling EA: Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study. Neuropharmacology; 2003 Feb;44(2):253-63
The Lens. Cited by Patents in .

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  • Daily treatment of AG at the dosage of 100 mg/kg or normal saline was given intraperitoneally into rats starting 2 h before or 30 min after brain injury.
  • Treatment with AG significantly reduced lesion volumes in the brains of rats after injury, as evaluated by high-resolution magnetic resonance imaging (MRI).
  • Apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL) and caspase-3 immunohistochemistry.
  • In rats receiving prophylactic or post-injury treatment of AG, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection.
  • It is suggested that inhibition of iNOS by AG may represent a potential therapeutic strategy for the treatment of traumatic brain injury.
  • [MeSH-major] Antigens, CD. Antigens, Neoplasm. Antigens, Surface. Avian Proteins. Blood Proteins. Brain Injuries / drug therapy. Enzyme Inhibitors / therapeutic use. Guanidines / therapeutic use
  • [MeSH-minor] Animals. Antigens, CD147. Caspase 3. Caspases / metabolism. Cerebral Cortex / cytology. Cerebral Cortex / metabolism. Cerebral Cortex / physiopathology. Disease Models, Animal. Hand Strength / physiology. Immunohistochemistry / methods. In Situ Nick-End Labeling / methods. Magnetic Resonance Imaging / methods. Male. Membrane Glycoproteins / metabolism. Motor Activity / drug effects. Nitric Oxide Synthase / antagonists & inhibitors. Nitric Oxide Synthase / genetics. Nitric Oxide Synthase / metabolism. Psychomotor Performance / drug effects. RNA, Messenger / analysis. Rats. Rats, Sprague-Dawley. Reflex, Acoustic / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Time Factors

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  • (PMID = 12623224.001).
  • [ISSN] 0028-3908
  • [Journal-full-title] Neuropharmacology
  • [ISO-abbreviation] Neuropharmacology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Avian Proteins; 0 / Blood Proteins; 0 / Bsg protein, Gallus gallus; 0 / Bsg protein, rat; 0 / Enzyme Inhibitors; 0 / Guanidines; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 136894-56-9 / Antigens, CD147; EC 1.14.13.39 / Nitric Oxide Synthase; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; SCQ4EZQ113 / pimagedine
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16. Marroni M, Agrawal ML, Kight K, Hallene KL, Hossain M, Cucullo L, Signorelli K, Namura S, Bingaman W, Janigro D: Relationship between expression of multiple drug resistance proteins and p53 tumor suppressor gene proteins in human brain astrocytes. Neuroscience; 2003;121(3):605-17
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  • [Title] Relationship between expression of multiple drug resistance proteins and p53 tumor suppressor gene proteins in human brain astrocytes.
  • Multiple drug resistance occurs when cells fail to respond to chemotherapy.
  • Although it has been established that the drug efflux protein P-glycoprotein protects the brain from xenobiotics, the mechanisms involved in the regulation of expression of multiple drug resistance genes and proteins are not fully understood.
  • Re-entry into the cell cycle and integrity of the p53 signaling pathway have been proposed as triggers of multiple drug resistance expression in tumor cells.
  • Whether this regulation occurs in non-tumor CNS tissue is not known.
  • Since multiple drug resistance overexpression has been reported in glia and blood vessels from epileptic brain, we investigated the level of expression of multidrug resistance protein, multidrug resistance-associated proteins and lung resistance protein in endothelial cells and astrocytes isolated from epileptic patients or studied in situ in surgical tissue samples by double label immunocytochemistry.
  • Reverse transcriptase-polymerase chain reaction and Western blot analyses revealed that multiple drug resistance, multidrug resistance protein, and lung resistance protein are expressed in these cells.
  • Our results suggest a possible link between loss of p53 function and expression of multiple drug resistance in non-tumor CNS cells.
  • [MeSH-minor] Adult. Astrocytoma / metabolism. Brain / anatomy & histology. Brain / pathology. Brain Neoplasms / metabolism. Cells, Cultured. Cerebral Cortex / cytology. Cerebral Cortex / metabolism. Chemokines, CC / metabolism. Endothelium / metabolism. Epilepsy / metabolism. Female. Gene Expression. Humans. Immunoblotting / methods. Immunohistochemistry / methods. In Situ Hybridization. Indoles / metabolism. Infant. Male. Microscopy, Confocal. Middle Aged. Neoplasm Proteins / metabolism. RNA / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction / methods. Vault Ribonucleoprotein Particles / metabolism

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  • (PMID = 14568021.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / 2R01 HL51614; United States / NINDS NIH HHS / NS / R01 NS38195
  • [Publication-type] Comparative Study; 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 / Chemokines, CC; 0 / Indoles; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / Tumor Suppressor Protein p53; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 139568-96-0 / Ccl6 protein, mouse; 47165-04-8 / DAPI; 63231-63-0 / RNA
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17. Quinkler M, Hahner S, Wortmann S, Johanssen S, Adam P, Ritter C, Strasburger C, Allolio B, Fassnacht M: Treatment of advanced adrenocortical carcinoma with erlotinib plus gemcitabine. J Clin Endocrinol Metab; 2008 Jun;93(6):2057-62
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  • [Title] Treatment of advanced adrenocortical carcinoma with erlotinib plus gemcitabine.
  • In advanced disease, mitotane given as monotherapy or combined either with etoposide, doxorubicin, and cisplatin or with streptozotocin is the recommended first-line therapy.
  • However, many patients have progressive disease despite treatment with these regimens.
  • OBJECTIVE: Our objective was to evaluate the efficacy of the epidermal growth factor receptor inhibitor erlotinib plus gemcitabine as salvage therapy in ACC patients with very advanced ACC.
  • PATIENTS AND INTERVENTION: Patients registered with the German ACC Registry with progressive ACC after two to four previous systemic therapies were offered treatment with erlotinib and gemcitabine.
  • MAIN OUTCOME MEASURE: We evaluated tumor response according to response evaluation criteria in solid tumors (RECIST) criteria after 12 wk of treatment.
  • One patient had to stop therapy after the first administration of gemcitabine due to cerebral seizure.
  • Nine of 10 patients had died after a median of 5.5 months after treatment initiation.
  • CONCLUSIONS: Salvage chemotherapy using erlotinib plus gemcitabine has very limited to no activity in patients with very advanced ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Deoxycytidine / analogs & derivatives. Quinazolines / administration & dosage
  • [MeSH-minor] Adult. Aged. Disease Progression. Drug Administration Routes. Drug Administration Schedule. Erlotinib Hydrochloride. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Salvage Therapy. Treatment Outcome

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  • [ErratumIn] J Clin Endocrinol Metab. 2008 Aug;93(8):3230. Ritte, Christian [corrected to Ritter, Christian]
  • (PMID = 18334586.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; DA87705X9K / Erlotinib Hydrochloride
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18. Kurul S, Cakmakçi H, Dirik E, Kovanlikaya A: Schilder's disease: case study with serial neuroimaging. J Child Neurol; 2003 Jan;18(1):58-61
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  • The disease often mimics intracranial neoplasm or abscess.
  • Cranial computed tomography and magnetic resonance imaging (MRI) showed large lesions in the subcortical white matter of the occipital and parietal lobes of both hemispheres that were indistinguishable from an abscess.
  • A diagnosis of acute disseminated encephalomyelitis was then suspected.
  • The patient had a dramatic clinical response to corticosteroid therapy.
  • [MeSH-major] Diffuse Cerebral Sclerosis of Schilder / diagnosis. Magnetic Resonance Imaging. Tomography, X-Ray Computed
  • [MeSH-minor] Administration, Oral. Adrenal Cortex Hormones / administration & dosage. Brain Abscess / diagnosis. Child. Corpus Callosum / pathology. Dominance, Cerebral / physiology. Dose-Response Relationship, Drug. Drug Administration Schedule. Encephalomyelitis, Acute Disseminated / diagnosis. Encephalomyelitis, Acute Disseminated / drug therapy. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Methylprednisolone / administration & dosage. Occipital Lobe / pathology. Optic Neuritis / diagnosis. Optic Neuritis / drug therapy. Parietal Lobe / pathology

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  • (PMID = 12661940.001).
  • [ISSN] 0883-0738
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; X4W7ZR7023 / Methylprednisolone
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19. Nasr Ben Ammar C, Chaari N, Kochbati L, Attia I, Ben Hamadi D, Chebbi A, Saadi A, Besbes M, Maalej M: [Brain radionecrosis in patients irradiated for nasopharyngeal carcinoma: about nine cases]. Cancer Radiother; 2007 Sep;11(5):234-40
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  • PURPOSE: To study the clinical, radiological, therapeutic and progressive aspects of brain radionecrosis after treatment for nasopharyngeal carcinoma.
  • PATIENTS AND METHODS: Nine patients (seven men and two women) of mean age 47.7 years old (extremes: 18-57 years old) were treated for UCNT (undifferentiated carcinoma of the nasopharynx) between 1989 and 2003 and developed cerebral radionecrosis.
  • The mean total dose was 73.5 Gy (70-75 Gy).
  • Dose per fraction was 2 to 2.5 Gy, one fraction daily.
  • One patient received adjuvant brachytherapy to the dose of 8 Gy and four patients also received chemotherapy.
  • The time to the appearance of neurological signs was 40.3 months (10 to 108 months).
  • After a mean follow-up period of 30.6 months (12-84 months), clinical outcomes were favorable in all cases receiving medical treatment (corticoids), with a stabilization of the radiological lesions in eight cases and complete radiological regression in one patient.
  • Imaging techniques (CT scan but more so MRI) play a major role in the diagnosis.
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / therapeutic use. Adult. Age Factors. Analgesics / therapeutic use. Blood-Brain Barrier. Brachytherapy. Dose Fractionation. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Nasopharynx / pathology. Necrosis. Neoplasm Staging. Radiotherapy Dosage. Remission Induction. Risk Factors. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 17631405.001).
  • [ISSN] 1278-3218
  • [Journal-full-title] Cancer radiothérapie : journal de la Société française de radiothérapie oncologique
  • [ISO-abbreviation] Cancer Radiother
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Analgesics
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20. Sisodiya SM, Lint WR, Harding BN, Squier MV, Thom M: Drug resistance in epilepsy: human epilepsy. Novartis Found Symp; 2002;243:167-74; discussion 174-9, 180-5
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  • [Title] Drug resistance in epilepsy: human epilepsy.
  • The basis of drug resistance in human epilepsy is not understood.
  • Parallels with resistance in cancer suggest that drug resistance proteins may have a role.
  • To examine this possibility, we have studied human brain tissue containing pathologies capable of causing refractory epilepsy.
  • Using immunohistochemistry for P glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP1), we examined both pathological tissue and control tissue.
  • In one particular type of malformation, we also demonstrate that dysplastic neurons express MRP1.
  • These findings suggest that drug resistance proteins may contribute to drug resistance in refractory epilepsy.
  • [MeSH-major] Anticonvulsants / therapeutic use. Brain Chemistry. Epilepsy / drug therapy. Multidrug Resistance-Associated Proteins / analysis. Nerve Tissue Proteins / analysis. P-Glycoprotein / analysis
  • [MeSH-minor] Antibodies, Monoclonal / immunology. Blood-Brain Barrier. Brain Neoplasms / chemistry. Brain Neoplasms / pathology. Cerebral Cortex / abnormalities. Drug Resistance / physiology. Drug Resistance, Multiple. Epilepsies, Partial / drug therapy. Epilepsies, Partial / metabolism. Epilepsies, Partial / pathology. Hippocampus / pathology. Humans. Immunohistochemistry. Neoplasm Proteins / analysis. Neuroectodermal Tumors, Primitive / chemistry. Neuroectodermal Tumors, Primitive / pathology. Neuroglia / metabolism. Sclerosis

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  • (PMID = 11990775.001).
  • [ISSN] 1528-2511
  • [Journal-full-title] Novartis Foundation symposium
  • [ISO-abbreviation] Novartis Found. Symp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Anticonvulsants; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / P-Glycoprotein
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21. Gold R, Rieckmann P: [Recent advances in the pathogenesis and immunotherapy of multiple sclerosis]. Nervenarzt; 2007 Sep;78 Suppl 1:15-24; quiz 25
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  • In addition findings with a direct effect on therapeutic decisions are presented which have contributed to improved immunotherapy.
  • Novel therapeutic approaches with monoclonal antibodies have increasing importance, yet side effects are not completely understood.
  • The pathogenetic insights presented here may open new avenues for novel immunotherapies and lead to individualized MS therapy in the future.
  • Limitations are given for primary progressive MS due to the lack of suitable tissue specimens and experimental models.
  • Neuroprotective treatment strategies aiming at the protection of glial and neuronal cells are still in early stages of development.
  • [MeSH-major] Immunotherapy / methods. Multiple Sclerosis, Chronic Progressive / drug therapy. Multiple Sclerosis, Relapsing-Remitting / drug therapy. Neuroprotective Agents / therapeutic use
  • [MeSH-minor] Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / adverse effects. Antibodies, Neoplasm / therapeutic use. Cerebral Cortex / drug effects. Cerebral Cortex / pathology. Clinical Trials as Topic. Glatiramer Acetate. Glucocorticoids / adverse effects. Glucocorticoids / therapeutic use. Humans. Immunoglobulin G / adverse effects. Immunoglobulin G / therapeutic use. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Interferon-beta / adverse effects. Interferon-beta / therapeutic use. Mitoxantrone / adverse effects. Mitoxantrone / therapeutic use. Natalizumab. Nerve Fibers, Myelinated / drug effects. Nerve Fibers, Myelinated / pathology. Neurons / drug effects. Neurons / pathology. Oligodendroglia / drug effects. Oligodendroglia / pathology. Peptides / adverse effects. Peptides / therapeutic use. Recombinant Proteins / adverse effects. Recombinant Proteins / therapeutic use

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  • (PMID = 17668159.001).
  • [ISSN] 0028-2804
  • [Journal-full-title] Der Nervenarzt
  • [ISO-abbreviation] Nervenarzt
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Glucocorticoids; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Natalizumab; 0 / Neuroprotective Agents; 0 / Peptides; 0 / Recombinant Proteins; 3A189DH42V / alemtuzumab; 5M691HL4BO / Glatiramer Acetate; 77238-31-4 / Interferon-beta; BZ114NVM5P / Mitoxantrone; CUJ2MVI71Y / daclizumab
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22. Gupta B, Levchenko TS, Torchilin VP: TAT peptide-modified liposomes provide enhanced gene delivery to intracranial human brain tumor xenografts in nude mice. Oncol Res; 2007;16(8):351-9
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  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. DNA / administration & dosage. Gene Products, tat / administration & dosage. Genes, tat / genetics. Genetic Therapy / methods
  • [MeSH-minor] Animals. Cerebral Cortex. Drug Administration Routes. Gene Transfer Techniques. Green Fluorescent Proteins / genetics. Humans. Injections, Intralesional. Liposomes. Mice. Mice, Nude. Neoplasm Transplantation. Transfection. Transplantation, Heterologous. Tumor Cells, Cultured. Up-Regulation. Xenograft Model Antitumor Assays

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  • (PMID = 17913043.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL55519
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tat; 0 / Liposomes; 147336-22-9 / Green Fluorescent Proteins; 9007-49-2 / DNA
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23. Emerich DF, Winn SR, Bartus RT: Injection of chemotherapeutic microspheres and glioma. IV: Eradicating tumors in rats. Cell Transplant; 2002;11(1):47-54
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  • Polymer microspheres can be easily injected into the brain to provide a local and sustained delivery of chemotherapeutics to a tumor or surrounding tissue subject to high rates of tumor recurrence following surgery.
  • In the first experiment, a previously grown cortical tumor was debulked and animals received either one or two treatments with carboplatin-loaded microspheres (either 200 or 800 microg total carboplatin per treatment).
  • In each case, the microspheres were injected along the perimeter of the resection cavity with each treatment separated by 20 days.
  • At the lowest dose tested (200 microg), median survival was increased an additional 40% over that in animals receiving one treatment.
  • At the higher dose (800 microg), one third of the animals receiving two separate treatments were long-term survivors (> 150 days) and showed complete eradication of the tumor on histological examination.
  • Moreover, they suggest that injectable chemotherapeutic microspheres may offer important advantages by (a) permitting multiple, temporally spaced injections to be made, as needed, and (b) providing the opportunity to deliver combinations of several different efficacious drugs directly to the tumor site to enhance survival beyond what can be achieved with delivery of any single chemotherapeutic agent.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Brain Neoplasms / drug therapy. Carboplatin / administration & dosage. Carmustine / administration & dosage. Glioma / drug therapy. Microspheres
  • [MeSH-minor] Animals. Cerebral Cortex / cytology. Cerebral Cortex / metabolism. Cerebral Cortex / surgery. Combined Modality Therapy. Delayed-Action Preparations. Drug Therapy, Combination. Injections. Male. Neoplasm Transplantation. Rats. Rats, Inbred F344. Time Factors

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  • (PMID = 12095219.001).
  • [ISSN] 0963-6897
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Delayed-Action Preparations; BG3F62OND5 / Carboplatin; U68WG3173Y / Carmustine
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24. Emerich DF, Winn SR, Bartus RT: Injection of chemotherapeutic microspheres and glioma. III: Parameters to optimize efficacy. Cell Transplant; 2002;11(1):35-45
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  • Using a rodent model of surgically resected glioma, we previously demonstrated that direct injections of chemotherapeutic microspheres into the tissue surrounding a resection cavity provide superior survival effects over injections of the same microspheres directly into the surgical cavity.
  • Careful attention to these principles is not only required if chemotherapeutic microspheres are to be used efficaciously, but these principles should provide a foundation to further optimize the potential of this and other polymeric delivery systems under development for local, intraparenchymal drug delivery to glioma.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Carboplatin / administration & dosage. Glioma / drug therapy. Microspheres
  • [MeSH-minor] Animals. Cerebral Cortex / drug effects. Delayed-Action Preparations. Immunohistochemistry. Injections. Male. Neoplasm Transplantation. Rats. Rats, Inbred F344. Time Factors

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  • (PMID = 12095218.001).
  • [ISSN] 0963-6897
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; BG3F62OND5 / Carboplatin
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25. Rao R, Vugman G, Leslie WT, Loew J, Venugopal P: Lymphomatoid granulomatosis treated with rituximab and chemotherapy. Clin Adv Hematol Oncol; 2003 Nov;1(11):658-60; discussion 660
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  • [Title] Lymphomatoid granulomatosis treated with rituximab and chemotherapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Immunotherapy. Lymphomatoid Granulomatosis / drug therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / analysis. Antigens, Neoplasm / analysis. Cerebral Cortex / pathology. Combined Modality Therapy. Cranial Irradiation. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Epilepsy, Tonic-Clonic / etiology. Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / isolation & purification. Humans. Lung Neoplasms / chemistry. Lung Neoplasms / drug therapy. Lung Neoplasms / virology. Magnetic Resonance Imaging. Male. Methotrexate / administration & dosage. Prednisone / administration & dosage. Remission Induction. Rituximab. Vincristine / administration & dosage. Vision Disorders / etiology

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  • (PMID = 16258464.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antigens, Neoplasm; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; CHOP protocol
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