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[Title] Promoting axon regeneration in the adult CNS by modulation of the PTEN/mTOR pathway.

The failure of axons to regenerate is a major obstacle for functional recovery after central nervous system (CNS) injury.

Deletion of PTEN (phosphatase and tensin homolog), a negative regulator of the mammalian target of rapamycin (mTOR) pathway, in adult retinal ganglion cells (RGCs) promotes robust axon regeneration after optic nerve injury.

In wild-type adult mice, the mTOR activity was suppressed and new protein synthesis was impaired in axotomized RGCs, which may contribute to the regeneration failure.

Thus, our results suggest the manipulation of intrinsic growth control pathways as a therapeutic approach to promote axon regeneration after CNS injury.

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[CommentIn] Science. 2008 Nov 7;322(5903):869-72 [18988832.001]

(PMID = 18988856.001).

[ISSN] 1095-9203

[Journal-full-title] Science (New York, N.Y.)

[ISO-abbreviation] Science

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS051788-04; United States / NINDS NIH HHS / NS / R01 NS058956-02; United States / NINDS NIH HHS / NS / R01 NS058956; United States / NINDS NIH HHS / NS / NS051788-04; United States / NINDS NIH HHS / NS / R01 NS051788; United States / NINDS NIH HHS / NS / NS058956-02

[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 / Carrier Proteins; 0 / Ribosomal Protein S6; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase

[Other-IDs] NLM/ NIHMS87526; NLM/ PMC2652400

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Scleroderma linearis: hemiatrophia faciei progressiva (Parry-Romberg syndrom) without any changes in CNS and linear scleroderma "en coup de sabre" with CNS tumor.

CASE PRESENTATION: We present two cases of a disease: a case of a 49-year-old woman with a typical image of hemifacial atrophy, without any changes of the nervous system and a case of a 33-year-old patient with an "en coup de sabre" scleroderma and with CNS tumor.

In the patient diagnosed with Parry-Romberg syndrome, with Borrelia burgdoferi infection and with minor neurological symptoms, despite a four-year case history, there was a lack of proper diagnosis and treatment.In the second patient only skin changes without any neurological symptoms could be observed and only a precise neurological diagnosis revealed the presence of CNS tumor.

[MeSH-minor] Adult. Borrelia burgdorferi. Cerebral Ventricle Neoplasms / complications. Cerebral Ventricle Neoplasms / pathology. Diagnosis, Differential. Electromyography. Female. Humans. Lyme Disease / complications. Magnetic Resonance Imaging. Middle Aged. Neurologic Examination. Tomography, Spiral Computed. Tomography, X-Ray Computed

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[Cites] J Rheumatol. 2003 Sep;30(9):1997-2004 [12966605.001]

[Cites] BMC Dermatol. 2001;1:9 [11741509.001]

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(PMID = 19635150.001).

[ISSN] 1471-2377

[Journal-full-title] BMC neurology

[ISO-abbreviation] BMC Neurol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2723072

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Intensive multimodality treatment for children with newly diagnosed CNS atypical teratoid rhabdoid tumor.

PURPOSE: Atypical teratoid rhabdoid tumor (ATRT) of the CNS is a highly malignant neoplasm primarily affecting young children, with a historic median survival ranging from 6 to 11 months.

Based on a previous pilot series, a prospective multi-institutional trial was conducted for patients with newly diagnosed CNS ATRT.

Gross total resection of the primary tumor was achieved in 11 patients.

CONCLUSION: This intensive multimodality regimen has resulted in a significant improvement in time to progression and overall survival for patients with this previously poor-prognosis tumor.

[MeSH-major] Brain Neoplasms / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy

[MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Humans. Infratentorial Neoplasms. Prognosis. Prospective Studies. Supratentorial Neoplasms. Young Adult

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(PMID = 19064966.001).

[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 / R01 CA046274; United States / NCI NIH HHS / CA / R01 CA046274-17A2; United States / NCI NIH HHS / CA / CA46274

[Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ PMC2645855

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detection of human herpesvirus-6 in adult central nervous system tumors: predominance of early and late viral antigens in glial tumors.

The purpose is to determine the incidence of active and latent human herpesvirus-6 (HHV-6) infection in a large cohort of adult primary and recurrent CNS tumors.

We screened a tissue microarray (TMA) containing more than 200 adult primary and recurrent CNS tumors with known clinical information for the presence of HHV-6 DNA by in situ hybridization (ISH) and protein by immunohistochemistry (IHC).

One hundred six of 224 (47%) CNS tumors were positive for HHV-6 U57 Major Capsid Protein (MCP) gene by ISH compared to 0/25 non tumor control brain (P = 0.001).

Fourteen of 30 (47%) tumors were HHV-6 MCP positive by nested PCR compared to 0/25 non-tumor brain controls (P = 0.001), revealing HHV-6 Variant A in 6 of 14 samples.

HHV-6A/B early (p41) and late (gp116/64/54) antigens were detected by IHC in 66 of 277 (24%) (P = 0.003) and 84 of 282 (35%) (P = 0.002) tumors, respectively, suggesting active infection.

Glial tumors were 3 times more positive by IHC compared to non glial tumors for both HHV-6 gp116/64/54 (P = 0.0002) and HHV-6 p41 (P = 0.004).

HHV-6 early and late antigens are detected in adult primary and recurrent CNS tumors more frequently in glial tumors.

We hypothesize that the glial-tropic features of HHV-6 may play an important modifying role in tumor biology that warrants further investigation.

[MeSH-major] Antigens, Viral. Central Nervous System Neoplasms / genetics. Central Nervous System Neoplasms / virology. Glioma / genetics. Glioma / virology. Herpesvirus 6, Human / isolation & purification

[MeSH-minor] Adult. Antigens, CD / metabolism. CD48 Antigen. Capsid Proteins / genetics. Capsid Proteins / metabolism. Humans. Survival Analysis. Viral Envelope Proteins / metabolism

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(PMID = 19424665.001).

[ISSN] 1573-7373

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / K12NS052159-01A

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Viral; 0 / CD48 Antigen; 0 / Capsid Proteins; 0 / Viral Envelope Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Complete response of CNS-involved olfactory neuroendocrine tumor using multimodal therapy.

INTRODUCTION: Locally advanced tumors in the olfactory area commonly have central nervous system (CNS) involvement and are often incurable.

CASE REPORT: We report the treatment of a 25-year-old male patient who presented with a large, neuroendocrine tumor arising from the ethmoid complex.

An endoscopic nasal biopsy demonstrated a poorly differentiated neuroendocrine tumor.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Brain Neoplasms / therapy. Ethmoid Bone / pathology. Neuroendocrine Tumors / therapy. Radiotherapy, Adjuvant. Skull Neoplasms / therapy

[MeSH-minor] Adult. Camptothecin / analogs & derivatives. Cisplatin / administration & dosage. Humans. Male. Organization and Administration

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[Copyright] (c) 2008 S. Karger AG, Basel.

(PMID = 18322415.001).

[ISSN] 1423-0240

[Journal-full-title] Onkologie

[ISO-abbreviation] Onkologie

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 7673326042 / irinotecan; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic factors for survival in adult patients with recurrent glioma enrolled onto the new approaches to brain tumor therapy CNS consortium phase I and II clinical trials.

The studies had similar inclusion criteria and were conducted within the New Approaches to Brain Tumor Therapy CNS Consortium.

RESULTS: Factors associated with an increased risk of death were increased age, lower Karnofsky performance score (KPS), initial and on-study histologies of glioblastoma multiforme (GBM), corticosteroid use, shorter time from original diagnosis to recurrence, and tumor outside frontal lobe.

Median survival time was poorest in non-GBM patients with KPS less than 80 or GBM patients, age 50 years, corticosteroid use (4.4 months; 95% CI, 3.6 to 5.4 months); median survival was best in patients with initial histology other than GBM with KPS 80 and tumor confined to the frontal lobe (25.7 months; 95% CI, 18.7 to 52.5), and was 7.0 months (95% CI, 6.2 to 8.0 months) for all patients.

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[CommentIn] J Clin Oncol. 2012 Feb 10;30(5):562-3; author reply 563-4 [22215743.001]

(PMID = 17577040.001).

[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 / U01 CA062475; United States / NCI NIH HHS / CA / CA62475

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ NIHMS507874; NLM/ PMC4118746

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Parathyroid adenoma and primary CNS tumors.

There are several case reports of MEN Type 1-associated central nervous system (CNS) tumors.

To determine if there is an association between parathyroid adenomas and CNS tumors, we used Swedish registry data to identify all individuals operated on for parathyroid adenomas between 1958-99 (n = 12,468).

Follow-up for the occurrence of CNS tumors in these individuals was through linkage with the Swedish Cancer Registry.

There were 70 observed cases of a CNS tumor diagnosed after a parathyroid adenoma, to be compared to 35 expected (standard incidence ratio [SIR] = 2.0; 95% confidence interval [CI] = 1.5-2.5).

These results strongly indicate an association between these tumor forms that may be genetic, environmental (such as radiation) or a combination of both.

[MeSH-major] Adenoma / epidemiology. Central Nervous System Neoplasms / epidemiology. Parathyroid Neoplasms / epidemiology

[MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Neoplasms, Second Primary / epidemiology. Registries. Retrospective Studies. Sweden / epidemiology

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[Copyright] (c) 2004 Wiley-Liss, Inc.

(PMID = 15515018.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Overcoming macrophage-mediated axonal dieback following CNS injury.

Trauma to the adult CNS initiates multiple processes including primary and secondary axotomy, inflammation, and glial scar formation that have devastating effects on neuronal regeneration.

These data provide valuable insight into the cellular and molecular mechanisms underlying macrophage-mediated axonal retraction and demonstrate modifications that can alleviate the detrimental effects of this unfavorable phenomenon on the postlesion CNS.

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(PMID = 19675231.001).

[ISSN] 1529-2401

[Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience

[ISO-abbreviation] J. Neurosci.

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS025713-17; United States / NINDS NIH HHS / NS / R37 NS025713; United States / NINDS NIH HHS / NS / NS25713; United States / NIA NIH HHS / AG / T32 AG00271; United States / NIA NIH HHS / AG / T32 AG000271; United States / NINDS NIH HHS / NS / R01 NS025713

[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 / Aggrecans; 0 / Matrix Metalloproteinase Inhibitors; 0 / Proteoglycans; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 4.2.2.20 / Chondroitin ABC Lyase

[Other-IDs] NLM/ NIHMS141238; NLM/ PMC2771342

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Long-term fate of neural precursor cells following transplantation into developing and adult CNS.

Successful strategies for transplantation of neural precursor cells for replacement of lost or dysfunctional CNS cells require long-term survival of grafted cells and integration with the host system, potentially for the life of the recipient.

Few studies have examined the long-term properties of transplanted neural precursor cells in the CNS, particularly in non-neurogenic regions of the adult.

The aim of the present study was to extensively characterize the fate of defined populations of neural precursor cells following transplantation into the developing and adult CNS (brain and spinal cord) for up to 15 months, including integration of graft-derived neurons with the host.

We found that in both developing and adult CNS grafted cells showed long-term survival, morphological maturation, extensive distribution and differentiation into all mature CNS cell types (neurons, astrocytes and oligodendrocytes).

Graft-derived neurons also formed synapses, as identified by electron microscopy, suggesting that transplanted neural precursor cells integrated with adult CNS.

We did not detect tumor formation, cells did not localize to unwanted locations and no pronounced immune response was present at the graft sites.

The long-term stability of neuronal-restricted precursors and glial-restricted precursors and the lack of adverse effects suggest that transplantation of lineage-restricted neural precursor cells can serve as an effective and safe replacement therapy for CNS injury and degeneration.

[MeSH-major] Cell Differentiation / physiology. Central Nervous System / physiology. Neurons / physiology. Stem Cell Transplantation / methods. Stem Cells / physiology

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[RepublishedFrom] Neuroscience. 2006 May 12;139(2):513-30 [16458439.001]

(PMID = 17120358.001).

[ISSN] 0306-4522

[Journal-full-title] Neuroscience

[ISO-abbreviation] Neuroscience

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / NS 37515; United States / NINDS NIH HHS / NS / NS24707

[Publication-type] Comparative Study; Corrected and Republished Article; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Gangliosides; 0 / Immunosuppressive Agents; 0 / Nerve Tissue Proteins; 0 / Neural Cell Adhesion Molecules; 0 / ganglioside A2B5

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Long-term fate of neural precursor cells following transplantation into developing and adult CNS.

Successful strategies for transplantation of neural precursor cells for replacement of lost or dysfunctional CNS cells require long-term survival of grafted cells and integration with the host system, potentially for the life of the recipient.

Few studies have examined the long-term properties of transplanted neural precursor cells in the CNS, particularly in non-neurogenic regions of the adult.

The aim of the present study was to extensively characterize the fate of defined populations of neural precursor cells following transplantation into the developing and adult CNS (brain and spinal cord) for up to 15 months, including integration of graft-derived neurons with the host.

We found that in both developing and adult CNS grafted cells showed long-term survival, morphological maturation, extensive distribution and differentiation into all mature CNS cell types (neurons, astrocytes and oligodendrocytes).

Graft-derived neurons also formed synapses, as identified by electron microscopy, suggesting that transplanted neural precursor cells integrated with adult CNS.

We did not detect tumor formation, cells did not localize to unwanted locations and no pronounced immune response was present at the graft sites.

The long-term stability of neuronal-restricted precursors and glial-restricted precursors and the lack of adverse effects suggest that transplantation of lineage-restricted neural precursor cells can serve as an effective and safe replacement therapy for CNS injury and degeneration.

[MeSH-major] Cell Transplantation / methods. Central Nervous System / physiology. Neurons / physiology. Stem Cells / physiology

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[ErratumIn] Neuroscience. 2006 Sep 29;142(1):285

[RepublishedIn] Neuroscience. 2006 Sep 29;142(1):287-304 [17120358.001]

(PMID = 16458439.001).

[ISSN] 0306-4522

[Journal-full-title] Neuroscience

[ISO-abbreviation] Neuroscience

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / NS 37515; United States / NINDS NIH HHS / NS / NS24707

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gangliosides; 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / Neural Cell Adhesion Molecules; 0 / RNA, Messenger; 0 / ganglioside A2B5; EC 3.1.3.1 / Alkaline Phosphatase; EC 4.2.1.11 / Phosphopyruvate Hydratase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Late recurrence and salvage therapy of CNS germinomas.

Central nervous system (CNS) germinoma is a curable tumor and its recurrence rate after initial therapy may be approximately 10% or higher.

All patients had been tumor-free for at least 6 months after the initial treatment.

Seventeen patients (68%) were salvaged and were tumor-free at the final observation.

At first recurrence, 11 patients were treated using radiation therapy with or without surgery and 7 out of the 11 patients died due to the recurrent tumor.

On the other hand, 13 patients who received salvage chemotherapy and radiotherapy were tumor-free at the last follow-up.

In conclusion, late recurrence is not a rare event in patients with CNS germinoma.

[MeSH-major] Central Nervous System Neoplasms / prevention & control. Germinoma / prevention & control. Salvage Therapy / methods

[MeSH-minor] Adolescent. Adult. Child. Female. Follow-Up Studies. Humans. Male. Remission Induction. Retrospective Studies. Secondary Prevention. Time Factors. Young Adult

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[Cites] J Clin Oncol. 2006 Dec 10;24(35):5503-11 [17158535.001]

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(PMID = 18604473.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

: e13007 Background: Malignant glioma (MG), an incurable primary CNS tumor, is characterized by frequent aberrant activation of EGFR, VEGFR, and PDGFR.

METHODS: Adult recurrent MG patients with ≤ 3 prior recurrences, KPS ≥ 60% and adequate organ function were stratified based on concurrent enzyme-inducing anticonvulsant use (EIAC).

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(PMID = 27962760.001).

[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] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Primary chemotherapy for intracranial germ cell tumors: results of the third international CNS germ cell tumor study.

BACKGROUND: The treatment of central nervous system (CNS) germ cell tumors (GCT) remains controversial.

METHODS: Between January 2001 and December 2004 newly diagnosed patients with CNS GCT were treated with one of two risk-tailored chemotherapy regimens.

Twenty-five patients aged 4 months to 24.5 years were stratified: Regimen A consisted of 4-6 cycles of carboplatin/etoposide alternating with cyclophosphamide/etoposide for low risk (LR) localized germinoma with normal cerebrospinal fluid (CSF) and serum tumor markers.

Our results indicate that, at the present time, standard treatment for CNS GCT continues to include irradiation either alone or combined with chemotherapy for pure germinomas and with chemotherapy for those with MMGCT.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Neoplasms, Germ Cell and Embryonal / drug therapy

[MeSH-minor] Adolescent. Adult. Carboplatin / administration & dosage. Carboplatin / adverse effects. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Infant. Male. Treatment Outcome. Young Adult

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[Copyright] Copyright 2009 Wiley-Liss, Inc.

(PMID = 20063410.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

[Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin

   

[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.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Essentials and pitfalls in the treatment of CNS hemangioblastomas and von Hippel-Lindau disease.

Hemangioblastomas are rare CNS tumors, which are mostly located in the posterior fossa or spinal cord and occasionally in spinal nerves.

They can occur sporadically or as a component tumor of von Hippel-Lindau (VHL) disease, an autosomal dominant tumor syndrome.

[MeSH-major] Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / surgery. Hemangioblastoma / pathology. Hemangioblastoma / surgery. Neurosurgical Procedures / methods. Spinal Cord Neoplasms / pathology. Spinal Cord Neoplasms / surgery. von Hippel-Lindau Disease / pathology. von Hippel-Lindau Disease / surgery

[MeSH-minor] Adult. Humans. Magnetic Resonance Imaging. Male

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[Copyright] Copyright Georg Thieme Verlag KG Stuttgart . New York.

(PMID = 20229452.001).

[ISSN] 1868-4912

[Journal-full-title] Central European neurosurgery

[ISO-abbreviation] Cent Eur Neurosurg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Protein biomarker identification in the CSF of patients with CNS lymphoma.

PURPOSE: Elucidation of the CSF proteome may yield insights into the pathogenesis of CNS disease.

We tested the hypothesis that individual CSF proteins distinguish CNS lymphoma from benign focal brain lesions.

METHODS: We used a liquid chromatography/mass spectrometry-based method to differentially quantify and identify several hundred CSF proteins in CNS lymphoma and control patients.

ATIII RNA transcripts were identified within CNS lymphomas, and ATIII protein was localized selectively to tumor neovasculature.

We propose that the discovery of CSF protein biomarkers will facilitate early and noninvasive diagnosis in patients with lesions not amenable to brain biopsy, as well as provide improved surrogates of prognosis and treatment response in CNS lymphoma and brain metastasis.

[MeSH-major] Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Lymphoma / cerebrospinal fluid. Neoplasm Proteins / cerebrospinal fluid

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antithrombin III / genetics. Antithrombin III / metabolism. Case-Control Studies. Chromatography, Liquid. Diagnosis, Differential. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunoblotting. Immunoenzyme Techniques. Leukemia, Myeloid / cerebrospinal fluid. Leukemia, Myeloid / pathology. Lymphoma, B-Cell / cerebrospinal fluid. Lymphoma, B-Cell / pathology. Lymphoma, B-Cell, Marginal Zone / cerebrospinal fluid. Lymphoma, B-Cell, Marginal Zone / pathology. Lymphoma, Large B-Cell, Diffuse / cerebrospinal fluid. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Non-Hodgkin / cerebrospinal fluid. Lymphoma, Non-Hodgkin / pathology. Male. Middle Aged. Proteomics. Sensitivity and Specificity. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Survival Rate

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[CommentIn] J Clin Oncol. 2009 May 1;27(13):2302-3; author reply 2303-4 [19332721.001]

(PMID = 18056677.001).

[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 / K23 CA100291

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 9000-94-6 / Antithrombin III

[Other-IDs] NLM/ NIHMS612770; NLM/ PMC4134101

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Age-incidence patterns of primary CNS tumors in children, adolescents, and adults in England.

Around 25% of all tumors in those 0-14 years of age and 9% in those 15-24 years of age involve the CNS.

In adults 25-84 years of age, the proportion of CNS tumors is 2%; 5-year overall survival is 10%-15%; and survivors have considerable morbidity.

Comprehensive up-to-date population-based incidence data on these tumors are lacking.

We present incidence rates for primary CNS tumors based on data derived from the high-quality national cancer registration system in England.

A total of 54,336 CNS tumors of malignant, benign, and uncertain behavior were registered across the whole of England from 1995 through 2003.

This is higher than previously reported for England because it includes nonmalignant CNS tumors and hence gives a more accurate picture of burden of disease.

In this article, we describe the changing patterns in the epidemiology of primary CNS tumors in these three age groups with respect to sex, tumor behavior, and histology using the current WHO classification.

[MeSH-major] Brain Neoplasms / epidemiology

[MeSH-minor] Adolescent. Adult. Age Distribution. Age Factors. Aged. Aged, 80 and over. Child. Child, Preschool. England / epidemiology. Female. Humans. Incidence. Infant. Infant, Newborn. Male. Middle Aged. Risk Factors. Survival Rate. Young Adult

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(PMID = 19033157.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ PMC2743220

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Survival and late mortality in long-term survivors of pediatric CNS tumors.

PURPOSE: To describe the pattern of survival and late mortality among contemporary long-term survivors of pediatric CNS tumor.

PATIENTS AND METHODS: The study population comprised 643 pediatric patients with primary CNS tumor treated at St Jude Children's Research Hospital (Memphis, TN) from 1985 to 2000 who survived > or = 5 years from diagnosis.

Patients were classified according to primary tumor type, location of tumor, and survival.

A significant difference in the survival rates according to original tumor type (P = .001) was seen.

Sixty-six (10%) of 643 patients experienced late mortality: 38 patients (58%) died of progressive disease while 14 patients (21%) died of second malignant tumor.

Twelve patients (18%), predominantly with diencephalic tumor location, died of a specific medical cause: cardiovascular disease (n = 2), cerebrovascular accident (n = 1), metabolic collapse and/or sepsis (n = 7), respiratory failure (n = 1), or shunt malfunction (n = 1).

CONCLUSION: Late mortality occurs in a substantial number of long-term survivors of pediatric CNS tumors and is most influenced by the initial tumor histopathology.

[MeSH-major] Cause of Death. Central Nervous System Neoplasms / mortality. Survivors / statistics & numerical data

[MeSH-minor] Adolescent. Adult. Age Distribution. Child. Child, Preschool. Cohort Studies. Disease Progression. Disease-Free Survival. Female. Humans. Incidence. Male. Neoplasm Staging. Prognosis. Registries. Retrospective Studies. Risk Assessment. Sex Distribution. Survival Analysis. Time Factors

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(PMID = 17442996.001).

[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 / P30 CA 21765

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum.

OBJECTIVE: The purpose of this study was to determine whether lymphoma and astrocytic tumor infiltrating the corpus callosum can be reliably differentiated with measurement of water diffusivity.

Regions of interest were drawn on apparent diffusion coefficient (ADC) maps inside the callosal tumor.

ADCs were normalized by calculation of the ratio between the ADC of the tumor and the ADC of an uninvolved region of corpus callosum.

RESULTS: The mean ADC of glioblastoma multiforme was 1.13 +/- 0.31 (SD) x 10(-3) mm(2)/s, and the mean tumor to corpus callosum ADC ratio was 1.51 +/- 0.46; of low-grade astrocytoma, 1.14 +/- 0.23 x 10(-3) mm(2)/s and 1.54 +/- 0.28; gliomatosis cerebri, 1.01 +/- 0.20 x 10(-3) mm(2)/s and 1.31 +/- 0.36; and lymphoma, 0.71 +/- 0.13 x 10(-3) mm(2)/s and 0.93 +/- 0.19.

The difference between the mean tumor to corpus callosum ADC ratio of lymphoma and that of all grades of astrocytoma (1.48 +/- 0.43) was statistically significant (p < 0.001).

The optimal ADC threshold for discriminating astrocytic tumor and lymphoma was 0.90 x 10(-3) mm(2)/s (sensitivity, 84%; specificity, 89%).

The optimal threshold for tumor to corpus callosum ADC ratio was 1.22 (sensitivity, 73%; specificity, 100%).

CONCLUSION: The water diffusivity and the ADC ratio of the tumor to normal-appearing corpus callosum of astrocytic tumor differ significantly from those of lymphoma infiltrating the corpus callosum, allowing reliable differentiation of the two types of tumor.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Corpus Callosum / pathology. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / pathology. Lymphoma / pathology. Water / metabolism

[MeSH-minor] Adult. Aged. Aged, 80 and over. Analysis of Variance. Female. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. ROC Curve. Retrospective Studies. Sensitivity and Specificity

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(PMID = 19843757.001).

[ISSN] 1546-3141

[Journal-full-title] AJR. American journal of roentgenology

[ISO-abbreviation] AJR Am J Roentgenol

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 059QF0KO0R / Water

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Descriptive profile of surgically-confirmed adult central nervous system tumors in Puerto Rico.

INTRODUCTION: Published studies regarding the incidence of central nervous system (CNS) tumors in Puerto Rico (PR) are exceedingly rare.

The general understanding is that the incidence of these tumors in Puerto Rico is similar to the one found in the United States of America (USA).

The objective of this study is to describe the specific profile of all the CNS tumors that are surgically intervened in Puerto Rico, through the creation of a database.

METHODS: A retrospective analysis of all the surgical procedures from January 1, 2002 to May 31, 2006 for adult CNS tumors in Puerto Rico was performed.

The information was organized to form a database of all the CNS neoplasms.

RESULTS: A total of 1,018 procedures for CNS tumors were performed on 1,005 patients.

The incidence rate of surgically intervened CNS tumors in Puerto Rico is 6 per 100,000 people.

CNS tumors were more common in women than in men (58% vs. 42%), respectively.

CONCLUSIONS: Our results reflect a unique histopathological distribution of operated CNS tumors in Puerto Rico.

In this series, primary tumors are more common than metastatic tumors.

Benign histological tumors were more frequent than more malignant variants.

Although this study reflects only the histologically diagnosed tumors, it is headway towards diagnosing the incidence of all CNS tumors in Puerto Rico.

[MeSH-major] Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / surgery

[MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Puerto Rico. Retrospective Studies. Young Adult

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(PMID = 19999240.001).

[ISSN] 0738-0658

[Journal-full-title] Puerto Rico health sciences journal

[ISO-abbreviation] P R Health Sci J

[Language] eng

[Publication-type] Journal Article

[Publication-country] Puerto Rico

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leptomeningeal metastasis of primary central nervous system (CNS) neoplasms.

Leptomeningeal dissemination of primary CNS tumors varies widely by histologic subtype.

In certain tumors including medulloblastoma, ependymoma, germ cell tumors, and primary CNS lymphoma, seeding of the cerebrospinal fluid space is a critical factor in determining stage, prognosis and appropriate therapy.

Other tumor types, such as glioma, may have radiographic evidence of leptomeningeal metastases without clear impact on prognosis or therapy.

[MeSH-major] Brain Neoplasms / pathology. Central Nervous System Neoplasms / pathology. Meningeal Neoplasms / secondary

[MeSH-minor] Adult. Child. Humans. Incidence

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(PMID = 16211884.001).

[ISSN] 0927-3042

[Journal-full-title] Cancer treatment and research

[ISO-abbreviation] Cancer Treat. Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 86

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation.

The gene responsible for neurofibromatosis type 1 (NF1) encodes a tumor suppressor that functions as a negative regulator of the Ras proto-oncogene.

Individuals with germline mutations in NF1 are predisposed to the development of benign and malignant tumors of the peripheral and central nervous system (CNS).

Children with this disease suffer a high incidence of optic gliomas, a benign but potentially debilitating tumor of the optic nerve; and an increased incidence of malignant astrocytoma, reactive astrogliosis and intellectual deficits.

In the present study, we have sought insight into the molecular and cellular basis of NF1-associated CNS pathologies.

We show that mice genetically engineered to lack NF1 in CNS exhibit a variety of defects in glial cells.

Primary among these is a developmental defect resulting in global reactive astrogliosis in the adult brain and increased proliferation of glial progenitor cells leading to enlarged optic nerves.

These data point to hyperproliferative glial progenitors as the source of the optic tumors and provide a genetic model for NF1-associated astrogliosis and optic glioma.

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(PMID = 16314489.001).

[ISSN] 0950-1991

[Journal-full-title] Development (Cambridge, England)

[ISO-abbreviation] Development

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / NS052606-01; United States / NINDS NIH HHS / NS / P50 NS052606; United States / NINDS NIH HHS / NS / P50 NS052606-01

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Neurofibromin 1

[Other-IDs] NLM/ NIHMS149022; NLM/ PMC2760350

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Modified ProMACE-MOPP hybrid regimen with moderate-dose methotrexate for patients with primary CNS lymphoma.

The object of this study was to assess the estimation of 2- and 5-year overall survival and tumor response and the frequency and severity of treatment morbidity with a modified ProMACE-MOPP hybrid protocol in patients with primary CNS lymphoma (PCNSL).

Eighteen patients were followed up with neuroimaging and neuropsychological assessments for evidence of CNS toxicity.

[MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Central Nervous System Neoplasms / therapy. Cranial Irradiation. Lymphoma / therapy. Methotrexate / administration & dosage

[MeSH-minor] Adult. Aged. Cyclophosphamide / administration & dosage. Cyclophosphamide / toxicity. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / toxicity. Etoposide / administration & dosage. Etoposide / toxicity. Female. Humans. Leukopenia / chemically induced. Male. Mechlorethamine / administration & dosage. Mechlorethamine / toxicity. Middle Aged. Pneumonia / etiology. Pneumonia / mortality. Prednisone / administration & dosage. Prednisone / toxicity. Procarbazine / administration & dosage. Procarbazine / toxicity. Retrospective Studies. Sepsis / etiology. Sepsis / mortality. Vincristine / administration & dosage. Vincristine / toxicity

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Hazardous Substances Data Bank. MECHLORETHAMINE .

Hazardous Substances Data Bank. PREDNISONE .

Hazardous Substances Data Bank. MECHLORETHAMINE HYDROCHLORIDE .

Hazardous Substances Data Bank. VINCRISTINE .

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(PMID = 15747120.001).

[ISSN] 0939-5555

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] Germany

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 35S93Y190K / Procarbazine; 50D9XSG0VR / Mechlorethamine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ProMACE-MOPP protocol

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Impact of radiotherapy for pediatric CNS atypical teratoid/rhabdoid tumor (single institute experience).

PURPOSE: To assess outcomes and prognostic factors in radiotherapy of pediatric central nervous system atypical teratoid/rhabdoid tumor (AT/RT).

METHODS AND MATERIALS: Seventeen patients with central nervous system AT/RT were retrospectively reviewed after curative radiotherapy as primary or adjuvant therapy between January 1990 and December 2003.

The 3 longest-surviving patients were older, underwent gross tumor removal, and completed both craniospinal and focal boost irradiation.

[MeSH-major] Brain Neoplasms / radiotherapy. Rhabdoid Tumor / radiotherapy. Teratoma / radiotherapy

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cranial Irradiation / methods. Disease-Free Survival. Female. Humans. Male. Multivariate Analysis. Radiotherapy Dosage. Retrospective Studies. Survival Analysis

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[CommentIn] Int J Radiat Oncol Biol Phys. 2006 Jul 15;65(4):1273; author reply 1273-4 [16798419.001]

(PMID = 16406394.001).

[ISSN] 0360-3016

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Microglial activation and TNFalpha production mediate altered CNS excitability following peripheral inflammation.

We hypothesized that peripheral inflammation leads to increased neuronal excitability arising from a CNS immune response.

We induced inflammation in the gut by intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) to adult male rats.

The TNBS-treated rats exhibited a marked, reversible inflammatory response within the hippocampus, characterized by microglial activation and increases in tumor necrosis factor alpha (TNFalpha) levels.

Central antagonism of TNFalpha using a monoclonal antibody or inhibition of microglial activation by i.c.v. injection of minocycline prevented the increase in seizure susceptibility.

Our finding of a microglia-dependent TNFalpha-mediated increase in CNS excitability provides insight into potential mechanisms underlying the disparate neurological and behavioral changes associated with chronic inflammation.

[MeSH-major] Central Nervous System / immunology. Colitis / immunology. Microglia / metabolism. Tumor Necrosis Factor-alpha / biosynthesis

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(PMID = 18955701.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid

[Other-IDs] NLM/ PMC2579393

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of CNS sarcoidosis with infliximab and mycophenolate mofetil.

OBJECTIVE: To describe the effects of the anti-tumor necrosis factor neutralizing antibody, infliximab, and the antiproliferative immunosuppressant, mycophenolate mofetil, in refractory neurosarcoidosis.

METHODS: We treated patients with biopsy-proven sarcoidosis and CNS involvement, who had failed treatment with steroids, with infliximab (5 mg/kg on weeks 0, 2, and 6, and then every 6-8 weeks thereafter).

A positive treatment response was attained irrespective of location or distribution of CNS involvement by sarcoidosis (dural/leptomeningeal based vs intraparenchymal; cord vs brain; single lesion vs multifocal).

[MeSH-major] Antibodies, Monoclonal / administration & dosage. Central Nervous System Diseases / drug therapy. Mycophenolic Acid / analogs & derivatives. Sarcoidosis / drug therapy

[MeSH-minor] Adult. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Infliximab. Male. Middle Aged. Treatment Outcome

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[CommentIn] Curr Neurol Neurosci Rep. 2009 Sep;9(5):339-40 [19664361.001]

(PMID = 19171830.001).

[ISSN] 1526-632X

[Journal-full-title] Neurology

[ISO-abbreviation] Neurology

[Language] eng

[Grant] United States / NIAID NIH HHS / AI / U19 AI056390; United States / NINDS NIH HHS / NS / NS047687-01

[Publication-type] Comparative Study; 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; B72HH48FLU / Infliximab; HU9DX48N0T / Mycophenolic Acid

[Other-IDs] NLM/ PMC2677503

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Primary rhabdoid tumor of the brain in an adult.

Rhabdoid tumor (RT) is an uncommon childhood neoplasm that typically arises within the kidney.

Since its description in 1978, several cases of primary extrarenal RT, including a CNS localization, have been reported.

The first case in the CNS was reported in 1985 and was defined as "rhabdoid tumor" initially, and was classified as grade IV in the most recent classification of the World Health Organization under the term of "atypical teratoid/rhabdoid tumor".

Nearly 200 cases of atypical teratoid/rhabdoid tumor of the CNS have been reported to date, most of them occurring in childhood.

This tumor, which was composed purely of rhabdoid cells with no additional primitive neuroectodermal, epithelial and mesenchymal components, was in a 27-year-old male patient.

In conclusion, RT should be considered also in the differential diagnosis of intracerebral neoplasms of adult patients.

[MeSH-major] Brain Neoplasms / pathology. Rhabdoid Tumor / pathology

[MeSH-minor] Adult. Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Meningioma / pathology

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(PMID = 16521480.001).

[ISSN] 0919-6544

[Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology

[ISO-abbreviation] Neuropathology

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diffuse leukoencephalopathy and brain edema: unusual presentations of CNS relapse of acute myeloid leukemia.

An isolated CNS relapse is rarely seen in acute myeloid leukemia.

In conjunction with normal findings in the peripheral blood-count with differential and the bone marrow examination a diagnosis of an isolated CNS relapse of the AML was made.

The case highlights the relevance of the CNS as a pharmacologic "sanctuary" for tumor cells in patients that on prior treatments have not received intrathecal chemotherapy or chemotherapeutics that cross the blood-brain barrier.

[MeSH-minor] Adult. Humans. Male. Recurrence

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(PMID = 18826442.001).

[ISSN] 1552-6569

[Journal-full-title] Journal of neuroimaging : official journal of the American Society of Neuroimaging

[ISO-abbreviation] J Neuroimaging

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] High-dose methotrexate is beneficial in parenchymal brain masses of uncertain origin suspicious for primary CNS lymphoma.

In patients with parenchymal brain masses of uncertain origin responsive to corticosteroids, primary CNS lymphoma (PCNSL) should be considered.

PCNSL is a rare but aggressive brain tumor that is highly sensitive to high-dose methotrexate (HDMTX)-based chemotherapy.

[MeSH-major] Brain Neoplasms / drug therapy. Central Nervous System Neoplasms / drug therapy. Lymphoma / drug therapy. Methotrexate / therapeutic use

[MeSH-minor] Adult. Aged. Antimetabolites, Antineoplastic / therapeutic use. Biopsy. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Recurrence. Stereotaxic Techniques

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(PMID = 17301290.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate

[Other-IDs] NLM/ PMC1871672

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Rat brain tumor models in experimental neuro-oncology: the C6, 9L, T9, RG2, F98, BT4C, RT-2 and CNS-1 gliomas.

In this review we will describe eight commonly used rat brain tumor models and their application for the development of novel therapeutic and diagnostic modalities.

The C6, 9L and T9 gliomas were induced by repeated injections of methylnitrosourea (MNU) to adult rats.

The 9L gliosarcoma has been used widely and has provided important information relating to brain tumor biology and therapy.

Both of these tumors arose in Fischer rats and can be immunogenic in syngeneic hosts, a fact that must be taken into consideration when used in therapy studies, especially if survival is the endpoint.

The RG2 and F98 gliomas were both chemically induced by administering ethylnitrosourea (ENU) to pregnant rats, the progeny of which developed brain tumors that subsequently were propagated in vitro and cloned.

The CNS-1 glioma was induced by administering MNU to a Lewis rat.

This tumor has been used for a variety of studies to evaluate new therapeutic modalities.

The Avian Sarcoma Virus (ASV) induced tumors, and a continuous cell line derived from one of them designated RT-2, have been useful for studies in which de novo tumor induction is an important requirement.

These tumors also are immunogenic and this limits their usefulness for therapy studies.

[MeSH-major] Brain Neoplasms. Glioma

[MeSH-minor] Animals. Cell Line, Tumor / pathology. Disease Models, Animal. Gene Expression Regulation, Neoplastic. Mice. Rats

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(PMID = 19381449.001).

[ISSN] 1573-7373

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA150153; United States / NINDS NIH HHS / NS / R01 NS064607; United States / NINDS NIH HHS / NS / R21 NS056203; United States / NINDS NIH HHS / NS / K01 NS059575; United States / NINDS NIH HHS / NS / K01 NS059575-02; United States / NINDS NIH HHS / NS / R01 NS064607-01; United States / NINDS NIH HHS / NS / R21 NS056203-02

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 149

[Other-IDs] NLM/ NIHMS127810; NLM/ PMC2730996

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I trial of lapatinib in children with refractory CNS malignancies: a Pediatric Brain Tumor Consortium study.

PURPOSE: To estimate the maximum-tolerated dose, dose-limiting toxicities (DLTs), and pharmacokinetic properties of lapatinib, a selective epidermal growth factor receptor (EGFR) and ERBB2 inhibitor, in children with refractory or recurrent CNS malignancies.

Expression of the four ERBB receptors and downstream signaling elements in tumor tissue was evaluated by immunohistochemistry.

Frequent, high-level expression of activated (phosphorylated) EGFR and ERBB2 receptors and downstream signal intermediates were observed in tumors, particularly in ependymomas that displayed prolonged stable disease on lapatinib therapy.

CONCLUSION: Lapatinib is well tolerated in children with recurrent CNS malignancies, with rash, diarrhea, and fatigue identified as DLTs.

[MeSH-major] Antineoplastic Agents / administration & dosage. Central Nervous System Neoplasms / drug therapy. Protein Kinase Inhibitors / administration & dosage. Quinazolines / administration & dosage

[MeSH-minor] Administration, Oral. Adolescent. Child. Child, Preschool. Diarrhea / chemically induced. Exanthema / chemically induced. Fatigue / chemically induced. Female. Humans. Infant. Male. Maximum Tolerated Dose. Phosphorylation. Receptor, Epidermal Growth Factor / analysis. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, ErbB-2 / analysis. Receptor, ErbB-2 / antagonists & inhibitors. Steroids / therapeutic use. Treatment Outcome. United States. Young Adult

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(PMID = 20713864.001).

[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 / R01 CA129541; United States / NCI NIH HHS / CA / U01 CA081457; United States / NCI NIH HHS / CA / U01CA81457

[Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Steroids; 0VUA21238F / lapatinib; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2

[Other-IDs] NLM/ PMC2953974

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Chemokines in multiple sclerosis: CXCL12 and CXCL13 up-regulation is differentially linked to CNS immune cell recruitment.

We report that immunohistologically CXCL12 was constitutively expressed in CNS parenchyma on blood vessel walls.

Quantitative PCR demonstrated that CXCL13 was produced in actively demyelinating multiple sclerosis lesions, but not in chronic inactive lesions or in the CNS of subjects who had no neurological disease.

The strong linkage of CXCL13 to immune cells and immunoglobulin levels in CSF suggests that this is one of the factors that attract and maintain B and T cells in inflamed CNS lesions.

[MeSH-major] Central Nervous System / immunology. Chemokines / cerebrospinal fluid. Multiple Sclerosis / immunology. Up-Regulation

[MeSH-minor] Acute Disease. Adult. B-Lymphocytes / immunology. Case-Control Studies. Cells, Cultured. Chemokine CXCL12. Chemokine CXCL13. Chemokines, CXC / cerebrospinal fluid. Chemotaxis, Leukocyte. Enzyme-Linked Immunosorbent Assay / methods. Female. Flow Cytometry. Humans. Immunoglobulins / immunology. Immunohistochemistry / methods. Interferon-gamma / immunology. Interleukin-1 / immunology. Interleukin-4 / immunology. Lymphocyte Activation. Male. Middle Aged. Polymerase Chain Reaction / methods. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / immunology

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(PMID = 16280350.001).

[ISSN] 1460-2156

[Journal-full-title] Brain : a journal of neurology

[ISO-abbreviation] Brain

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / P01 NS38667

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / CXCL12 protein, human; 0 / CXCL13 protein, human; 0 / Chemokine CXCL12; 0 / Chemokine CXCL13; 0 / Chemokines; 0 / Chemokines, CXC; 0 / Immunoglobulins; 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparative analysis of germ cell transcription factors in CNS germinoma reveals diagnostic utility of NANOG.

Expression of NANOG has been detected in fetal germ cells and in gonadal germ cell tumors.

To assess the diagnostic utility of NANOG in central nervous system (CNS) germ cell tumors, we analyzed its expression by immunohistochemistry in a series of 12 CNS germinomas and compared its expression with other stem cell markers.

Strong nuclear expression of NANOG was demonstrated in >90% of the tumor cells in all cases.

NANOG was not detected in tumor types frequently considered in the differential diagnosis of CNS germinoma: pineoblastoma, primitive neuroectodermal tumors, medulloblastoma, lymphoma, pituitary adenoma, atypical teratoid/rhabdoid tumor, Langerhans cell histiocytosis, and gliomas.

These findings demonstrate that NANOG is a sensitive and specific marker of CNS germinoma.

Compared with other currently used markers, NANOG may have superior diagnostic characteristics and can facilitate identification of germinomas in minute surgical biopsies commonly obtained from these tumors.

These findings also suggest a potential biologic role for NANOG in maintenance of CNS germinoma.

[MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Germinoma / metabolism. Homeodomain Proteins / metabolism

[MeSH-minor] Adolescent. Adult. Alkaline Phosphatase / metabolism. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Child. HMGB Proteins / metabolism. Humans. Isoenzymes / metabolism. Octamer Transcription Factor-3 / metabolism. SOXB1 Transcription Factors. Transcription Factors / metabolism

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(PMID = 17122519.001).

[ISSN] 0147-5185

[Journal-full-title] The American journal of surgical pathology

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / NS047213

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Isoenzymes; 0 / NANOG protein, human; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors; 0 / Transcription Factors; 0 / germ-cell AP isoenzyme; EC 3.1.3.1 / Alkaline Phosphatase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Factors influencing PCR detection of viruses in cerebrospinal fluid of patients with suspected CNS infections.

The likelihood of central nervous system (CNS) infection was classified as likely, possible, or unlikely.

Of episodes likely to be CNS viral infections, 30% were PCR positive compared to 5% categorised as unlikely.

Enteroviruses and HSV were found predominantly in the likely CNS viral infection group, whereas EBV was found mainly in the unlikely group.

[MeSH-major] Central Nervous System Viral Diseases / diagnosis. Enterovirus / isolation & purification. Herpesviridae / isolation & purification. JC Virus / isolation & purification. Polymerase Chain Reaction

[MeSH-minor] Adolescent. Adult. Animals. Cerebrospinal Fluid / parasitology. Cerebrospinal Fluid / virology. Child. Child, Preschool. Enterovirus Infections / diagnosis. Female. Herpesviridae Infections / diagnosis. Humans. Infant. Male. Polyomavirus Infections / diagnosis. Predictive Value of Tests. Toxoplasma / isolation & purification. Toxoplasmosis / diagnosis. Tumor Virus Infections / diagnosis

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[CommentIn] J Neurol Neurosurg Psychiatry. 2005 Jan;76(1):10 [15607987.001]

(PMID = 15608000.001).

[ISSN] 0022-3050

[Journal-full-title] Journal of neurology, neurosurgery, and psychiatry

[ISO-abbreviation] J. Neurol. Neurosurg. Psychiatry

[Language] eng

[Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Other-IDs] NLM/ PMC1739313

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] CSF analysis of IgH gene rearrangement in CNS lymphoma: relationship to the disease course.

PURPOSE: To assess whether clonal IgH genes in CSF of patients with CNS lymphoma correlates with the disease course.

METHODS: Seventy-three CSF specimens from 32 patients (27 with primary CNS lymphoma and 5 with an isolated parenchymal CNS relapse of systemic lymphoma) were examined.

CNS disease was defined as active when leptomeningeal and/or parenchymal brain involvement was evident on neuroimaging.

Patients were considered to have a complete response when imaging confirmed absence of a tumor mass or leptomeningeal seeding.

The PCR study has high specificity and positive results are indicative for the presence of active disease, even when the tumor seems confined to the brain parenchyma.

[MeSH-major] Central Nervous System Neoplasms / genetics. Gene Rearrangement. Immunoglobulin Heavy Chains / cerebrospinal fluid. Immunoglobulin Heavy Chains / genetics. Lymphoma / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. False Negative Reactions. False Positive Reactions. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction. Reproducibility of Results. Sensitivity and Specificity

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(PMID = 16678210.001).

[ISSN] 0022-510X

[Journal-full-title] Journal of the neurological sciences

[ISO-abbreviation] J. Neurol. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Immunoglobulin Heavy Chains

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] CNS tumor 22 years after spinal neuroblastoma IV: diagnostic dilemma between recurrence and secondary malignancy.

We present the very unusual case of a young woman suffering from a brain tumor 22 years after a stage IV spinal neuroblastoma as an infant, demonstrating the difficulties of differentiating late neuroblastoma relapse from secondary supratentorial primitive neuroectodermal tumor (sPNET).

Lacking specific immunohistochemical features, the first cerebral tumor at the age of 21 was regarded as sPNET, and we pursued a therapeutic approach consisting of neurosurgical resection as well as irradiation and high-dose alkylator-based chemotherapy according to the HIT2000 protocol.

Moreover, the lack of PNET-specific translocations (EWS/FLI1 gene fusion) in both brain tumors as well as the development of hepatic metastases was more compatible with the diagnosis of a very late relapse 22 years after initial stage IV spinal neuroblastoma.

[MeSH-major] Brain Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Neoplasms, Second Primary / pathology. Neuroblastoma / pathology. Spinal Neoplasms / pathology

[MeSH-minor] Adult. DNA, Neoplasm / genetics. Diagnosis, Differential. Female. Genetic Markers. Humans. Immunohistochemistry. Infant. Magnetic Resonance Imaging. Neoplasm Staging. Time Factors

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(PMID = 19258732.001).

[ISSN] 1423-0305

[Journal-full-title] Pediatric neurosurgery

[ISO-abbreviation] Pediatr Neurosurg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Genetic Markers

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Imaging changes and cognitive outcome in primary CNS lymphoma after enhanced chemotherapy delivery.

We hypothesized that this would also be true in primary CNS lymphoma (PCNSL) patients who attained a complete response (CR) after treatment with chemotherapy and osmotic blood-brain barrier disruption (BBBD).

We hypothesized that cognitive function loss measured after tissue diagnosis but before BBBD-enhanced chemotherapy could be correlated with brain changes visualized by imaging, whereas a correlation would not be present after therapy if the patient attained a complete tumor response, analogous to the findings in children.

METHODS: Sixteen primary CNS lymphoma patients were followed after CR (no enhancing tumor) by using a methotrexate-based regimen.

Zone I was defined as enhancing tumor, and zone II as surrounding abnormal MR T2 signal intensity or low-attenuation CT.

[MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / diagnosis. Brain Neoplasms / drug therapy. Cognition / drug effects. Lymphoma / diagnosis. Lymphoma / drug therapy. Magnetic Resonance Imaging. Methotrexate / administration & dosage. Tomography, X-Ray Computed

[MeSH-minor] Adolescent. Adult. Aged. Blood-Brain Barrier. Child. Female. Humans. Male. Middle Aged. Neuropsychological Tests. Remission Induction

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[CommentIn] AJNR Am J Neuroradiol. 2005 Feb;26(2):205-6 [15709113.001]

(PMID = 15709122.001).

[ISSN] 0195-6108

[Journal-full-title] AJNR. American journal of neuroradiology

[ISO-abbreviation] AJNR Am J Neuroradiol

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / NS 33618; United States / NINDS NIH HHS / NS / NS 34608; United States / NINDS NIH HHS / NS / R01 NS 44687

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; YL5FZ2Y5U1 / Methotrexate

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detection of subclinical systemic disease in primary CNS lymphoma by polymerase chain reaction of the rearranged immunoglobulin heavy-chain genes.

PURPOSE: To search for subclinical systemic disease in bone marrow and peripheral blood in patients with primary CNS lymphoma (PCNSL) to elucidate whether extracerebral relapse may represent a sequel of initial occult systemic disease rather than true extracerebral spread.

RESULTS: Identical dominant PCR products were found in bone marrow aspirates, blood samples, and tumor biopsy specimens of two patients, indicating that the same tumor cell population is present in the CNS and in extracerebral sites.

An oligoclonal IgH rearrangement pattern was found in the tumor specimen of two other patients, whereas bone marrow and blood samples demonstrated the same dominant PCR products.

[MeSH-major] Bone Marrow Neoplasms / diagnosis. Brain Neoplasms / diagnosis. Immunoglobulin Heavy Chains / genetics. Lymphoma, Non-Hodgkin / diagnosis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow / chemistry. Female. Gene Rearrangement. Humans. Male. Middle Aged. Neoplasm Staging / methods. Polymerase Chain Reaction. Recurrence

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(PMID = 16966685.001).

[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] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Immunoglobulin Heavy Chains

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Primary CNS lymphoma of T-cell origin: a descriptive analysis from the international primary CNS lymphoma collaborative group.

PURPOSE: To describe the demographic and tumor related characteristics and outcomes for patients with primary T-cell CNS lymphoma (TPCNSL).

Univariate and multivariate analyses were conducted for age (</= 60 v > 60 years), PS (0 or 1 v 2, 3, or 4), involvement of deep structures of the CNS (no v yes), and methotrexate (MTX) use in the primary treatment (yes v no).

[MeSH-major] Central Nervous System Neoplasms / pathology. Lymphoma, T-Cell / pathology

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antimetabolites, Antineoplastic / therapeutic use. Child. Child, Preschool. Cohort Studies. Female. Health Status. Humans. Male. Methotrexate / therapeutic use. Middle Aged. Multivariate Analysis. Prognosis. Retrospective Studies. Survival Analysis

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(PMID = 15800313.001).

[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

[Publication-type] Journal Article; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinicopathologic and genetic profile of intracranial marginal zone lymphoma: a primary low-grade CNS lymphoma that mimics meningioma.

PURPOSE: Although rare overall, marginal zone B-cell lymphoma (MZBCL) is the most common primary low-grade CNS lymphoma reported in the literature.

The aim of this study is to elucidate the biology and genetic features of this unusual tumor.

PATIENTS AND METHODS: Fifteen CNS MZBCLs were studied clinically, pathologically, and genetically, including fluorescent in situ hybridization analyses with commercially available MALT1 and IgH break-apart and centromere 3, 7, 12, and 18 probes.

RESULTS: CNS MZBCLs preferentially affect middle-aged women (female-to-male ratio, 4:1), with 93% presenting as dural-based masses mimicking meningioma.

Like MZBCLs outside of the CNS, they consisted of CD20+, CD3- small B lymphocytes with varying degrees of plasmacytic differentiation and predominantly kappa light-chain restriction (78%).

CONCLUSION: Our data suggest that intracranial MZBCL is an indolent primary CNS lymphoma that typically presents as a meningioma-like dural-based mass.

Trisomy 3, but not MALT1 or IgH translocation, is a common genetic abnormality that may contribute to the pathogenesis of this CNS lymphoma.

[MeSH-major] Central Nervous System Neoplasms / genetics. Central Nervous System Neoplasms / pathology. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / pathology

[MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 3. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Meningioma / pathology. Middle Aged. Translocation, Genetic. Trisomy

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(PMID = 16009945.001).

[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

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] p73 is an essential regulator of neural stem cell maintenance in embryonal and adult CNS neurogenesis.

In both embryonic and adult neurogenesis, p73 has a critical role in maintaining an adequate neurogenic pool by promoting self-renewal and proliferation and inhibiting premature senescence of neural stem and early progenitor cells.

Thus, products of the p73 gene locus are essential maintenance factors in the central nervous system, whose broad action stretches across the entire differentiation arch from stem cells to mature postmitotic neurons.

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(PMID = 21076477.001).

[ISSN] 1476-5403

[Journal-full-title] Cell death and differentiation

[ISO-abbreviation] Cell Death Differ.

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS042168; United States / NCI NIH HHS / CA / CA093853-10; United States / NCI NIH HHS / CA / CA93853; United States / NIGMS NIH HHS / GM / T32 GM007518; United States / NCI NIH HHS / CA / R01 CA093853; United States / NCI NIH HHS / CA / R01 CA093853-10; United States / NINDS NIH HHS / NS / NS42168

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Receptors, Notch; 0 / SOXB1 Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73

[Other-IDs] NLM/ NIHMS338733; NLM/ PMC3260880