[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 28 of about 28
3. Mitchell DA, Fecci PE, Sampson JH: Immunotherapy of malignant brain tumors. Immunol Rev; 2008 Apr;222:70-100
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunotherapy of malignant brain tumors.
  • Despite aggressive multi-modality therapy including surgery, radiation, and chemotherapy, the prognosis for patients with malignant primary brain tumors remains very poor.
  • Moreover, the non-specific nature of conventional therapy for brain tumors often results in incapacitating damage to surrounding normal brain and systemic tissues.
  • Thus, there is an urgent need for the development of therapeutic strategies that precisely target tumor cells while minimizing collateral damage to neighboring eloquent cerebral cortex.
  • The rationale for using the immune system to target brain tumors is based on the premise that the inherent specificity of immunologic reactivity could meet the clear need for more specific and precise therapy.
  • The success of this modality is dependent on our ability to understand the mechanisms of immune regulation within the central nervous system (CNS), as well as counter the broad defects in host cell-mediated immunity that malignant gliomas are known to elicit.
  • Recent advances in our understanding of tumor-induced and host-mediated immunosuppressive mechanisms, the development of effective strategies to combat these suppressive effects, and a better understanding of how to deliver immunologic effector molecules more efficiently to CNS tumors have all facilitated significant progress toward the realization of true clinical benefit from immunotherapeutic treatment of malignant gliomas.
  • [MeSH-major] Antigens, Neoplasm / immunology. Brain Neoplasms / immunology. Immunotherapy / methods
  • [MeSH-minor] Adjuvants, Immunologic. Amyloid beta-Peptides / immunology. Animals. Antigen-Presenting Cells / immunology. Blood-Brain Barrier / immunology. Cancer Vaccines. Cell Culture Techniques. Humans. Immune Tolerance. Immunity, Innate. Immunologic Memory. Immunologic Surveillance. Immunotherapy, Adoptive / methods. Killer Cells, Lymphokine-Activated. Lymphocytes, Tumor-Infiltrating / immunology. Lymphocytes, Tumor-Infiltrating / transplantation. Mice. Models, Animal. Rats. Toll-Like Receptors / agonists

  • 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. 2005 Nov-Dec;28(6):582-92 [16224276.001]
  • [Cites] J Neurooncol. 1990 Apr;8(2):173-88 [2193121.001]
  • [Cites] Neuro Oncol. 2005 Jan;7(1):90-6 [15701286.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):1089-96 [15705911.001]
  • [Cites] J Exp Med. 2005 Mar 7;201(5):779-91 [15753211.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] J Neurooncol. 2005 Mar;72(1):35-46 [15803373.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4160-7 [15930352.001]
  • [Cites] Clin Cancer Res. 2005 Aug 1;11(15):5515-25 [16061868.001]
  • [Cites] Urology. 2005 Nov;66(5 Suppl):10-4 [16194701.001]
  • [Cites] Immunol Invest. 2007;36(1):3-23 [17190647.001]
  • [Cites] J Immunother. 2005 Nov-Dec;28(6):599-609 [16224278.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):323-35 [16226707.001]
  • [Cites] Nucl Med Commun. 2005 Dec;26(12):1049-57 [16264350.001]
  • [Cites] Nat Med. 2005 Nov;11(11):1230-7 [16227990.001]
  • [Cites] J Clin Invest. 2005 Dec;115(12):3623-33 [16308572.001]
  • [Cites] J Immunol. 2006 Jan 1;176(1):157-64 [16365406.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):115-22 [16382120.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Jan;3(1):24-40 [16407877.001]
  • [Cites] J Immunother. 2006 Mar-Apr;29(2):208-14 [16531821.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3294-302 [16540683.001]
  • [Cites] J Neuroimmunol. 2006 May;174(1-2):74-81 [16504307.001]
  • [Cites] Cancer Biol Ther. 2006 Apr;5(4):375-9 [16575203.001]
  • [Cites] Neurosurg Focus. 2006;20(4):E12 [16709017.001]
  • [Cites] Neurosurg Focus. 2006;20(4):E14 [16709019.001]
  • [Cites] Chem Immunol Allergy. 2007;92:140-54 [17264490.001]
  • [Cites] Neurosurgery. 2007 Feb;60(2 Suppl 1):ONS89-98; discussion ONS98-9 [17297371.001]
  • [Cites] AJR Am J Roentgenol. 2007 Mar;188(3):703-9 [17312057.001]
  • [Cites] J Transl Med. 2007;5:10 [17295916.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):837-44 [17327604.001]
  • [Cites] Cancer Immunol Immunother. 2007 May;56(5):739-45 [17195077.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4071-6 [17360479.001]
  • [Cites] Expert Opin Biol Ther. 2007 Apr;7(4):439-48 [17373896.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2158-67 [17404100.001]
  • [Cites] Int J Cancer. 2007 Jun 15;120(12):2723-33 [17315189.001]
  • [Cites] Front Biosci. 2007;12:4050-60 [17485358.001]
  • [Cites] Br J Cancer. 2007 Jun 18;96(12):1788-95 [17519900.001]
  • [Cites] Neuro Oncol. 2007 Jul;9(3):343-53 [17435179.001]
  • [Cites] J Immunol. 2007 Jul 15;179(2):845-53 [17617575.001]
  • [Cites] Expert Opin Biol Ther. 2007 Aug;7(8):1245-56 [17696822.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):7983-6 [17804706.001]
  • [Cites] Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5280-9 [17875756.001]
  • [Cites] J Immunol. 2007 Oct 1;179(7):4919-28 [17878392.001]
  • [Cites] Nature. 2007 Sep 27;449(7161):419-26 [17898760.001]
  • [Cites] Curr Opin Oncol. 2007 Nov;19(6):598-605 [17906459.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9630-6 [17942891.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4722-9 [17947719.001]
  • [Cites] J Immunother. 2007 Nov-Dec;30(8):789-97 [18049330.001]
  • [Cites] Handb Exp Pharmacol. 2008;(181):131-50 [18071944.001]
  • [Cites] J Nucl Med. 2008 Jan;49(1):30-8 [18077533.001]
  • [Cites] Neuro Oncol. 2008 Feb;10(1):10-8 [17951512.001]
  • [Cites] Neuro Oncol. 2008 Feb;10(1):98-103 [18079360.001]
  • [Cites] Br J Exp Pathol. 1948 Feb;29(1):58-69 [18865105.001]
  • [Cites] Curr Opin Mol Ther. 1999 Dec;1(6):720-6 [19629869.001]
  • [Cites] J Neuropathol Exp Neurol. 1988 May;47(3):191-205 [3367154.001]
  • [Cites] J Immunol. 1988 Jun 15;140(12):4217-23 [3131428.001]
  • [Cites] Nature. 1988 Jun 23;333(6175):742-6 [3260350.001]
  • [Cites] J Immunol. 1988 Aug 15;141(4):1126-30 [2456341.001]
  • [Cites] Ann Surg. 1988 Aug;208(2):121-35 [3041925.001]
  • [Cites] Eur J Immunol. 1988 Oct;18(10):1623-6 [3142781.001]
  • [Cites] Neurosurgery. 1988 Dec;23(6):725-32 [2851116.001]
  • [Cites] Annu Rev Immunol. 1989;7:145-73 [2523712.001]
  • [Cites] Cancer Res. 1989 May 15;49(10):2807-13 [2469537.001]
  • [Cites] Cancer Immunol Immunother. 1989;29(2):93-100 [2720709.001]
  • [Cites] Radiobiol Radiother (Berl). 1988;29(6):631-58 [3253788.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Sep;86(18):7149-53 [2476813.001]
  • [Cites] J Immunol. 1989 Nov 15;143(10):3222-9 [2809198.001]
  • [Cites] J Pathol. 1989 Oct;159(2):143-9 [2530324.001]
  • [Cites] J Neuroimmunol. 1989 Dec;25(2-3):185-93 [2584396.001]
  • [Cites] Cancer Res. 1990 Feb 1;50(3 Suppl):814s-819s [2404582.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1486-90 [2137615.001]
  • [Cites] J Neurosurg. 1990 Jun;72(6):941-5 [2159987.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jun;87(11):4207-11 [1693434.001]
  • [Cites] J Neurosurg. 1992 Jan;76(1):1-12 [1727147.001]
  • [Cites] J Clin Invest. 1990 Jul;86(1):80-6 [2365829.001]
  • [Cites] J Neurosurg. 1992 Feb;76(2):251-60 [1730954.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2965-9 [1557402.001]
  • [Cites] Annu Rev Biochem. 1992;61:331-54 [1497314.001]
  • [Cites] Curr Opin Oncol. 1992 Jun;4(3):533-9 [1379833.001]
  • [Cites] J Neurosurg. 1992 Nov;77(5):820-1 [1403131.001]
  • [Cites] Cancer Surv. 1992;13:23-37 [1423324.001]
  • [Cites] In Vitro Cell Dev Biol. 1992 Sep-Oct;28A(9-10):609-14 [1331021.001]
  • [Cites] J Exp Med. 1992 Dec 1;176(6):1693-702 [1460426.001]
  • [Cites] Immunol Today. 1992 Dec;13(12):507-12 [1463583.001]
  • [Cites] J Neuroimmunol. 1992 Dec;41(2):195-202 [1469079.001]
  • [Cites] Int Arch Allergy Immunol. 1992;99(1):1-7 [1483057.001]
  • [Cites] J Neurol Sci. 1992 Dec;113(2):144-51 [1336795.001]
  • [Cites] Eur J Immunol. 1993 Jun;23(6):1364-72 [7684687.001]
  • [Cites] J Neurooncol. 1993 Feb;15(2):141-55 [8509819.001]
  • [Cites] Phys Med Biol. 1993 Aug;38(8):1121-30 [8367523.001]
  • [Cites] J Neuroimmunol. 1993 Nov-Dec;48(2):189-98 [8227316.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1169-78 [7505205.001]
  • [Cites] Int J Cancer. 1994 Jan 2;56(1):72-7 [8262681.001]
  • [Cites] Brain Pathol. 1992 Oct;2(4):269-76 [1341962.001]
  • [Cites] J Neurosci Res. 1993 Nov 1;36(4):382-90 [7903705.001]
  • [Cites] Immunol Today. 1993 Nov;14(11):523-5 [8274193.001]
  • [Cites] Am J Physiol. 1994 Jan;266(1 Pt 2):R292-305 [8304553.001]
  • [Cites] Eur Cytokine Netw. 1993 Sep-Oct;4(5):331-41 [8117934.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2076-80 [8134351.001]
  • [Cites] Ann Neurol. 1994;36 Suppl:S47-53 [7517126.001]
  • [Cites] Immunol Today. 1994 May;15(5):218-24 [8024682.001]
  • [Cites] Int J Cancer. 1994 Aug 15;58(4):574-81 [8056454.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5414-9 [7923174.001]
  • [Cites] Immunology. 1994 Jul;82(3):365-9 [7959869.001]
  • [Cites] J Leukoc Biol. 1994 Dec;56(6):732-40 [7996050.001]
  • [Cites] J Neurooncol. 1994;20(1):35-45 [7807182.001]
  • [Cites] Immunol Today. 1994 Dec;15(12):566-71 [7848517.001]
  • [Cites] J Neurosurg. 1995 Jun;82(6):1021-9 [7539062.001]
  • [Cites] Annu Rev Immunol. 1995;13:545-86 [7612234.001]
  • [Cites] Int J Cancer. 1995 Jul 17;62(2):145-8 [7622287.001]
  • [Cites] J Immunol. 1995 Aug 1;155(3):1151-64 [7636184.001]
  • [Cites] Clin Neuropathol. 1995 May-Jun;14(3):169-74 [7671460.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9829-33 [7568227.001]
  • [Cites] Brain Res Brain Res Rev. 1995 Mar;20(3):269-87 [7550361.001]
  • [Cites] Microsc Res Tech. 1995 Nov 1;32(4):267-85 [8573777.001]
  • [Cites] Neurol Clin. 1995 Nov;13(4):827-46 [8583999.001]
  • [Cites] Semin Cancer Biol. 1995 Oct;6(5):307-17 [8562908.001]
  • [Cites] Science. 1996 Mar 22;271(5256):1734-6 [8596936.001]
  • [Cites] Cancer. 1995 Sep 1;76(5):840-52 [8625188.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1047-53 [8644846.001]
  • [Cites] Eur J Cancer. 1996 Apr;32A(4):636-40 [8695267.001]
  • [Cites] Clin Exp Immunol. 1996 Aug;105(2):344-52 [8706344.001]
  • [Cites] J Exp Med. 1996 Aug 1;184(2):387-96 [8760792.001]
  • [Cites] Cell Immunol. 1996 Aug 1;171(2):277-84 [8806798.001]
  • [Cites] Immunol Rev. 1996 Feb;149:231-43 [9005217.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10399-404 [8816812.001]
  • [Cites] Alzheimer Dis Assoc Disord. 2006 Apr-Jun;20(2):118-23 [16772748.001]
  • [Cites] Trends Mol Med. 2006 Jun;12(6):244-6 [16650803.001]
  • [Cites] Neurosurg Focus. 2000;9(6):e1 [16817684.001]
  • [Cites] Clin Cancer Res. 2006 Jul 15;12(14 Pt 1):4294-305 [16857805.001]
  • [Cites] Neurodegener Dis. 2004;1(1):20-8 [16908970.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7843-8 [16912155.001]
  • [Cites] J Leukoc Biol. 2006 Oct;80(4):797-801 [16885505.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10247-52 [17079441.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Mol Cancer. 2006;5:67 [17140455.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):331-6 [16504379.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Apr 1;38(1):9-20 [9211998.001]
  • [Cites] Nat Med. 2007 Jan;13(1):84-8 [17159987.001]
  • [Cites] Neuroreport. 1997 May 27;8(8):1995-8 [9223091.001]
  • [Cites] Cancer Treat Res. 1996;88:235-48 [9239484.001]
  • [Cites] Cancer Res. 1997 Sep 15;57(18):4130-40 [9307304.001]
  • [Cites] J Exp Med. 1997 Oct 6;186(7):1177-82 [9314567.001]
  • [Cites] Neuroimmunomodulation. 1997 Jan-Feb;4(1):49-56 [9326745.001]
  • [Cites] J Immunol. 1997 Nov 1;159(9):4415-25 [9379040.001]
  • [Cites] Cancer Immunol Immunother. 1997 Oct;45(2):77-87 [9390198.001]
  • [Cites] Nat Med. 1997 Dec;3(12):1362-8 [9396606.001]
  • [Cites] J Immunol. 1998 Mar 15;160(6):2896-904 [9510193.001]
  • [Cites] Brain Pathol. 1998 Apr;8(2):285-93 [9546287.001]
  • [Cites] Parasite Immunol. 1998 Mar;20(3):111-9 [9568614.001]
  • [Cites] J Immunol. 1998 Feb 1;160(3):1212-8 [9570536.001]
  • [Cites] J Neurovirol. 1998 Apr;4(2):148-58 [9584952.001]
  • [Cites] J Immunol. 1998 Jun 1;160(11):5320-30 [9605131.001]
  • [Cites] Hum Gene Ther. 1998 May 1;9(7):989-95 [9607410.001]
  • [Cites] Cancer J Sci Am. 1998 May;4 Suppl 1:S100-5 [9619278.001]
  • [Cites] Eur J Pediatr. 1998 May;157(5):410-5 [9625340.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2202-12 [9626222.001]
  • [Cites] J Exp Med. 1998 Jul 20;188(2):287-96 [9670041.001]
  • [Cites] J Neuroimmunol. 1998 Oct 1;90(2):137-42 [9817441.001]
  • [Cites] Clin Cancer Res. 1995 Nov;1(11):1253-8 [9815919.001]
  • [Cites] Clin Cancer Res. 1996 Jun;2(6):963-72 [9816257.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):56-8 [9892184.001]
  • [Cites] Eur J Cancer. 1998 Oct;34(11):1807-11 [9893673.001]
  • [Cites] J Exp Med. 1999 Jan 18;189(2):279-88 [9892610.001]
  • [Cites] Bull Mem Acad R Med Belg. 1998;153(5-6):255-61; discussion 261-2 [9988932.001]
  • [Cites] J Exp Med. 1999 Mar 1;189(5):877-82 [10049952.001]
  • [Cites] J Immunol. 1999 Apr 15;162(8):4882-92 [10202033.001]
  • [Cites] J Immunol. 1999 May 1;162(9):5317-26 [10228007.001]
  • [Cites] Clin Cancer Res. 1999 May;5(5):985-90 [10353730.001]
  • [Cites] Acta Oncol. 1999;38(3):351-9 [10380827.001]
  • [Cites] Jpn J Cancer Res. 1999 May;90(5):536-45 [10391094.001]
  • [Cites] Nature. 1999 Jul 8;400(6740):173-7 [10408445.001]
  • [Cites] J Immunol. 1999 Sep 15;163(6):3260-8 [10477595.001]
  • [Cites] J Immunother. 2004 Nov-Dec;27(6):452-9 [15534489.001]
  • [Cites] J Immunol. 2004 Dec 1;173(11):6526-31 [15557141.001]
  • [Cites] Methods Mol Med. 2005;109:55-70 [15585913.001]
  • [Cites] Clin Cancer Res. 1999 Oct;5(10):2963-70 [10537366.001]
  • [Cites] J Immunol. 1999 Nov 15;163(10):5211-8 [10553041.001]
  • [Cites] J Immunother. 1999 Nov;22(6):497-505 [10570748.001]
  • [Cites] J Neuroimmunol. 1999 Nov 15;101(2):111-27 [10580795.001]
  • [Cites] J Immunol. 2000 Jan 1;164(1):183-90 [10605010.001]
  • [Cites] J Neurol Sci. 2000 Jan 1;172(1):70-2 [10620663.001]
  • [Cites] J Immunol. 2000 Mar 1;164(5):2487-95 [10679086.001]
  • [Cites] Immunol Today. 2000 Mar;21(3):141-7 [10689302.001]
  • [Cites] J Neuroimmunol. 1999 Dec;100(1-2):216-32 [10695732.001]
  • [Cites] Nat Med. 2000 Mar;6(3):332-6 [10700237.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1168-72 [10728667.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1383-7 [10728703.001]
  • [Cites] Neurosurgery. 2000 Apr;46(4):778-91; discussion 791-2 [10764250.001]
  • [Cites] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422.001]
  • [Cites] J Biol Response Mod. 1990 Aug;9(4):431-8 [2395007.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8602-6 [2236070.001]
  • [Cites] Cancer Res. 1990 Dec 15;50(24):8017-22 [2253244.001]
  • [Cites] Neurosurgery. 1991 Jan;28(1):16-23 [1994273.001]
  • [Cites] FASEB J. 1991 Feb;5(2):171-7 [1825981.001]
  • [Cites] Immunol Ser. 1989;48:93-9 [2488328.001]
  • [Cites] Neurol Res. 1990 Dec;12(4):265-73 [1982172.001]
  • [Cites] Eur J Cancer. 1991;27(5):646-50 [1711354.001]
  • [Cites] Transplant Proc. 1991 Jun;23(3 Suppl 3):97-101 [1648844.001]
  • [Cites] J Cell Biol. 1991 Nov;115(4):1127-36 [1720121.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;22(1):225-30 [1309204.001]
  • [Cites] J Neurooncol. 2000 May;48(1):21-6 [11026693.001]
  • [Cites] Science. 1991 Dec 13;254(5038):1643-7 [1840703.001]
  • [Cites] J Clin Oncol. 2000 Nov 15;18(22):3862-72 [11078500.001]
  • [Cites] Hum Mol Genet. 2001 Feb 1;10(3):271-82 [11159946.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):842-7 [11221866.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):376-88 [11208829.001]
  • [Cites] J Immunol. 2001 Mar 15;166(6):4254-9 [11238679.001]
  • [Cites] Nat Med. 2001 Mar;7(3):369-72 [11231639.001]
  • [Cites] Hum Gene Ther. 2001 Mar 20;12(5):575-95 [11268289.001]
  • [Cites] Cancer. 2001 May 1;91(9):1809-13 [11335907.001]
  • [Cites] Clin Cancer Res. 2001 May;7(5):1204-13 [11350885.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3466-9 [11369638.001]
  • [Cites] J Exp Med. 2001 Jun 4;193(11):1285-94 [11390435.001]
  • [Cites] J Exp Med. 2001 Jun 4;193(11):1303-10 [11390437.001]
  • [Cites] J Immunol. 2001 Jun 15;166(12):7282-9 [11390478.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4766-72 [11406550.001]
  • [Cites] Exp Nephrol. 2001;9(4):275-83 [11423727.001]
  • [Cites] Immunol Res. 2001;23(2-3):263-72 [11444391.001]
  • [Cites] Curr Top Microbiol Immunol. 2001;258:221-9 [11443864.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8850-5 [11438712.001]
  • [Cites] J Immunol. 2001 Aug 1;167(3):1137-40 [11466326.001]
  • [Cites] Blood. 2001 Aug 1;98(3):505-12 [11468143.001]
  • [Cites] Brain Tumor Pathol. 2001;18(1):37-42 [11517972.001]
  • [Cites] J Exp Med. 2001 Sep 3;194(5):629-44 [11535631.001]
  • [Cites] Neuro Oncol. 1999 Jan;1(1):33-42 [11550300.001]
  • [Cites] J Exp Med. 2001 Sep 17;194(6):823-32 [11560997.001]
  • [Cites] J Immunol. 2001 Oct 15;167(8):4271-5 [11591749.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2736-44 [11675346.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8643-6 [11751377.001]
  • [Cites] Hematol Oncol Clin North Am. 2001 Dec;15(6):1053-71 [11770298.001]
  • [Cites] J Immunol. 2002 Jan 15;168(2):613-20 [11777953.001]
  • [Cites] Neurosurgery. 2002 Jan;50(1):158-64; discussion 164-6 [11844246.001]
  • [Cites] Oncogene. 2002 Jan 21;21(4):656-63 [11850793.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1389-97 [11870184.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2009-16 [11877273.001]
  • [Cites] J Immunol. 2002 May 1;168(9):4272-6 [11970966.001]
  • [Cites] J Immunother. 2002 May-Jun;25(3):243-51 [12000866.001]
  • [Cites] Curr Top Microbiol Immunol. 2002;265:1-22 [12014185.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8213-8 [12034883.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3347-50 [12067971.001]
  • [Cites] J Exp Med. 2002 Jun 17;195(12):1575-84 [12070285.001]
  • [Cites] Lancet Oncol. 2002 Jun;3(6):357-63 [12107023.001]
  • [Cites] J Exp Med. 2002 Jul 15;196(2):247-53 [12119349.001]
  • [Cites] J Exp Med. 2002 Jul 15;196(2):255-60 [12119350.001]
  • [Cites] J Clin Invest. 2002 Jul;110(2):157-9 [12122106.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3914-9 [12124318.001]
  • [Cites] Nat Med. 2002 Aug;8(8):793-800 [12091876.001]
  • [Cites] J Immunol Methods. 2002 Jun 1;264(1-2):135-51 [12191517.001]
  • [Cites] J Immunol. 2002 Sep 1;169(5):2756-61 [12193750.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5267-72 [12234995.001]
  • [Cites] Exp Hematol. 2002 Oct;30(10):1178-84 [12384149.001]
  • [Cites] J Immunol. 2002 Nov 1;169(9):4712-6 [12391178.001]
  • [Cites] Science. 2002 Oct 25;298(5594):850-4 [12242449.001]
  • [Cites] Exp Neurol. 1996 Oct;141(2):214-24 [8812155.001]
  • [Cites] Brain Pathol. 1996 Jul;6(3):275-88 [8864284.001]
  • [Cites] Neurosurgery. 1996 Sep;39(3):478-83 [8875477.001]
  • [Cites] Nature. 1996 Oct 31;383(6603):787-93 [8893001.001]
  • [Cites] J Exp Med. 1996 Nov 1;184(5):1737-45 [8920862.001]
  • [Cites] Eur J Immunol. 1996 Nov;26(11):2709-16 [8921959.001]
  • [Cites] Immunol Rev. 1996 Oct;153:27-46 [9010718.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2318-26 [9036980.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):4109-12 [9108113.001]
  • [Cites] Am J Pathol. 1997 Jun;150(6):2143-52 [9176405.001]
  • [Cites] Biochem J. 1997 Jun 15;324 ( Pt 3):855-61 [9210410.001]
  • [Cites] Brain Pathol. 1997 Jul;7(3):863-9 [9217971.001]
  • [Cites] Blood. 2003 Jun 15;101(12):5076-83 [12609834.001]
  • [Cites] J Immunother. 2003 Jul-Aug;26(4):332-42 [12843795.001]
  • [Cites] J Immunother. 2003 Jul-Aug;26(4):374-83 [12843800.001]
  • [Cites] Neurology. 2003 Jul 8;61(1):46-54 [12847155.001]
  • [Cites] J Exp Med. 2003 Jul 21;198(2):249-58 [12874258.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8886-91 [12857946.001]
  • [Cites] Cancer. 2003 Sep 1;98(5):1089-99 [12942579.001]
  • [Cites] J Neurooncol. 2003 Aug-Sep;64(1-2):161-76 [12952297.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):889-901 [12975455.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10878-83 [12949259.001]
  • [Cites] Br J Cancer. 2003 Oct 6;89(7):1172-9 [14520441.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Clin Cancer Res. 2003 Oct 1;9(12):4404-8 [14555512.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6501-5 [14559843.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7462-7 [14612546.001]
  • [Cites] Scand J Immunol. 2003 Nov;58(5):578-86 [14629630.001]
  • [Cites] Eur J Immunol. 2003 Dec;33(12):3473-83 [14635058.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] J Clin Invest. 2004 Jan;113(2):310-7 [14722622.001]
  • [Cites] Brain Res Brain Res Rev. 2004 Jan;44(1):65-81 [14739003.001]
  • [Cites] J Immunol. 2004 Apr 15;172(8):4686-90 [15067043.001]
  • [Cites] J Immunol. 2004 May 1;172(9):5149-53 [15100250.001]
  • [Cites] J Immunol. 2004 May 1;172(9):5213-21 [15100259.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1646-54 [15117987.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4973-9 [15256471.001]
  • [Cites] Anticancer Res. 2004 May-Jun;24(3b):1861-71 [15274367.001]
  • [Cites] J Immunother. 2004 Sep-Oct;27(5):398-404 [15314549.001]
  • [Cites] Nat Med. 2004 Sep;10(9):942-9 [15322536.001]
  • [Cites] Immunology. 1971 Dec;21(6):903-14 [4943147.001]
  • [Cites] Br J Cancer. 1971 Dec;25(4):711-20 [5004175.001]
  • [Cites] J Exp Med. 1972 Dec 1;136(6):1631-47 [4345108.001]
  • [Cites] Acta Pathol Microbiol Scand B Microbiol Immunol. 1973 Dec;81(6):768-74 [4131383.001]
  • [Cites] Surg Neurol. 1974 Nov;2(6):419-23 [4372736.001]
  • [Cites] Lancet. 1975 Jun 21;1(7921):1389-90 [48983.001]
  • [Cites] Cancer. 1976 Apr;37(4):1869-73 [769940.001]
  • [Cites] Adv Neurol. 1976;15:327-35 [937155.001]
  • [Cites] Clin Exp Immunol. 1976 Apr;24(1):54-62 [1084818.001]
  • [Cites] J Neurosurg. 1977 Apr;46(4):467-76 [191575.001]
  • [Cites] Clin Exp Immunol. 1977 Jul;29(1):61-6 [330067.001]
  • [Cites] Cancer. 1977 Sep;40(3):1037-44 [198084.001]
  • [Cites] Cancer Res. 1977 Dec;37(12):4267-75 [72598.001]
  • [Cites] Clin Exp Immunol. 1978 Jan;31(1):116-25 [639343.001]
  • [Cites] Ann Neurol. 1978 Sep;4(3):219-24 [718133.001]
  • [Cites] J Neurosurg. 1978 Dec;49(6):854-61 [731302.001]
  • [Cites] Cancer. 1980 Jan 1;45(1):112-25 [6985826.001]
  • [Cites] Clin Exp Immunol. 1980 Feb;39(2):395-402 [6966992.001]
  • [Cites] Clin Neurol Neurosurg. 1980;82(3):157-68 [6260411.001]
  • [Cites] J Neuropathol Exp Neurol. 1981 May;40(3):201-29 [6260907.001]
  • [Cites] J Neurosurg. 1981 Jul;55(1):32-42 [6165811.001]
  • [Cites] J Exp Med. 1981 Aug 1;154(2):347-61 [6943285.001]
  • [Cites] Neurosurgery. 1982 Feb;10(2):203-9 [6280097.001]
  • [Cites] Crit Rev Immunol. 2000;20(1):17-56 [10770269.001]
  • [Cites] J Neurooncol. 1999;45(2):141-57 [10778730.001]
  • [Cites] Immunity. 2000 Apr;12(4):431-40 [10795741.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):3081-7 [10850460.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7503-8 [10852962.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2157-65 [10873064.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8548-53 [10890891.001]
  • [Cites] Immunol Invest. 2000 Aug;29(3):319-36 [10933613.001]
  • [Cites] Nat Med. 2000 Aug;6(8):916-9 [10932230.001]
  • [Cites] J Immunol. 2000 Sep 15;165(6):3105-10 [10975823.001]
  • [Cites] Nat Med. 2000 Oct;6(10):1160-6 [11017149.001]
  • [Cites] Semin Oncol. 2000 Oct;27(5 Suppl 9):20-6 [11049053.001]
  • [Cites] J Immunol. 1986 Mar 1;136(5):1899-907 [2936812.001]
  • [Cites] Semin Oncol. 1986 Mar;13(1):94-109 [2420011.001]
  • [Cites] J Immunol. 1986 May 15;136(10):3916-20 [2871107.001]
  • [Cites] J Immunol. 1986 Jun 1;136(11):4054-62 [2422272.001]
  • [Cites] J Exp Med. 1986 May 1;163(5):1037-50 [2871125.001]
  • [Cites] J Neurosurg. 1986 May;64(5):743-9 [3517250.001]
  • [Cites] J Exp Med. 1987 Jan 1;165(1):146-56 [2432148.001]
  • [Cites] Cell. 1987 Apr 24;49(2):273-80 [3494522.001]
  • [Cites] J Neuroimmunol. 1987 May;15(1):37-56 [3571486.001]
  • [Cites] J Neurooncol. 1987;4(4):329-36 [3494820.001]
  • [Cites] J Neurosurg. 1987 Aug;67(2):231-6 [2885402.001]
  • [Cites] Nature. 1987 Jul 16-22;328(6127):267-70 [3496540.001]
  • [Cites] EMBO J. 1987 Jun;6(6):1633-6 [3497030.001]
  • [Cites] J Exp Med. 1987 Oct 1;166(4):991-8 [3498791.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903 [3477813.001]
  • [Cites] Science. 1988 Jan 15;239(4837):290-2 [3276004.001]
  • [Cites] Cancer. 1988 Feb 15;61(4):738-43 [3338036.001]
  • [Cites] EMBO J. 1987 Dec 1;6(12):3673-7 [3322813.001]
  • [Cites] J Neurosurg. 1988 Mar;68(3):438-48 [3257792.001]
  • [Cites] J Immunol. 1988 Apr 1;140(7):2312-6 [3280680.001]
  • [Cites] J Immunol. 1988 May 1;140(9):3026-32 [3129508.001]
  • [Cites] Br J Cancer. 2002 Oct 21;87(9):1006-12 [12434293.001]
  • [Cites] Int Immunol. 2002 Dec;14(12):1397-406 [12456587.001]
  • [Cites] Nat Med. 2002 Dec;8(12):1369-75 [12415261.001]
  • [Cites] Tissue Antigens. 2002 Oct;60(4):319-27 [12472661.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16168-73 [12427970.001]
  • [Cites] Hum Immunol. 2003 Jan;64(1):56-68 [12507815.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):606-12 [12576425.001]
  • [Cites] Cancer Immunol Immunother. 2003 Feb;52(2):80-8 [12594571.001]
  • [Cites] Eur J Immunol. 2003 Feb;33(2):556-66 [12645955.001]
  • [Cites] Cytokine Growth Factor Rev. 2003 Apr;14(2):85-9 [12651220.001]
  • [Cites] J Drug Target. 2002 Nov;10(7):529-33 [12683719.001]
  • [Cites] Int J Cancer. 2003 Jul 1;105(4):520-6 [12712444.001]
  • [Cites] Nat Med. 2003 May;9(5):562-7 [12704383.001]
  • [Cites] Cancer. 1982 Oct 1;50(7):1273-9 [6213292.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Mar;80(5):1337-41 [6298788.001]
  • [Cites] Cancer Res. 1983 Jun;43(6):2796-805 [6342760.001]
  • [Cites] J Neurosurg. 1983 Aug;59(2):201-7 [6864286.001]
  • [Cites] J Immunol. 1984 Mar;132(3):1208-15 [6319491.001]
  • [Cites] J Immunol. 1984 Apr;132(4):1837-44 [6607949.001]
  • [Cites] Cancer Res. 1984 Oct;44(10):4679-87 [6590117.001]
  • [Cites] J Neurooncol. 1984;2(2):147-51 [6090602.001]
  • [Cites] Nature. 1984 Nov 8-14;312(5990):162-3 [6095085.001]
  • [Cites] Nature. 1985 Jan 10-18;313(5998):144-7 [2981413.001]
  • [Cites] J Immunol. 1985 Mar;134(3):1545-50 [3155771.001]
  • [Cites] J Cell Physiol. 1985 Nov;125(2):251-8 [4055909.001]
  • [Cites] Cancer Res. 1986 Apr;46(4 Pt 2):2101-4 [3512079.001]
  • (PMID = 18363995.001).
  • [ISSN] 1600-065X
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Amyloid beta-Peptides; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Toll-Like Receptors
  • [Number-of-references] 401
  • [Other-IDs] NLM/ NIHMS396799; NLM/ PMC3418681
  •  go-up   go-down


Advertisement
4. Chen YY, Tiang XY, Li Z, Luo BN, Huang Q: Sporadic meningioangiomatosis-associated atypical meningioma mimicking parenchymal invasion of brain: a case report and review of the literature. Diagn Pathol; 2010;5:39
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sporadic meningioangiomatosis-associated atypical meningioma mimicking parenchymal invasion of brain: a case report and review of the literature.
  • Meningioangiomatosis is a rare hamartomatous lesion or meningiovascular malformation in brain.
  • He had no stigmata of neurofibromatosis type 2.
  • The adjacent brain parenchyma showed the histological features of meningioangiomatosis.
  • The patient had been followed-up for 11 months without adjuvant radiotherapy or chemotherapy.
  • No tumor recurrence was found during this period.
  • Meningioangiomatosis-associated meningioma is more likely to occur in younger patients and histologically to mimic parenchymal invasion of brain.
  • We suggest that postoperative radiotherapy or chemotherapy should be given careful consideration to avoid over-treatment due to erroneously interpret as malignant meningioma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Central Nervous System Vascular Malformations / diagnosis. Cerebral Cortex / pathology. Meningeal Neoplasms / diagnosis. Meningioma / diagnosis
  • [MeSH-minor] Adult. Biopsy. Diagnosis, Differential. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Treatment Outcome

  • Genetic Alliance. consumer health - Meningioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosurg. 2000 Apr;92(4):706-10 [10761664.001]
  • [Cites] Acta Cytol. 2009 Jan-Feb;53(1):93-7 [19248561.001]
  • [Cites] Pediatr Dev Pathol. 2001 Nov-Dec;4(6):568-72 [11826364.001]
  • [Cites] Neuropathol Appl Neurobiol. 2002 Feb;28(1):48-56 [11849563.001]
  • [Cites] Nervenarzt. 2002 Oct;73(10):990-4 [12376888.001]
  • [Cites] Neuropathol Appl Neurobiol. 2003 Apr;29(2):170-4 [12662324.001]
  • [Cites] Brain Pathol. 2003 Oct;13(4):643-5 [14655769.001]
  • [Cites] Am J Clin Pathol. 1974 Oct;62(4):481-7 [4212953.001]
  • [Cites] J Neurosurg. 1982 Jan;56(1):154-7 [7054414.001]
  • [Cites] Acta Neuropathol. 1987;73(4):361-4 [3618128.001]
  • [Cites] J Neurosurg. 1990 Nov;73(5):715-9 [2213161.001]
  • [Cites] Pathol Res Pract. 1992 Feb;188(1-2):145-7 [1594484.001]
  • [Cites] J Neurosurg. 1993 Feb;78(2):287-9 [8421212.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 May;56(5):485-9 [9143261.001]
  • [Cites] Am J Surg Pathol. 1999 Aug;23(8):872-5 [10435554.001]
  • [Cites] Brain Pathol. 2005 Jan;15(1):55-65 [15779237.001]
  • [Cites] Childs Nerv Syst. 2006 Jan;22(1):78-83 [16389566.001]
  • [Cites] Surg Neurol. 2006 Jun;65(6):595-603 [16720184.001]
  • [Cites] Am J Surg Pathol. 2002 Jan;26(1):125-9 [11756780.001]
  • (PMID = 20565869.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2904739
  •  go-up   go-down


5. Winters BS, Shepard SR, Foty RA: Biophysical measurement of brain tumor cohesion. Int J Cancer; 2005 Apr 10;114(3):371-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biophysical measurement of brain tumor cohesion.
  • An advantage of using 3D multicellular spheres to study tumor biology is that they better approximate the interactions encountered by cells in vivo.
  • This liquid-like behavior enables us to measure a key property influencing tumor behavior, namely, intercellular cohesion.
  • We have developed a method, tissue surface tensiometry (TST), to measure the cohesivity, expressible as surface tension (sigma), of tissue aggregates under physiologic conditions.
  • This study utilizes TST to measure the cohesivity of 3 widely used malignant astrocytoma cell lines of different in vitro invasive potentials.
  • We compare invasiveness with aggregate cohesivity and with the expression of N-cadherin, a key mediator of cell-cell cohesion in neural tissues.
  • We show that the cell lines exhibit liquid-like behavior since they form spheroids whose surface tension is both force- and volume-independent; that aggregates from each cell line have a distinct surface tension that correlates with their in vitro invasive capacity; that dexamethasone (Dex), a widely used therapeutic agent for the treatment of tumor-related cerebral edema, increases aggregate cohesivity and decreases invasiveness; that dexamethasone treatment decreases invasion in a dose-dependent manner but only when cells are in direct contact with one another; and that dex-mediated decreased invasiveness correlates with increased aggregate cohesivity as measured by TST but not with N-cadherin expression or function.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Adhesion. Models, Biological. Neoplasm Invasiveness / physiopathology. Spheroids, Cellular
  • [MeSH-minor] Biophysical Phenomena. Biophysics. Brain Edema / drug therapy. Brain Edema / physiopathology. Dexamethasone / pharmacology. Glucocorticoids / pharmacology. Humans. Tensile Strength. Thermodynamics

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551307.001).
  • [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
  • [Chemical-registry-number] 0 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone
  •  go-up   go-down


6. Hirth A, Pedersen PH, Wester K, Mörk S, Helgestad J: Cerebral atypical teratoid/rhabdoid tumor of infancy: long-term survival after multimodal treatment, also including triple intrathecal chemotherapy and gamma knife radiosurgery--case report. Pediatr Hematol Oncol; 2003 Jun;20(4):327-32
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebral atypical teratoid/rhabdoid tumor of infancy: long-term survival after multimodal treatment, also including triple intrathecal chemotherapy and gamma knife radiosurgery--case report.
  • Cerebral atypical teratoid/rhabdoid tumors (AT/RT) of infancy are highly malignant and have a poor prognosis.
  • He was treated with complete surgery, followed by multiagent chemotherapy.
  • Later he had a second resection and intrathecal chemotherapy and Gamma knife radiosurgery was added to the treatment.
  • Intrathecal chemotherapy and Gamma knife radiosurgery of single recurrent or residual tumors might increase survival.
  • [MeSH-major] Brain Neoplasms / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Humans. Infant. Injections, Spinal. Magnetic Resonance Imaging. Male. Neoplasm Recurrence, Local. Radiosurgery. Survivors. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12746165.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


7. Beuthien-Baumann B, Hahn G, Winkler C, Heubner G: Differentiation between recurrent tumor and radiation necrosis in a child with anaplastic ependymoma after chemotherapy and radiation therapy. Strahlenther Onkol; 2003 Dec;179(12):819-22
MedlinePlus Health Information. consumer health - Radiation Therapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differentiation between recurrent tumor and radiation necrosis in a child with anaplastic ependymoma after chemotherapy and radiation therapy.
  • BACKGROUND: In patients after treatment for malignant brain tumors, a clear distinction between tumor recurrence and radiation necrosis can be challenging.
  • This case report describes the diagnostic workup in a child with anaplastic ependymoma and inconclusive MRI (magnetic resonance imaging) and PET (positron emission tomography) findings.
  • CASE REPORT: 1.5 years after resection, hyperfractionated radiotherapy and chemotherapy of an anaplastic ependymoma in the right parietal region, the cranial MRI of an 11-year-old girl showed multiple small contrast-enhanced lesions in the frontal cortex.
  • In the following months, these lesions increased in number and size and neurologic symptoms developed.
  • Diagnostic workup included repeated MRI scans, PET with an (18)F-amino acid and (18)F-fluorodeoxyglucose (FDG), as well as a brain biopsy.
  • Although not typical, this result was suspicious of tumor seeding, the more since the lesions appeared in gray matter areas outside the high-dose-rate irradiation field.
  • A biopsy, performed 6 months later when the clinical appearance worsened, showed no tumor tissue.
  • FDG PET, performed after the size and number of the lesions had increased, showed no intensely increased glucose metabolism, a high-grade recurrent tumor was therefore very unlikely.
  • CONCLUSION: The final interpretation of the lesions was multiple focal radiation necrosis based on perfusion abnormalities after chemotherapy and conformal hyperfractionated radiotherapy, probably due to an individually enhanced vulnerability of the cerebral vessels.
  • [MeSH-major] Brain Diseases / etiology. Brain Neoplasms / radiotherapy. Ependymoma / radiotherapy. Magnetic Resonance Imaging. Necrosis. Neoplasm Recurrence, Local / diagnosis. Radiation Injuries / diagnosis. Radiotherapy / adverse effects. Tomography, Emission-Computed
  • [MeSH-minor] Biopsy. Brain / pathology. Child. Combined Modality Therapy. Diagnosis, Differential. Dose Fractionation. Female. Follow-Up Studies. Humans. Radiotherapy Dosage. Radiotherapy, Conformal. Time Factors


8. Alexiou GA, Moschovi M, Stefanaki K, Prodromou C, Sfakianos G, Prodromou N: Malignant progression of a pleomorphic xanthoastrocytoma in a child. Neuropediatrics; 2010 Aug;41(2):69-71
Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant progression of a pleomorphic xanthoastrocytoma in a child.
  • Pleomorphic xanthoastrocytoma (PXA) is a recently recognized rare cerebral neoplasm that predominantly affects young patients.
  • 1 year later follow-up magnetic resonance imaging (MRI) revealed tumor relapse.
  • Histology revealed that the presence of a malignant PXA with anaplastic features.
  • The patient received radiotherapy and 9 months later on follow-up MRI a new tumor recurrence was noted.
  • A third craniotomy was performed and the tumor removed.
  • The patient was referred to the oncology department and received chemotherapy with temozolamide.
  • 8 months later the patient was stable without tumor recurrence.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Brain Neoplasms / physiopathology. Glioblastoma / diagnosis
  • [MeSH-minor] Child, Preschool. Disease Progression. Gadolinium. Humans. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed / methods

  • Genetic Alliance. consumer health - Pleomorphic xanthoastrocytoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 20799153.001).
  • [ISSN] 1439-1899
  • [Journal-full-title] Neuropediatrics
  • [ISO-abbreviation] Neuropediatrics
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] AU0V1LM3JT / Gadolinium
  •  go-up   go-down


9. Lutterbach J, Spetzger U, Bartelt S, Pagenstecher A: Malignant germ cell tumors metastatic to the brain: a model for a curable neoplasm? The Freiburg experience and a review of the literature. J Neurooncol; 2002 Jun;58(2):147-56
MedlinePlus Health Information. consumer health - Testicular Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant germ cell tumors metastatic to the brain: a model for a curable neoplasm? The Freiburg experience and a review of the literature.
  • The aim of this study on malignant germ cell tumors metastasizing to the brain is (a) to report our institutional experience, (b) to present three patients surviving for more than seven years, and (c) to review the literature with regard to long-term survival.
  • From 1985 to 2000, 916 consecutive patients were treated with whole brain radiation therapy for brain metastases at our hospital.
  • Eleven patients had cerebral lesions from histologically proven malignant germ cell tumors.
  • Brain metastases were diagnosed at presentation (n = 2), following complete remission (n = 3), or along with extracerebral tumor progression (n = 6).
  • Seven patients had a single brain metastasis.
  • Eight patients reached the planned total dose of 50 Gy.
  • Eight patients had chemotherapy.
  • The long-term survivors all had an isolated cerebral relapse after complete remission, presented with a single brain metastasis, and were treated with resection and whole brain radiation therapy to a total dose of 50 Gy.
  • The first patient died from a late relapse 89 months after the diagnosis of brain metastasis, the second patient is well and alive at 95 months.
  • He is alive at 194 months, the longest survival for brain metastases from malignant germ cell tumors ever reported.
  • Altogether, our study demonstrates that advanced extracerebral disease at initial diagnosis and isolated cerebral relapse after complete remission do not preclude long-term survival.
  • Resection and whole brain radiation therapy might result in durable cerebral control with minimal morbidity.
  • [MeSH-major] Brain Neoplasms / secondary. Germinoma / secondary. Testicular Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Humans. Male. Middle Aged. Survival Analysis

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br Med J. 1979 Jan 27;1(6158):233-4 [421046.001]
  • [Cites] Int J Urol. 1997 Sep;4(5):527-9 [9354961.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):594-603 [9053482.001]
  • [Cites] Cancer. 1980 Sep 15;46(6):1339-44 [6158370.001]
  • [Cites] J Clin Oncol. 1994 Mar;12(3):627-42 [8120563.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):297-302 [10661335.001]
  • [Cites] Med Oncol. 2000 Nov;17(4):279-86 [11114706.001]
  • [Cites] Urologe A. 1998 Nov;37(6):635-47 [9887493.001]
  • [Cites] Med Pediatr Oncol. 1992;20(1):68-70 [1370071.001]
  • [Cites] Oncol Rep. 2001 Mar-Apr;8(2):219-23 [11182030.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jul 1;29(4):711-7 [8040016.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1449-54 [9193339.001]
  • [Cites] N Engl J Med. 1987 Jun 4;316(23):1435-40 [2437455.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Oct 1;51(2):426-34 [11567817.001]
  • [Cites] Cancer. 1986 Jun 1;57(11):2108-13 [2421864.001]
  • [Cites] Cancer. 1981 Mar 1;47(5):978-81 [7194730.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;22(1):17-22 [1370066.001]
  • [Cites] Br J Urol. 1987 Oct;60(4):364-7 [2825897.001]
  • [Cites] Clin Exp Metastasis. 1994 May;12(3):226-30 [8194197.001]
  • [Cites] Br J Cancer. 1979 Mar;39(3):217-23 [88952.001]
  • [Cites] BJU Int. 1999 Mar;83(4):457-61 [10210571.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 2):2630-2 [10068265.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Mar 1;37(4):745-51 [9128946.001]
  • [Cites] Ann Oncol. 1997 May;8(5):477-83 [9233528.001]
  • [Cites] Cancer. 1983 Nov 1;52(9):1728-35 [6684500.001]
  • [Cites] Ital J Neurol Sci. 1997 Jun;18(3):173-5 [9241566.001]
  • [Cites] Neurosurgery. 1989 Nov;25(5):814-9 [2555732.001]
  • [Cites] Cancer. 1982 Jan 1;49(1):12-8 [6274499.001]
  • [Cites] J Clin Oncol. 1984 Dec;2(12):1397-403 [6210350.001]
  • [Cites] Cancer. 1979 Dec;44(6):2349-53 [228844.001]
  • [Cites] Cancer. 1999 Feb 15;85(4):988-97 [10091779.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Aug 1;42(1):155-9 [9747833.001]
  • [Cites] N Engl J Med. 1990 Feb 22;322(8):494-500 [2405271.001]
  • [Cites] Neurol Med Chir (Tokyo). 1991 May;31(5):277-82 [1717863.001]
  • [Cites] J Natl Cancer Inst. 2000 Jul 19;92(14):1165-71 [10904090.001]
  • (PMID = 12164687.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 37
  •  go-up   go-down


10. Raco A, Raimondi AJ, D'Alonzo A, Esposito V, Valentino V: Radiosurgery in the management of pediatric brain tumors. Childs Nerv Syst; 2000 May;16(5):287-95
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiosurgery in the management of pediatric brain tumors.
  • A total of 114 patients with benign and malignant intracranial tumors were treated by Valentino at the Flaminia Radiosurgical Center using a Philips 6-MeV linear accelerator between 1987 and 1995.
  • The tumor locations break down as follows: 36 in the cerebral hemispheres, 14 in the region of the hypothalamus/optic chiasm, 21 in the III ventricle/pineal region, 3 in the basal ganglia, 27 in the posterior fossa, 13 in the brain stem.
  • Seventy-nine patients had multivariate/combined treatment consisting of surgery or biopsy followed by chemotherapy, radiotherapy and/or radiosurgery.
  • Thirty-five were not operated on or biopsied but were treated primarily by radiosurgery, which was associated with chemotherapy and conventional radiotherapy.
  • The short- and long-term results were evaluated separately for each pathology in an attempt to derive guidelines for future treatment.
  • For tumors of the pineal region, we are of the opinion that radiosurgery is the treatment of choice in children and that more than one-third of patients can be cured by this means.
  • The remaining patients require surgery and/or chemotherapy in addition.
  • For medulloblastomas radiosurgery may be useful to control local recurrence if coupled with chemotherapy.
  • We fear that limiting treatment to radiosurgery, rather than prescribing conventional radiotherapy when indicated, could permit CNS seeding.
  • In glial tumors radiosurgery helped either to "sterilize" the tumor bed after removal or to treat remnants of the lesions in critical areas; for diffuse brain stem gliomas it should be considered the treatment of choice.
  • [MeSH-major] Brain / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery. Radiosurgery / methods
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Karnofsky Performance Status. Male. Neoplasm Recurrence, Local. Neoplasm Seeding. Neoplasm, Residual / surgery. Prognosis. Radiotherapy. Reoperation. Retrospective Studies. Survival Analysis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10883372.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
  •  go-up   go-down


11. Alavi S, Rashidi A, Khatami AR, Arzanian MT: Rhabdoid tumor of the kidney presenting with hemiplegia: report of a case. Pediatr Hematol Oncol; 2007 Mar;24(2):123-8
MedlinePlus Health Information. consumer health - Kidney Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rhabdoid tumor of the kidney presenting with hemiplegia: report of a case.
  • Rhabdoid tumor of the kidney (RTK) is a rare and highly malignant neoplasm of infancy, with a strong tendency for early metastasis to distant regions.
  • RTK is unique in its significant association with primary or metastatic brain tumors.
  • The patient was found thereafter to have RTK concurrent with pulmonary metastases, a brain tumor, and a cerebral ischemic lesion.
  • Intensive chemotherapy consisting of carboplatin and etoposide alternating with cyclophosphamide was unsuccessful and the patient died 5 months later because of severe respiratory distress resulting from widespread pulmonary metastases.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Hemiplegia / complications. Kidney Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Rhabdoid Tumor / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Ischemia / drug therapy. Brain Ischemia / pathology. Fatal Outcome. Female. Humans. Infant. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Hemiplegia.
  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17454778.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


12. Preusser M, Haberler C, Hainfellner JA: Malignant glioma: neuropathology and neurobiology. Wien Med Wochenschr; 2006 Jun;156(11-12):332-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant glioma: neuropathology and neurobiology.
  • Malignant gliomas may manifest at any age including congenital and childhood cases.
  • The sole unequivocal risk factor is therapeutic ionizing irradiation.
  • Malignant gliomas comprise a spectrum of different tumor subtypes.
  • Within this spectrum, glioblastoma, anaplastic astrocytoma and anaplastic oligodendroglioma share as basic features preferential location in cerebral hemispheres, diffuse infiltration of brain tissue, fast tumor growth with fatal outcome within months or years.
  • Invasion is regarded as one of the main reasons for poor therapeutic success, because it makes complete surgical removal of gliomas impossible.
  • Invasion of glioma cells requires interaction with the extracellular matrix and with surrounding cells of the healthy brain tissue.
  • Vascular proliferates and tissue necrosis are characteristic features of malignant gliomas, in particular glioblastoma.
  • These features are most likely the consequence of rapidly increasing tumor mass that is inadequately oxygenized by the preexisting vasculature.
  • In malignant glioma, distinct molecular pathways including the p53 pathway, the RB pathway and the EGFR pathway show frequent alterations that seem to be pathogenetically relevant.
  • Methylguanine-methyltransferase (MGMT) promoter methylation status in glioblastoma and 1p19q deletion status in anaplastic oligodendroglioma are associated with response to chemotherapy.
  • The role of neuropathology and neurobiology in neurooncology is 1. to provide a clinically meaningful classification of brain tumors on basis of pathobiological factors, 2. to clarify etiology and pathogenesis of brain tumors as rational basis for development of new diagnostic tests and therapies, and 3. to translate testing for new clinically relevant molecular parameters into clinical application.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Adult. Brain / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Child. Chromosome Aberrations. Female. Humans. Infant. Male. Neoplasm Invasiveness / pathology. Prognosis


13. Kim L, Glantz MJ: Neoplastic meningitis. Curr Treat Options Oncol; 2001 Dec;2(6):517-27
MedlinePlus Health Information. consumer health - Meningitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The frequency of neoplastic meningitis is increasing because of heightened clinical suspicion, improved neuroimaging techniques, and longer survival in patients with extraneural cancer Longer survival allows residual tumor cells within central nervous system sanctuary sites time to become symptomatic.
  • Affected patients may present with cerebral, cranial nerve, or spinal signs and symptoms, depending on the specific sites of central nervous system (CNS) involvement.
  • As a result, the standard diagnostic test for neoplastic meningitis remains the cytologic identification of malignant cells in cerebrospinal fluid (CSF).
  • Although CSF cytology is useful, malignant cells are not detected in as many as one third of patients who have compelling clinical or radiographic evidence of neoplastic meningitis.
  • Novel assays are being tested that may enhance the early identification of malignant cells in CSF.
  • By the time symptoms appear, most tumors have disseminated widely within the CNS, due to cortical irritation, compression of nervous system structures, or obstruction of CSF flow.
  • At this stage surgery, cranial irradiation, and chemotherapy are rarely, if ever, curative.
  • The goals of treatment are to improve or to stabilize the neurologic status of patients and to prolong survival.
  • If only symptomatic areas are treated, reseeding of the neuraxis with tumor cells will occur.
  • Therefore, intrathecal chemotherapy remains a mainstay of therapy.
  • Currently, four therapeutic agents are available for intrathecal treatment: methotrexate, ara-C, sustained-release ara-C (DepoCyt; Chiron Therapeutics, San Francisco, CA), and thiotepa.
  • Unfortunately, intrathecal chemotherapy does not treat bulky disease in the subarachnoid space, and often is slow to stabilize progressive neurologic deficits.
  • For these reasons, radiation therapy to sites of symptomatic disease and sites of bulky disease on imaging studies is recommended.
  • Alternative approaches (which offer less toxicity, enhanced therapeutic effect, and prolonged survival) are being investigated.
  • [MeSH-major] Brain Neoplasms / pathology. Meningitis / etiology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / blood. Carcinoma / cerebrospinal fluid. Carcinoma / secondary. Combined Modality Therapy. Cranial Irradiation. Diagnostic Imaging. Epidemiologic Methods. Glioma / pathology. Humans. Neoplasm Invasiveness. Palliative Care. Risk Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1994 Sep 1;54(17):4710-4 [8062269.001]
  • [Cites] J Clin Oncol. 1993 Nov;11(11):2186-93 [8229133.001]
  • [Cites] Cancer Treat Rep. 1982 Dec;66(12):2105-6 [6958367.001]
  • [Cites] Cancer. 1995 Jun 15;75(12):2919-31 [7773943.001]
  • [Cites] Eur J Cancer Clin Oncol. 1987 Jan;23(1):1-4 [3297711.001]
  • [Cites] J Natl Cancer Inst. 1988 Oct 5;80(15):1211-6 [3418727.001]
  • [Cites] Cancer. 2001 Aug 15;92(4):856-62 [11550158.001]
  • [Cites] J Clin Oncol. 1987 Oct;5(10):1655-62 [3309199.001]
  • [Cites] J Neurooncol. 1989 Nov;7(4):319-28 [2585028.001]
  • [Cites] Arch Neurol. 1997 Jan;54(1):16-7 [9006407.001]
  • [Cites] J Nucl Med. 1971 Aug;12(8):555-7 [5093427.001]
  • [Cites] Clin Cancer Res. 1996 Jun;2(6):963-72 [9816257.001]
  • [Cites] J Clin Oncol. 1989 Nov;7(11):1701-9 [2809683.001]
  • [Cites] J Neurol. 1999 Sep;246(9):810-4 [10525979.001]
  • [Cites] J Neurooncol. 1998 Jun-Jul;38(2-3):225-32 [9696376.001]
  • [Cites] J Clin Oncol. 1993 Mar;11(3):561-9 [8445432.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1991 Feb;54(2):119-23 [2019836.001]
  • [Cites] Am J Med. 1982 Nov;73(5):641-7 [6814249.001]
  • [Cites] Ann Neurol. 1980 Dec;8(6):597-604 [7212647.001]
  • [Cites] Neurology. 2000 Apr 25;54(8):1670-6 [10762512.001]
  • [Cites] Cancer. 1998 Mar 1;82(5):923-30 [9486583.001]
  • [Cites] Cancer. 1995 Jul 15;76(2):232-6 [8625097.001]
  • [Cites] N Engl J Med. 1975 Jul 24;293(4):161-6 [806016.001]
  • [Cites] Neurosurg Focus. 1998 Jun 15;4(6):e4 [17154444.001]
  • [Cites] Cancer Res. 1986 Jan;46(1):169-74 [2933145.001]
  • [Cites] Neurology. 1994 Aug;44(8):1463-9 [8058150.001]
  • [Cites] Kaohsiung J Med Sci. 1997 Oct;13(10):626-30 [9385779.001]
  • [Cites] Cancer. 1982 Feb 15;49(4):759-72 [6895713.001]
  • [Cites] Arch Neurol. 1996 Jul;53(7):626-32 [8929170.001]
  • [Cites] J Natl Cancer Inst. 1992 Aug 5;84(15):1203-4 [1635089.001]
  • [Cites] Cancer Treat Rev. 1999 Apr;25(2):103-19 [10395835.001]
  • [Cites] J Neuropathol Exp Neurol. 1992 May;51(3):235-45 [1583530.001]
  • [Cites] J Neurooncol. 1990 Dec;9(3):225-9 [2086737.001]
  • [Cites] J Cancer Res Clin Oncol. 2001 Jan;127(1):2-8 [11206266.001]
  • [Cites] Invest New Drugs. 1985;3(3):293-6 [4066222.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1561-7 [9552066.001]
  • [Cites] Cancer. 1978 Jul;42(1):283-6 [667799.001]
  • [Cites] Ann Neurol. 1995 Jul;38(1):51-7 [7611725.001]
  • [Cites] J Neurosurg. 1996 Oct;85(4):648-54 [8814169.001]
  • [Cites] Cancer. 1996 Feb 1;77(3):543-8 [8630963.001]
  • [Cites] Cancer Chemother Pharmacol. 1995;36(2):121-4 [7767947.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3110-6 [10506606.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3394-402 [10589750.001]
  • [Cites] Eur J Nucl Med. 1984;9(3):125-8 [6325197.001]
  • [Cites] J Neurooncol. 1994;19(3):239-44 [7807174.001]
  • [Cites] Neurology. 1998 Apr;50(4):1173-5 [9566421.001]
  • [Cites] Cancer. 1998 Feb 15;82(4):733-9 [9477107.001]
  • [Cites] Am J Med. 1981 Jul;71(1):26-32 [6264785.001]
  • [Cites] Cancer Treat Rep. 1977 Jul;61(4):733-43 [577896.001]
  • [Cites] J Neurooncol. 1998 Jun-Jul;38(2-3):245-52 [9696379.001]
  • [Cites] Neurology. 1991 Nov;41(11):1765-9 [1944906.001]
  • [Cites] J Neurooncol. 1997 May;32(3):215-23 [9049883.001]
  • [Cites] Ann Oncol. 1996 Oct;7(8):773-86 [8922190.001]
  • [Cites] CA Cancer J Clin. 2001 Jan-Feb;51(1):15-36 [11577478.001]
  • [Cites] J Immunother Emphasis Tumor Immunol. 1993 Jan;13(1):49-54 [8435432.001]
  • (PMID = 12057097.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 63
  •  go-up   go-down


14. Donovan DJ, Smith AB, Petermann GW: Atypical teratoid/rhabdoid tumor of the velum interpositum presenting as a spontaneous intraventricular hemorrhage in an infant: case report with long-term survival. Pediatr Neurosurg; 2006;42(3):187-92
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical teratoid/rhabdoid tumor of the velum interpositum presenting as a spontaneous intraventricular hemorrhage in an infant: case report with long-term survival.
  • Atypical teratoid/rhabdoid tumors (ATRT) of infancy are highly malignant neoplasms that are most common in the first 2 years of life.
  • Serial imaging studies and two ventriculoscopic biopsies were required to establish the diagnosis of the tumor in this unique location and in the midst of an evolving hematoma.
  • After surgical resection, the patient received adjuvant chemotherapy.
  • At 4-year follow-up, the child is neurologically intact, meeting normal developmental milestones, and imaging studies show no evidence of tumor.
  • ATRT were previously associated with an extremely poor prognosis, but more recent evidence with complete surgical resection and adjuvant chemotherapy shows extended survival in some cases, supporting an aggressive and comprehensive approach to give these patients the best chance for a good outcome.
  • Spontaneous brain hemorrhage in a full-term infant requires a diligent and persistent search to rule out an underlying neoplasm.
  • [MeSH-major] Brain Neoplasms / surgery. Cerebral Hemorrhage / etiology. Cerebral Ventricle Neoplasms / surgery. Rhabdoid Tumor / surgery. Survivors. Teratoma / surgery
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Chemotherapy, Adjuvant. Craniotomy. Diagnosis, Differential. Epilepsy, Generalized / diagnosis. Epilepsy, Generalized / etiology. Epilepsy, Generalized / surgery. Epilepsy, Tonic-Clonic / diagnosis. Epilepsy, Tonic-Clonic / etiology. Epilepsy, Tonic-Clonic / surgery. Female. Humans. Hydrocephalus / diagnosis. Hydrocephalus / surgery. Infant. Lateral Ventricles / pathology. Lateral Ventricles / surgery. Magnetic Resonance Imaging. Microscopy, Electron. Reoperation. Third Ventricle / pathology. Third Ventricle / surgery. Tomography, X-Ray Computed. Ventriculoperitoneal Shunt. Ventriculostomy

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 S. Karger AG, Basel
  • (PMID = 16636624.001).
  • [ISSN] 1016-2291
  • [Journal-full-title] Pediatric neurosurgery
  • [ISO-abbreviation] Pediatr Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


15. Yamada K, Goto S, Kochi M, Ushio Y: Stereotactic biopsy for multifocal, diffuse, and deep-seated brain tumors using Leksell's system. J Clin Neurosci; 2004 Apr;11(3):263-7
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stereotactic biopsy for multifocal, diffuse, and deep-seated brain tumors using Leksell's system.
  • Using the Leksell stereotactic system, we selectively performed 91 biopsies for surgically inaccessible brain lesions.
  • Sixty-nine (75.8%) lesions were primary tumors; 44 (48.4%) were malignant gliomas, 18 (19.8%) malignant lymphomas, and five (5.5%) low-grade gliomas.
  • Thirteen (14.3%) cases had previously undergone radiation and/or chemotherapy for brain tumors, seven had recurrent glioma (five with malignant transformation) and six manifested radiation necrosis.
  • None of the patients died due to the stereotactic procedure; one (1.1%) exhibited morbidity due to complicated hemorrhage.
  • We found asymptomatic minor bleeding occurred in nine (9.9%) patients; the rate of hemorrhage was significantly higher in patients with preoperative angiographic evidence of tumor stain.
  • All five patients younger than 15 years underwent the procedure without complications.
  • The Leksell stereotactic system is useful for diagnostic tissue sampling and contributes effectively to the selection of appropriate therapy in patients with malignant brain tumors.
  • While it carries a low morbidity rate without mortality in our series, care must be taken for selected target sites in highly vascularized lesions exhibiting positive tumor stains.
  • [MeSH-major] Biopsy / methods. Brain Neoplasms / diagnosis. Stereotaxic Techniques
  • [MeSH-minor] Adolescent. Adult. Aged. Cerebral Angiography. Cerebral Hemorrhage / epidemiology. Cerebral Hemorrhage / etiology. Cerebral Hemorrhage / pathology. Child. Child, Preschool. Electric Stimulation. Female. Humans. Infant. Male. Middle Aged. Neoplasm Recurrence, Local. Neurosurgical Procedures. Postoperative Care. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Biopsy.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14975414.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  •  go-up   go-down


16. Taomoto K, Ohnishi H, Kamada Y, Kuga Y, Kohaya N, Nakashima K, Ichioka T, Tominaga T, Nakamura M, Nakazato Y: A rare case of malignant glioma suspected to have arisen from a cavernous sinus. Brain Tumor Pathol; 2007;24(2):75-80
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rare case of malignant glioma suspected to have arisen from a cavernous sinus.
  • The extraparenchymal tumor located around the right trigeminal ganglion was totally removed, except for an intracavernous lesion, by the orbitozygomatic approach.
  • The solid tumor was completely separated from the brainstem and seemed to be a trigeminal schwannoma arising from the trigeminal ganglion or cavernous sinus at surgery.
  • A histological examination, however, found a typical malignant glioma that consisted primarily of astrocytic tumor cells.
  • Immunohistochemical staining showed the tumor cells stained intensely for GFAP, S-100 protein, and vimentin, but not for NFP, Schwann/2E, CD34, and CD68.
  • The tumor recurred after a short time, and then it rapidly disseminated into the subarachnoid space and left the cerebral hemisphere.
  • The patient died 1 year after the initial symptoms in spite of aggressive surgery, radiation, and chemotherapy with temozolomide.
  • There are no previous reports of a malignant glioma arising from either the cavernous sinus or the trigeminal ganglion.
  • From the pathogenetic point of view, this malignant glioma is an extremely rare case that developed clinically and neuroradiologically from the cavernous sinus and was suspected be being derived from ectopic glial tissue.
  • [MeSH-major] Brain Neoplasms / pathology. Cavernous Sinus / pathology. Glioma / pathology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Fatal Outcome. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Middle Aged. Neurosurgical Procedures. Radiosurgery. Radiotherapy

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18095135.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


17. de Bouyn-Icher C, Minard-Colin V, Isapof A, Khuong Quang DA, Redon I, Hartmann O: [Malignant solid tumors in neonates: a study of 71 cases]. Arch Pediatr; 2006 Dec;13(12):1486-94
MedlinePlus Health Information. consumer health - Neuroblastoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Malignant solid tumors in neonates: a study of 71 cases].
  • Malignant neonatal tumors are rare and comprise 2% of childhood malignancies.
  • Clinical features, histologic types, prognosis were very different from those seen in older children, facing oncologists with diagnostic, therapeutic and ethical problems.
  • PATIENTS AND METHODS: In a retrospective study from January 1987 to January 2004, we reviewed the management of neonates treated at the Institute Gustave Roussy for a malignant solid tumor for whom symptoms started in the first month of life.
  • RESULTS: Seventy-one neonates were treated, comprising 1,2% of the overall patients treated during the same period of time.
  • Of these 71 patients, 42 (59%) presented with neuroblastomas, 12 (17%) with mesenchymal tumors, 6(8%) with cerebral tumors and 11 with various other types of tumors.
  • Thirty-eight neonates received chemotherapy, administered at a 30 to 50% reduced dose.
  • Hematologic toxicities and infections were the main therapeutic complications.
  • There has been no therapy-related mortality.
  • CONCLUSIONS: Neonatal malignant solid tumors, except for cerebral tumors, have a good prognosis.
  • The young age of patients resulted in problems of treatment tolerance.
  • The therapeutic regimen should take into account the risk of acute iatrogenic toxicity and long term sequelae.
  • Surgery remains the treatment of choice but chemotherapy, with dose reduction, managed by expert teams, is essential and safer in a lot of case.
  • [MeSH-major] Brain Neoplasms / epidemiology. Mesenchymoma / epidemiology. Neuroblastoma / epidemiology
  • [MeSH-minor] Adolescent. Age Factors. Antineoplastic Agents / therapeutic use. Brain / pathology. Child. Child, Preschool. Female. France / epidemiology. Humans. Incidence. Infant. Infant, Newborn. Male. Neoplasm Staging. Prenatal Diagnosis. Prognosis. Radiotherapy Dosage. Retrospective Studies. Risk Factors. Sex Factors. Survival Analysis

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17137765.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


18. Giordana MT, Ghimenti C, Leonardo E, Balteri I, Iudicello M, Duò D: Molecular genetic study of a metastatic oligodendroglioma. J Neurooncol; 2004 Feb;66(3):265-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It may be instrumental in defining the distant tumor as metastatic oligodendroglioma and give clues to the genetic events associated with the highly malignant transformation.
  • We present the case of a patient with multiple bone metastases from a cerebral oligodendroglioma.
  • The patient received procarbazine, lomustine, vincristine chemotherapy and radiotherapy after the second surgery.
  • The computed tomography-guided biopsy of the bone lesions revealed tumor cells positive for GFAP, S-100 and Leu-7 and negative for cytokeratin, LCA and EMA.
  • The genetic analysis of DNA from the original tumor, the bone metastasis and the autoptic brain tumor showed LOH of 1p; heterozygous deletion of CDKN2A/p 16 was detected as additional alteration in the metastasis and in the intracranial tumor at autopsy.
  • Repeated brain surgery and extended survival may have acted as promoter of extraneural dissemination.
  • Loss of CDKN2A most probably played an important role in the malignant progression: its involvement in metastatic potential remains to be clarified.
  • Our data confirm that malignant transformation of oliogodendrogliomas may be undetected by histology and underscore the importance of genetic analysis.
  • Coincidentally with intensive anticancer therapy, chemotherapy included, employed in patients with oligodendroglioma and the ensuing long survival, the frequency of metastatic oliogodendrogliomas may increase.
  • [MeSH-major] Bone Neoplasms / genetics. Brain Neoplasms / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Deletion. Oligodendroglioma / genetics
  • [MeSH-minor] Biomarkers, Tumor / analysis. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Combined Modality Therapy. DNA, Neoplasm / analysis. Humans. Loss of Heterozygosity / genetics. Male. Microsatellite Repeats. Middle Aged. Molecular Biology. Neoplasm Proteins / analysis

  • Genetic Alliance. consumer health - Oligodendroglioma.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Chromosomes Cancer. 2002 Oct;35(2):170-5 [12203781.001]
  • [Cites] Am J Pathol. 1999 Aug;155(2):375-86 [10433931.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(3):636-45 [10653879.001]
  • [Cites] J Neurooncol. 1988;6(1):53-9 [3294352.001]
  • [Cites] Neurology. 1989 Dec;39(12):1593-6 [2685656.001]
  • [Cites] Lancet Oncol. 2002 Aug;3(8):498-507 [12147436.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] Oncology. 1998 Jul-Aug;55(4):345-8 [9663425.001]
  • [Cites] J Neurosurg. 2002 Mar;96(3):559-64 [11892633.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1969 Jun;32(3):249-53 [5795118.001]
  • [Cites] Neurosurgery. 1981 Mar;8(3):391-6 [7242888.001]
  • [Cites] Acta Neuropathol. 2002 Mar;103(3):267-75 [11907807.001]
  • [Cites] Ann Neurol. 1990 May;27(5):573-4 [2360797.001]
  • [Cites] Med Hypotheses. 1992 Sep;39(1):88-9 [1435399.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Dec;60(12):1181-9 [11764090.001]
  • [Cites] J Neurooncol. 2001 Jun;53(2):107-14 [11716064.001]
  • [Cites] Clin Neuropathol. 1988 May-Jun;7(3):131-3 [3203482.001]
  • [Cites] Int J Cancer. 2000 Nov 15;88(4):554-7 [11058870.001]
  • [Cites] Oncogene. 1996 Sep 5;13(5):983-94 [8806688.001]
  • [Cites] J Neurosurg. 1968 Apr;28(4):373-9 [5643931.001]
  • [Cites] Clin Cancer Res. 2002 Jan;8(1):196-201 [11801559.001]
  • (PMID = 15015656.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins
  •  go-up   go-down


19. Roser F, Nakamura M, Brandis A, Hans V, Vorkapic P, Samii M: Transition from meningeal melanocytoma to primary cerebral melanoma. Case report. J Neurosurg; 2004 Sep;101(3):528-31
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transition from meningeal melanocytoma to primary cerebral melanoma. Case report.
  • The authors describe the first case of an intracranial transition of a melanocytoma into a primary malignant melanoma within a short time.
  • A 37-year-old woman presented with progressive brainstem syndrome due to a tumor, originally diagnosed and treated 12 years earlier, that extended from the petroclival area to the anterior craniocervical junction.
  • The histological workup following subtotal tumor resection of the initial tumor had revealed the typical features of a fibrous melanocytic meningioma without increased proliferation.
  • Ten years after the patient had completed treatment for the melanocytic meningioma, control neuroimaging demonstrated growth of the residual tumor with compression of the brainstem.
  • Another neurosurgical intervention revealed a dark tumor of hard consistency.
  • At this time immunohistochemical examinations demonstrated melanocytic features (expression of vimentin, S100 protein, and melan A) of the lesion with focally increased proliferation (5% of Ki-67-positive cells) but no higher mitotic activity.
  • Clinical signs of deterioration along with imaging-confirmed tumor progression precipitated another operation within 7 months.
  • Pleomorphic changes and a focal high mitotic activity led to the diagnosis of a primary cerebral malignant melanoma.
  • The patient's later clinical course consisted of a rapid diffuse meningeal spread of the lesion throughout the entire brain and spine.
  • Despite whole-brain and stereotactic radiation therapy as well as chemotherapy, the patient died 4 months after the last neuropathological diagnosis.
  • The biological behavior of a melanocytoma is variable and recurrence may happen after subtotal resection, but intracranial transition into a malignant melanoma has not been observed previously.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Melanoma / pathology. Meningeal Neoplasms / pathology. Meningioma / pathology. Neoplasm, Residual / pathology. Nevus / pathology
  • [MeSH-minor] Adult. Brain Stem / pathology. Cell Division. Disease Progression. Fatal Outcome. Female. Follow-Up Studies. Humans. Magnetic Resonance Angiography. Meninges / pathology. Neoplasm Invasiveness / pathology. Reoperation

  • MedlinePlus Health Information. consumer health - Birthmarks.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Moles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15352613.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


20. Toledano Delgado R, Garcia N, Riva-Amarante E, Rodríguez Pascual J, García Leal R, Sendra Tello J: [Spinal leptomeningeal metastasis from cerebral glioblastoma: case report]. Neurologia; 2006 Sep;21(7):378-81
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Spinal leptomeningeal metastasis from cerebral glioblastoma: case report].
  • INTRODUCTION: Glioblastoma multiforme (GBM) is the most common primary malignant tumor of the central nervous system.
  • Most of the time it is diagnosed late and misdiagnosis is a common problem.
  • CASE REPORT: We present a case of a 65-year-old man with a right temporal GBM treated by surgical resection, radiotherapy and chemotherapy, who is readmitted 10 months later as he developed an ataxic gait.
  • A new cerebral magnetic resonance imaging (MRI) showed multiple cerebellar metastasis.
  • Awareness of this complication might facilitate more rapid diagnosis and treatment.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Meningeal Neoplasms / secondary. Spinal Cord Neoplasms / secondary
  • [MeSH-minor] Aged. Humans. Lumbar Vertebrae / pathology. Male. Neoplasm Invasiveness

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16977559.001).
  • [ISSN] 0213-4853
  • [Journal-full-title] Neurología (Barcelona, Spain)
  • [ISO-abbreviation] Neurologia
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


21. Tange Y, Miyazaki M, Iwata J, Aiko Y, Sakamoto S, Mori K: Novel antitumor effect of carboplatin delivered by intracerebral microinfusion in a rat malignant glioma model. Neurol Med Chir (Tokyo); 2009 Dec;49(12):572-9
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel antitumor effect of carboplatin delivered by intracerebral microinfusion in a rat malignant glioma model.
  • Carboplatin loaded osmotic mini-pumps were implanted in 24 9L malignant glioma-bearing rats to investigate the implications of direct intracerebral microinfusion.
  • The tumor volume was serially measured by magnetic resonance (MR) imaging with gadolinium as the enhanced area, and the survival periods and histological findings were also examined.
  • Separately, to examine the effects of intracerebral carboplatin infusion on vascular permeability, tumor-bearing rats received intravenous administration of 2% Evans blue at 21 days after infusion.
  • The high dose group showed transient increase of enhanced volume at 21 days associated with mass effect, and significantly decreased tumor volume at 28 and 35 days compared with the control and low dose groups.
  • The high dose group showed significant longer survival time than the control and low dose groups.
  • Histological examination of the high dose group at 21 days showed the central tumor necrotic area around the infusion site and Evans blue leakage into the surrounding enhanced rim and the necrotic core.
  • The present study demonstrated quantitatively using MR imaging that intracerebral carboplatin microinfusion significantly inhibited the rapid growth of experimental rat glioma but that the high dose required carries the risk of transient swelling of the target tumor.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Carboplatin / administration & dosage. Glioma / drug therapy. Infusion Pumps, Implantable. Microinjections / instrumentation
  • [MeSH-minor] Animals. Brain Edema / chemically induced. Brain Edema / diagnosis. Brain Edema / physiopathology. Cell Line, Tumor. Cerebral Cortex / drug effects. Cerebral Cortex / pathology. Disease Models, Animal. Dose-Response Relationship, Drug. Evans Blue. Injections, Intravenous. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness / pathology. Rats. Rats, Inbred F344. Survival Rate. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20035131.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 45PG892GO1 / Evans Blue; BG3F62OND5 / Carboplatin
  •  go-up   go-down


22. Farhadi MR, Capelle HH, Erber R, Ullrich A, Vajkoczy P: Combined inhibition of vascular endothelial growth factor and platelet-derived growth factor signaling: effects on the angiogenesis, microcirculation, and growth of orthotopic malignant gliomas. J Neurosurg; 2005 Feb;102(2):363-70
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined inhibition of vascular endothelial growth factor and platelet-derived growth factor signaling: effects on the angiogenesis, microcirculation, and growth of orthotopic malignant gliomas.
  • OBJECT: The goal of this study was to determine the effects of SU6668, a polyvalent receptor tyrosine kinase inhibitor against vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and fibroblast growth factor-1 on tumor growth, angiogenesis, and microcirculation in an orthotopic malignant glioma model.
  • METHODS: Fluorescently labeled C6 malignant glioma cells were implanted into a long-term cranial window, which had been prepared in nude mice.
  • The animals were treated with intraperitoneal injections of SU6668 (75 mg/kg/day) immediately (five animals) or 7 days (five animals) following tumor implantation.
  • Control mice received intraperitoneal injections of vehicle (50 microl dimethylsulfoxide) immediately (five animals) or 7 days (four animals) after tumor implantation.
  • Tumor growth, angiogenesis, and microcirculation were assessed by performing intravital fluorescence videomicroscopy over a 14-day observation period.
  • To assess the effects of SU6668 on overall survival, C6 glioma cells were implanted stereotactically into the brains of 24 additional animals and treatment was initiated on Day 7.
  • In both the immediate and delayed experimental setting, SU6668 treatment resulted in a significant reduction of total and functional tumor vessel densities (both p < 0.05), reflecting a suppression of angiogenesis and impairment of tumor perfusion.
  • As a consequence, tumor growth was significantly inhibited (p < 0.05).
  • Histological analysis demonstrated reduced tumor growth and less mass effect on the adjacent brain of treated animals.
  • The survival experiments confirmed the importance of our results in that survival was significantly prolonged following SU6668 therapy (p < 0.05).
  • This also applies to malignant gliomas, despite the uniqueness of the cerebral microenvironment and the singular pathobiology of this tumor entity.
  • [MeSH-major] Brain Neoplasms / blood supply. Glioma / blood supply. Indoles / pharmacology. Neovascularization, Pathologic / physiopathology. Platelet-Derived Growth Factor / antagonists & inhibitors. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrroles / pharmacology. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Brain / drug effects. Brain / pathology. Cell Division / drug effects. Cell Division / physiology. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Mice. Mice, Nude. Microcirculation / drug effects. Microcirculation / physiology. Microscopy, Fluorescence. Microscopy, Video. Neoplasm Transplantation. Rats. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor beta / physiology. Transplantation, Heterologous. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / physiology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15739567.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indoles; 0 / Platelet-Derived Growth Factor; 0 / Pyrroles; 0 / Vascular Endothelial Growth Factor A; 9RL37ZZ665 / orantinib; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


23. Tabatabai G, Frank B, Wick A, Lemke D, von Kürthy G, Obermüller U, Heckl S, Christ G, Weller M, Wick W: Synergistic antiglioma activity of radiotherapy and enzastaurin. Ann Neurol; 2007 Feb;61(2):153-61
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Radiotherapy is an essential treatment modality for malignant gliomas, but it exerts adverse effects via promotion of glioma cell invasion in experimental glioma.
  • Here, we investigate the combination of the protein kinase C-beta inhibitor enzastaurin (ENZA) and radiotherapy in vitro and in vivo in comparison with either treatment alone.
  • After orthotopic intracerebral implantation of LNT-229 glioma cells in nude mice, the effects of in situ cerebral irradiation and oral application of ENZA on survival, tumor size, VEGF expression, apoptosis, and microvessel density in vivo were analyzed.
  • RESULTS: Combining cerebral irradiation with ENZA leads to longer survival in vivo.
  • ENZA diminishes tumor volume, irradiation-induced tumor satellite formation, upregulation of VEGF expression in vitro and in vivo, as well as enhanced microvessel density in vivo.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy. Indoles / therapeutic use. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / radiation effects. Combined Modality Therapy. Magnetic Resonance Imaging. Mice. Mice, Nude. Neoplasm Transplantation. Protein Kinase C / antagonists & inhibitors. Protein Kinase C beta. Survival Analysis. Up-Regulation. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17212356.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indoles; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C beta; UC96G28EQF / enzastaurin
  •  go-up   go-down


24. Bähr O, Rieger J, Duffner F, Meyermann R, Weller M, Wick W: P-glycoprotein and multidrug resistance-associated protein mediate specific patterns of multidrug resistance in malignant glioma cell lines, but not in primary glioma cells. Brain Pathol; 2003 Oct;13(4):482-94
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P-glycoprotein and multidrug resistance-associated protein mediate specific patterns of multidrug resistance in malignant glioma cell lines, but not in primary glioma cells.
  • Understanding and overcoming multidrug resistance (MDR) may be a promising strategy to develop more effective pharmacotherapies for malignant gliomas.
  • In the present study, human malignant glioma cell lines (n=12) exhibited heterogeneous mRNA and protein expression and functional activity of the mdr gene-encoded P-glycoprotein (PGP) and MDR-associated protein (MRP).
  • The human cerebral endothelial cell line, SV-HCEC, exhibited the strongest PGP activity of all cell lines.
  • Five primary human glioblastomas and one anaplastic astrocytoma displayed heterogenous protein levels of PGP and MRP-1 in tumor cells and of PGP in biopsy specimens in vivo, but no functional activity of these proteins upon ex vivo culturing.
  • These data suggest that the glioma cell line-associated MDR-type drug resistance is a result of long-term culturing and that cerebral endothelial, but not glioma cells, may contribute to MDR-type drug resistance of gliomas in vivo.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm / physiology. Glioma / pathology. Multidrug Resistance-Associated Proteins / physiology. P-Glycoprotein / physiology
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Calcium Channel Blockers / pharmacology. Dose-Response Relationship, Drug. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Flow Cytometry / methods. Humans. Immunohistochemistry / methods. Indomethacin / pharmacology. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction / methods. Rhodamine 123 / metabolism. Tumor Cells, Cultured. Verapamil / pharmacology. Vincristine / pharmacology

  • Genetic Alliance. consumer health - Glioma.
  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • Hazardous Substances Data Bank. INDOMETHACIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14655754.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents, Phytogenic; 0 / Calcium Channel Blockers; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / RNA, Messenger; 1N3CZ14C5O / Rhodamine 123; 5J49Q6B70F / Vincristine; CJ0O37KU29 / Verapamil; XXE1CET956 / Indomethacin
  •  go-up   go-down


25. Clavo B, Robaina F, Catalá L, Valcárcel B, Morera J, Caramés MA, Ruiz-Egea E, Panero F, Lloret M, Hernández MA: Increased locoregional blood flow in brain tumors after cervical spinal cord stimulation. J Neurosurg; 2003 Jun;98(6):1263-70
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased locoregional blood flow in brain tumors after cervical spinal cord stimulation.
  • OBJECT: Patients with high-grade gliomas have poor prognoses following standard treatment.
  • Generally, malignant brain tumors have a decreased blood flow that results in increased resistance to radiation and reduced delivery of chemotherapeutic agents and oxygen.
  • The aim of the present study was to assess the effect of spinal cord stimulation (SCS) on locoregional blood flow in high-grade tumors in the brain.
  • METHODS: Fifteen patients (11 with Grade III and four with Grade IV brain tumors) had SCS devices inserted prior to scheduled radiotherapy.
  • 1) single-photon emission computerized tomography (SPECT) scanning;.
  • 2) middle cerebral artery (MCA) blood flow velocity measurements (centimeters/second) with the aid of transcranial Doppler (TCD) ultrasonography; and 3) common carotid artery (CCA) blood flow volume quantification (milliliters/minute) based on time-domain processing by using color Doppler ultrasonography.
  • The indices demonstrated on SPECT scanning before SCS were significantly lower (p < 0.001) in tumor sites compared with those in peritumoral sites (32%) and healthy contralateral areas (41%).
  • 1) a mean increase of 15% in tumor blood flow in 75% of patients (p = 0.033), as demonstrated on SPECT scanning: 2) a mean increase of greater than 18% in systolic and diastolic blood flow velocities in both tumorous and healthy MCAs in all but one patient (p < 0.002), as exhibited on TCD ultrasonography; and 3) a mean increase of greater than 60% in blood flow volume in tumorous and healthy CCAs in all patients (p < 0.013), as revealed on color Doppler ultrasonography studies.
  • CONCLUSIONS: Preliminary data show that SCS can modify locoregional blood flow in high-grade malignant tumors in the brain, thus indicating that SCS could be used to improve blood flow, oxygenation, and drug delivery to such tumors and could be a useful adjuvant in chemoradiotherapy.
  • [MeSH-major] Brain Neoplasms / blood supply. Brain Neoplasms / therapy. Spinal Cord / physiology
  • [MeSH-minor] Adult. Aged. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Blood Flow Velocity. Carotid Artery, Common / physiology. Combined Modality Therapy. Dose Fractionation. Electric Stimulation / instrumentation. Female. Follow-Up Studies. Humans. Hydroxyurea / therapeutic use. Male. Middle Aged. Middle Cerebral Artery / ultrasonography. Neoplasm Staging. Tegafur / therapeutic use. Tomography, Emission-Computed, Single-Photon. Ultrasonography, Doppler, Color. Ultrasonography, Doppler, Transcranial

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Neurosurg. 2004 Feb;100(2):357; author reply 357-8 [15086248.001]
  • (PMID = 12816274.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 1548R74NSZ / Tegafur; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


26. Yang WQ, Senger D, Muzik H, Shi ZQ, Johnson D, Brasher PM, Rewcastle NB, Hamilton M, Rutka J, Wolff J, Wetmore C, Curran T, Lee PW, Forsyth PA: Reovirus prolongs survival and reduces the frequency of spinal and leptomeningeal metastases from medulloblastoma. Cancer Res; 2003 Jun 15;63(12):3162-72
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Medulloblastoma (MB), the most common pediatric brain tumor, is a highly malignant disease with a 5-year survival rate of only 60%.
  • Tumor cells invade surrounding tissue and disseminate through cerebral spinal fluid, making treatment difficult.
  • Human reovirus type 3 exploits an activated Ras pathway in tumor cells to support productive infection as an oncolytic virus.
  • Here, we examined the ability of human reovirus to kill MB cells lines and surgical specimens in vitro and inhibit tumor growth/metastases in vivo.
  • These data suggest that this oncolytic virus may be a potentially effective novel therapy against human MB.
  • Its ability to reduce metastases to the spinal cord could allow a reduction in the dose/field of total neuroaxis cerebral-spinal radiotherapy currently used to treat/prevent cerebral spinal fluid dissemination.
  • [MeSH-major] Biological Therapy. Cerebellar Neoplasms / therapy. Mammalian orthoreovirus 3 / physiology. Medulloblastoma / secondary. Meningeal Neoplasms / secondary. Spinal Cord Neoplasms / secondary
  • [MeSH-minor] Animals. Drug Administration Schedule. Enzyme Activation. Eukaryotic Initiation Factor-2 / antagonists & inhibitors. Female. Genes, Reporter. Genes, p53. Green Fluorescent Proteins. Humans. Injections, Spinal. Luminescent Proteins / analysis. Luminescent Proteins / genetics. Mice. Mice, Nude. Neoplasm Proteins / physiology. Proto-Oncogene Proteins p21(ras) / physiology. Signal Transduction. Transcription, Genetic. Tumor Cells, Cultured. Virus Replication. Xenograft Model Antitumor Assays. eIF-2 Kinase / antagonists & inhibitors. eIF-2 Kinase / physiology

  • Genetic Alliance. consumer health - Medulloblastoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12810644.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Eukaryotic Initiation Factor-2; 0 / Luminescent Proteins; 0 / Neoplasm Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.11.1 / eIF-2 Kinase; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  •  go-up   go-down


27. Guo M, Roman RJ, Fenstermacher JD, Brown SL, Falck JR, Arbab AS, Edwards PA, Scicli AG: 9L gliosarcoma cell proliferation and tumor growth in rats are suppressed by N-hydroxy-N'-(4-butyl-2-methylphenol) formamidine (HET0016), a selective inhibitor of CYP4A. J Pharmacol Exp Ther; 2006 Apr;317(1):97-108
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 9L gliosarcoma cell proliferation and tumor growth in rats are suppressed by N-hydroxy-N'-(4-butyl-2-methylphenol) formamidine (HET0016), a selective inhibitor of CYP4A.
  • This was accompanied by a 4-fold reduction in the mitotic index, a 3- to 4-fold increase in the apoptotic index, and a approximately 50% decrease in vascularization in the tumor.
  • HET0016 treatment increased mean survival time of the animals from 17 to 22 days.
  • The normal surrounding brain tissue, however, avidly makes 20-HETE, and this activity is selectively inhibited by HET0016.
  • These results suggest that HET0016 may be the prototype of a class of antigrowth compounds that may be efficacious for treating malignant brain tumors.
  • In vivo, it may act in part by inhibiting the formation of 20-HETE by the surrounding tissue.
  • [MeSH-major] Amidines / therapeutic use. Brain Neoplasms / drug therapy. Cell Proliferation / drug effects. Cytochrome P-450 CYP4A / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Gliosarcoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Arachidonic Acid / metabolism. Cell Line, Tumor. Cerebral Cortex / pathology. Male. Neoplasm Transplantation. Rats. Rats, Inbred F344

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16352703.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY014385; United States / NHLBI NIH HHS / HL / HL36279; United States / NIGMS NIH HHS / GM / GM31278; United States / NHLBI NIH HHS / HL / HL29587; United States / NHLBI NIH HHS / HL / R37 HL036279; United States / NHLBI NIH HHS / HL / HL059996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amidines; 0 / Enzyme Inhibitors; 0 / N-hydroxy-N'-(4-butyl-2-methylphenyl)formamidine; 27YG812J1I / Arachidonic Acid; EC 1.14.15.3 / Cytochrome P-450 CYP4A
  •  go-up   go-down






Advertisement