[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 7 of about 7
1. Benesch M, Siegler N, Hoff Kv, Lassay L, Kropshofer G, Müller H, Sommer C, Rutkowski S, Fleischhack G, Urban C: Safety and toxicity of intrathecal liposomal cytarabine (Depocyte) in children and adolescents with recurrent or refractory brain tumors: a multi-institutional retrospective study. Anticancer Drugs; 2009 Oct;20(9):794-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety and toxicity of intrathecal liposomal cytarabine (Depocyte) in children and adolescents with recurrent or refractory brain tumors: a multi-institutional retrospective study.
  • This retrospective study aimed to evaluate the safety and toxicity of intrathecal liposomal cytarabine (Depocyte) in children and adolescents with refractory or recurrent brain tumors.
  • Nineteen heavily pretreated patients (males, n = 14; females, n = 5; median age at diagnosis 8.5 years; range, 1.4-22 years) were given intrathecal liposomal cytarabine on a compassionate use basis for recurrent refractory medulloblastoma (n = 12), mixed germ cell tumor (n = 2), central nervous system primitive neuroectodermal tumors of the pons (n = 1), anaplastic ependymoma (n = 1), anaplastic oligodendroglioma (n = 1), atypical teratoid rhabdoid tumor (n = 1), or rhabdoid papillary meningioma (n = 1).
  • In conclusion, although intrathecal liposomal cytarabine was generally well tolerated, it should be used cautiously and only with dexamethasone prophylaxis in extensively pretreated patients with recurrent brain tumors.
  • Proof of efficacy requires a prospective single-agent phase II study.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Brain Neoplasms / drug therapy. Cytarabine / administration & dosage. Cytarabine / adverse effects
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Compassionate Use Trials. Delayed-Action Preparations. Drug Resistance, Neoplasm. Female. Humans. Infant. Injections, Spinal. Liposomes / administration & dosage. Male. Retrospective Studies. Salvage Therapy. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19617818.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Delayed-Action Preparations; 0 / Liposomes; 04079A1RDZ / Cytarabine
  •  go-up   go-down


2. Rao RD, James CD: Altered molecular pathways in gliomas: an overview of clinically relevant issues. Semin Oncol; 2004 Oct;31(5):595-604
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary central nervous system (CNS) tumors constitute a small fraction of the overall incidence of human cancer, but they represent a major source of cancer-related morbidity and mortality.
  • The most common CNS tumor subtype in adults, high-grade astrocytoma, confers a dismal prognosis with a median survival of only 1 to 2 years.
  • Other common adult CNS tumors, ie, low-grade astrocytomas and oligodendrogliomas, carry a less ominous, yet still poor prognosis.
  • This research has, however, greatly increased our understanding of the underlying molecular biology of these tumors, examples of which include the determination of elevated epidermal growth factor receptor (EGFR) as well as platelet-derived growth factor receptor (PDGF) signaling, and the inactivation of p53 , p16 , and PTEN tumor-suppressor genes (TSGs) that negatively regulate specific enzymatic activities in normal glial cells.
  • Such observations have greatly improved our understanding of the pathogenesis of these tumors and have potential diagnostic as well as therapeutic relevance.
  • With respect to the latter of these two issues, the identification of aberrant enzymatic activities in gliomas has promoted the development of novel therapeutic agents that target specific signaling effectors, and whose inhibition should, in theory, prove to be cytostatic, if not cytotoxic, to tumor cells.
  • Several clinical trials are currently underway for testing these therapeutic agents in patients with primary brain tumors, and it is hoped that the targeting of pro-tumorigenic enzymatic activities will lead to better patient outcomes.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Glioma / genetics
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Astrocytoma / diagnosis. Astrocytoma / drug therapy. Astrocytoma / genetics. Astrocytoma / metabolism. Drug Delivery Systems. Genes, p53. Genes, ras. Humans. Neovascularization, Pathologic. Oligodendroglioma / diagnosis. Oligodendroglioma / drug therapy. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Phosphatidylinositol 3-Kinases. Prognosis. Receptor, Epidermal Growth Factor. Receptors, Platelet-Derived Growth Factor

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15497113.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Number-of-references] 123
  •  go-up   go-down


3. da Fonseca CO, Linden R, Futuro D, Gattass CR, Quirico-Santos T: Ras pathway activation in gliomas: a strategic target for intranasal administration of perillyl alcohol. Arch Immunol Ther Exp (Warsz); 2008 Jul-Aug;56(4):267-76
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant gliomas commonly overexpress the oncogenes EGFR and PDGFR and contain mutations and deletions of the tumor suppressor genes PTEN and TP53.
  • Follow-up studies revealed that POH suppresses the synthesis of small G proteins, including Ras.
  • Intranasal delivery allows drugs that do not cross the blood-brain barrier to enter the central nervous system.
  • MATERIALS AND METHODS: Applying this method, a phase I/II clinical trial of POH was performed in patients with relapsed malignant gliomas after standard treatment: surgery, radiotherapy, and chemotherapy.
  • The cohort consisted of 37 patients, including 29 with glioblastoma multiforme (GBM), 5 with grade III astrocytoma (AA), and 3 with anaplastic oligodendroglioma (AO).
  • Complete response was defined as neurological stability or improvement of conditions, disappearance of CT/MRI tumor image, and corticosteroid withdraw; partial response (PR) as > or =50 reduction of CT/MRI tumor image, neurological stability, or improvement of conditions and corticosteroid requirement; progressive course (PC) as > or =25 increase in CT/MRI tumor image or the appearance of a new lesion; and stable disease as a lack of any changes in the CT/MR tumor image or neurological status.
  • RESULTS: After six months of treatment, PR was observed in 3.4% (n=1) of the patients with GBM and 33.3% (n=1) with AO; stable disease in 44.8% (n=13) with GBM, 60% (n=3) with AA, and 33.3% (n=1) with AO; and PC in 51.7% (n=15) with GBM, 40% (n=2), with AA and 33.3% (n=1) AO.
  • There were no toxicity events and the regression of tumor size in some patients is suggestive of antitumor activity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Mitogen-Activated Protein Kinase Kinases / metabolism. Monoterpenes / therapeutic use. ras Proteins / metabolism
  • [MeSH-minor] Administration, Intranasal. Adult. Aged. Apoptosis / drug effects. Astrocytoma / drug therapy. Astrocytoma / metabolism. Disease-Free Survival. Female. Glioblastoma / drug therapy. Glioblastoma / metabolism. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / metabolism. Oligodendroglioma / drug therapy. Oligodendroglioma / metabolism. Signal Transduction / drug effects


Advertisement
4. Zalutsky MR, Reardon DA, Akabani G, Coleman RE, Friedman AH, Friedman HS, McLendon RE, Wong TZ, Bigner DD: Clinical experience with alpha-particle emitting 211At: treatment of recurrent brain tumor patients with 211At-labeled chimeric antitenascin monoclonal antibody 81C6. J Nucl Med; 2008 Jan;49(1):30-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical experience with alpha-particle emitting 211At: treatment of recurrent brain tumor patients with 211At-labeled chimeric antitenascin monoclonal antibody 81C6.
  • alpha-Particle-emitting radionuclides, such as (211)At, with a 7.2-h half-life, may be optimally suited for the molecularly targeted radiotherapy of strategically sensitive tumor sites, such as those in the central nervous system.
  • Because of the much shorter range and more potent cytotoxicity of alpha-particles than of beta-particles, (211)At-labeled agents may be ideal for the eradication of tumor cells remaining after surgical debulking of malignant brain tumors.
  • The main goal of this study was to investigate the feasibility and safety of this approach in patients with recurrent malignant brain tumors.
  • Six patients experienced grade 2 neurotoxicity within 6 wk of (211)At-ch81C6 administration; this neurotoxicity resolved fully in all but 1 patient.
  • No toxicities of grade 3 or higher were attributable to the treatment.
  • The median survival times for all patients, those with glioblastoma multiforme, and those with anaplastic astrocytoma or oligodendroglioma were 54, 52, and 116 wk, respectively.
  • Specifically, the regional administration of (211)At-ch81C6 is feasible, safe, and associated with a promising antitumor benefit in patients with malignant central nervous system tumors.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunother. 1997 May;20(3):214-43 [9181460.001]
  • [Cites] Appl Radiat Isot. 1996 Feb;47(2):135-43 [8852627.001]
  • [Cites] Radiat Res. 1998 Feb;149(2):155-62 [9457895.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2202-12 [9626222.001]
  • [Cites] Nucl Med Biol. 1998 May;25(4):351-7 [9639296.001]
  • [Cites] Blood. 1998 Sep 15;92(6):1933-40 [9731050.001]
  • [Cites] Clin Cancer Res. 1998 Oct;4(10):2495-502 [9796983.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Sep 1;45(2):491-9 [10487576.001]
  • [Cites] J Nucl Med. 2005 Jan;46 Suppl 1:199S-204S [15653670.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] J Nucl Med. 2005 Jun;46(6):1042-51 [15937318.001]
  • [Cites] Clin Cancer Res. 2005 Jun 15;11(12):4451-9 [15958630.001]
  • [Cites] J Nucl Med. 2005 Aug;46(8):1393-400 [16085599.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):115-22 [16382120.001]
  • [Cites] J Nucl Med. 2006 Jun;47(6):912-8 [16741299.001]
  • [Cites] Clin Cancer Res. 1999 Oct;5(10 Suppl):3275s-3280s [10541375.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2572-8 [10561324.001]
  • [Cites] Curr Pharm Des. 2000 Sep;6(14):1433-55 [10903402.001]
  • [Cites] J Nucl Med. 2001 Oct;42(10):1508-15 [11585865.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1389-97 [11870184.001]
  • [Cites] Int J Cancer. 2002 Mar 20;98(3):362-9 [11920587.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1233-9 [12149203.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Nov 15;54(4):1259-75 [12419456.001]
  • [Cites] Cancer Res. 1983 Jun;43(6):2796-805 [6342760.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1987 Nov;13(11):1767-73 [3667382.001]
  • [Cites] Cancer Res. 1989 May 15;49(10):2807-13 [2469537.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;24(1):55-7 [1512163.001]
  • [Cites] Invest Radiol. 1993 Jun;28(6):488-96 [7686539.001]
  • [Cites] Lancet. 1995 Apr 22;345(8956):1008-12 [7723496.001]
  • [Cites] Nucl Med Biol. 1996 May;23(4):449-58 [8832699.001]
  • [Cites] Nucl Med Biol. 1997 Apr;24(3):255-61 [9228660.001]
  • (PMID = 18077533.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NINDS NIH HHS / NS / NS20023; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NCI NIH HHS / CA / R01 CA042324; United States / NINDS NIH HHS / NS / P50 NS020023-268624; United States / NCI NIH HHS / CA / CA014236-35S59008; United States / NCI NIH HHS / CA / CA108786; United States / NCI NIH HHS / CA / CA42324; United States / NCI NIH HHS / CA / CA11898; United States / NCRR NIH HHS / RR / M01 RR30; United States / NINDS NIH HHS / NS / NS020023-268624; United States / NCI NIH HHS / CA / R37 CA042324; United States / NCI NIH HHS / CA / P30 CA014236; United States / NCI NIH HHS / CA / R37 CA042324-23; United States / NCI NIH HHS / CA / P30 CA014236-35S59008; United States / NCI NIH HHS / CA / R37 CA011898
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Radioisotopes; 0 / Radiopharmaceuticals; 0 / Tenascin; XI595HAL7H / Astatine
  • [Other-IDs] NLM/ NIHMS180689; NLM/ PMC2832604
  •  go-up   go-down


5. Desjardins A, Quinn JA, Vredenburgh JJ, Sathornsumetee S, Friedman AH, Herndon JE, McLendon RE, Provenzale JM, Rich JN, Sampson JH, Gururangan S, Dowell JM, Salvado A, Friedman HS, Reardon DA: Phase II study of imatinib mesylate and hydroxyurea for recurrent grade III malignant gliomas. J Neurooncol; 2007 May;83(1):53-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of imatinib mesylate and hydroxyurea for recurrent grade III malignant gliomas.
  • We performed the current phase 2 study to evaluate this regimen among patients with recurrent WHO grade III malignant glioma (MG).
  • PATIENTS AND METHOD: Patients with grade III MG at any recurrence, received imatinib mesylate plus hydroxyurea (500 mg twice a day) orally on a continuous, daily schedule.
  • The imatinib mesylate dose was 500 mg twice a day for patients on enzyme inducing anti-epileptic drugs (EIAEDs) and 400 mg once a day for those not on EIAEDs.
  • The most common grade 3 or greater toxicities were hematologic and complicated less than 4% of administered courses.
  • CONCLUSION: Imatinib mesylate plus hydroxyurea, is well tolerated and associated with anti-tumor activity in some patients with recurrent grade 3 MG.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Central Nervous System Neoplasms / drug therapy. Oligodendroglioma / drug therapy
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Benzamides. Female. Follow-Up Studies. Humans. Hydroxyurea / administration & dosage. Imatinib Mesylate. Male. Middle Aged. Neoplasm Recurrence, Local. Piperazines / administration & dosage. Prognosis. Pyrimidines / administration & dosage. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2000 Feb;18(3):636-45 [10653879.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jan 1;40(1):57-63 [9422558.001]
  • [Cites] Cancer. 2001 Jul 15;92(2):420-33 [11466698.001]
  • [Cites] N Engl J Med. 2001 Jan 11;344(2):114-23 [11150363.001]
  • [Cites] Lancet. 2003 Jan 25;361(9354):323-31 [12559880.001]
  • [Cites] Nat Med. 2006 Aug;12(8):908-16 [16862153.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):839-45 [11309331.001]
  • [Cites] Surg Neurol. 2003 Nov;60(5):443-56 [14572971.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] J Clin Oncol. 1999 Sep;17 (9):2762-71 [10561351.001]
  • [Cites] J Neurosurg. 2000 Jun;92(6):983-90 [10839259.001]
  • [Cites] Semin Oncol. 2004 Oct;31(5):618-34 [15497115.001]
  • [Cites] Cancer Treat Rev. 2005 Apr;31(2):79-89 [15847978.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2572-8 [10561324.001]
  • [Cites] J Neurosurg. 1979 Oct;51(4):526-32 [225456.001]
  • [Cites] Semin Oncol. 1992 Jun;19(3 Suppl 9):34-9 [1641655.001]
  • [Cites] Lancet. 2002 Mar 23;359(9311):1011-8 [11937180.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2585-97 [8453582.001]
  • [Cites] J Clin Oncol. 1994 Aug;12(8):1607-15 [8040673.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9359-68 [16361636.001]
  • [Cites] Ann Oncol. 2005 Oct;16(10):1702-8 [16033874.001]
  • (PMID = 17245623.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA11898; United States / NCRR NIH HHS / RR / M01 RR30; United States / NINDS NIH HHS / NS / NS20023; United States / NCI NIH HHS / CA / P50-CA108786-01
  • [Publication-type] Clinical Trial, Phase II; Controlled Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


6. Sbalchiero E, Azzalin A, Palumbo S, Barbieri G, Arias A, Simonelli L, Ferretti L, Comincini S: Altered cellular distribution and sub-cellular sorting of doppel (Dpl) protein in human astrocytoma cell lines. Cell Oncol; 2008;30(4):337-47
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Doppel, a prion-like protein, is a GPI-membrane anchored protein generally not expressed in the Central Nervous System (CNS) of different mammalian species, including human.
  • Nevertheless, in astrocytomas, a particular kind of glial tumors, the doppel encoding gene (PRND) is over-expressed and the corresponding protein product (Dpl) is ectopically localized in the cytoplasm of the tumor cells.
  • Noticeably, none of the examined tumor cells showed a membrane-Dpl localization.
  • Additionally, Dpl showed altered expression and traffic using the acidotropic agent ammonium chloride, leading to the accumulation of Dpl in nascent exocytic vesicles.
  • Altogether, these results indicated that in the astrocytic tumor cells Dpl has an altered biosynthetic trafficking, likely derived from abnormal post-translational processes: these modifications do not permit the localization of Dpl in correspondence of the plasma membrane and lead to its intracellular accumulation in the lysosomes.
  • In these proteolytic compartments, the astrocytic tumor cells might provide to the degradation of the excess of a potentially cytotoxic Dpl product.
  • [MeSH-major] Astrocytes / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Oligodendroglioma / metabolism. Prions / metabolism
  • [MeSH-minor] Adult. Ammonium Chloride / pharmacology. Cell Compartmentation. Cell Culture Techniques. Cell Membrane / metabolism. Cell Membrane / ultrastructure. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic. Glycosylation. Glycosylphosphatidylinositols / genetics. Glycosylphosphatidylinositols / metabolism. HeLa Cells. Humans. Lysosomes / metabolism. Lysosomes / ultrastructure. Male. Mutant Proteins / analysis. Mutant Proteins / genetics. Mutant Proteins / metabolism. Protein Transport. Recombinant Proteins / analysis. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AMMONIUM CHLORIDE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18607068.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Glycosylphosphatidylinositols; 0 / Mutant Proteins; 0 / PRND protein, human; 0 / Prions; 0 / Recombinant Proteins; 01Q9PC255D / Ammonium Chloride
  • [Other-IDs] NLM/ PMC4618817
  •  go-up   go-down


7. Khan MK, Hunter GK, Vogelbaum M, Suh JH, Chao ST: Evidence-based adjuvant therapy for gliomas: current concepts and newer developments. Indian J Cancer; 2009 Apr-Jun;46(2):96-107
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Of the 18,820 new cases of primary central nervous system (CNS) tumors diagnosed annually in the United States, gliomas account for over 60% with 30-40% of them being glioblastoma multiforme (GBM), 10% being anaplastic astrocytoma (AA), and 10% being low grade gliomas (LGGs).
  • This is in contrast to one study from West Bengal, India, in which only 7.9% of the brain tumors were GBMs, while 46.8% were astrocytomas.
  • Of all adult primary CNS tumors, GBM is the most common and the most malignant with about 7,000 to 8,000 new cases annually in the United States.
  • Common to these approaches is the use of adjuvant radiation therapy, even as surgery alone, with or without chemotherapy, may be the mainstay for some lower grade and low-risk gliomas.
  • Specifically, the database is searched using the following keywords, with various combinations: glioma, low-grade, anaplastic, astrocytoma, oligodendroglioma, oligoastrocytoma, glioblastoma multiforme, chemotherapy, radiation, new concepts, phase III, MGMT, CDX-110 (Celldex), temozolomide, 1p/19q deletion, and bevacizumab.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Chemotherapy, Adjuvant. Evidence-Based Medicine. Glioma / therapy. Radiotherapy, Adjuvant
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Astrocytoma / therapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioblastoma / therapy. Humans

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19346643.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 64
  •  go-up   go-down






Advertisement