[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 29 of about 29
1. Chang HK, Kim JH: Classical malignant rhabdoid tumor of central nervous system in 9-year-old Korean. Yonsei Med J; 2001 Feb;42(1):142-6
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] Classical malignant rhabdoid tumor of central nervous system in 9-year-old Korean.
  • A Malignant rhabdoid tumor (MRT) arising in the right temporoparietal lobe of a 9-year-old boy is described along with the results of an immunohistochemical study.
  • The child underwent a subtotal resection of the tumor, followed by radiotherapy and systemic chemotherapy, but died three years after surgery.
  • A MRT, a primary neoplasm of the central nervous system (CNS), is an entity of unknown histogenesis with a dismal prognosis, which only occurs in early childhood.
  • Histologically similar tumors with more varied morphological features have been designated as an atypical teratoid/rhabdoid tumor.
  • However, a classical MRT is extremely rare in the CNS and our case represents a classical CNS MRT.
  • [MeSH-major] Brain Neoplasms / metabolism. Rhabdoid Tumor / metabolism

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11293495.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
  •  go-up   go-down


2. Daniel RA, Rozanska AL, Mulligan EA, Drew Y, Thomas HD, Castelbuono DJ, Hostomsky Z, Plummer ER, Tweddle DA, Boddy AV, Clifford SC, Curtin NJ: Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699. Br J Cancer; 2010 Nov 9;103(10):1588-96
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] Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699.
  • BACKGROUND: Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour.
  • AG-014699 was not toxic, accumulated and reduced PARP activity ≥75% in xenograft and brain tissues.
  • CONCLUSION: We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699.

  • Genetic Alliance. consumer health - Medulloblastoma.
  • Genetic Alliance. consumer health - Medulloblastoma, childhood.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3402-9 [15867241.001]
  • [Cites] Nat Rev Drug Discov. 2005 May;4(5):421-40 [15864271.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Jan;45(1):47-60 [16149064.001]
  • [Cites] Neurosurg Focus. 2005 Nov;19(5):E10 [16398460.001]
  • [Cites] Childs Nerv Syst. 2006 Jul;22(7):652-61 [16565851.001]
  • [Cites] Eur J Cancer. 2006 Sep;42(14):2335-42 [16899365.001]
  • [Cites] Clin Cancer Res. 2007 Mar 15;13(6):1663-74 [17363519.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):945-56 [17363489.001]
  • [Cites] Clin Cancer Res. 2007 May 1;13(9):2728-37 [17473206.001]
  • [Cites] Expert Opin Ther Targets. 2007 Jun;11(6):783-99 [17504016.001]
  • [Cites] Cancer. 2007 Oct 1;110(7):1542-50 [17705175.001]
  • [Cites] Clin Cancer Res. 2007 Nov 15;13(22 Pt 1):6712-8 [18006772.001]
  • [Cites] Nat Clin Pract Oncol. 2008 Aug;5(8):476-86 [18542116.001]
  • [Cites] Arch Dis Child Educ Pract Ed. 2008 Oct;93(5):137-44 [18809691.001]
  • [Cites] Clin Cancer Res. 2008 Dec 1;14(23):7917-23 [19047122.001]
  • [Cites] Cancer Res. 2009 Jan 1;69(1):120-7 [19117994.001]
  • [Cites] Clin Cancer Res. 2009 Feb 15;15(4):1241-9 [19174487.001]
  • [Cites] Childs Nerv Syst. 2009 May;25(5):535-41 [19107490.001]
  • [Cites] N Engl J Med. 2009 Jul 9;361(2):123-34 [19553641.001]
  • [Cites] Br J Neurosurg. 2009 Aug;23(4):364-75 [19637007.001]
  • [Cites] Clin Cancer Res. 2009 Oct 1;15(19):6106-12 [19789326.001]
  • [Cites] Semin Oncol. 2001 Aug;28(4 Suppl 13):3-12 [11550133.001]
  • [Cites] Clin Cancer Res. 2000 Mar;6(3):998-1007 [10741727.001]
  • [Cites] Neuro Oncol. 2009 Oct;11(5):458-67 [19179424.001]
  • [Cites] J Clin Oncol. 2003 Jul 1;21(13):2525-8 [12829671.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14):5370-9 [14614022.001]
  • [Cites] J Natl Cancer Inst. 2004 Jan 7;96(1):56-67 [14709739.001]
  • [Cites] Clin Cancer Res. 2004 Feb 1;10(3):881-9 [14871963.001]
  • [Cites] J Med Chem. 2004 Aug 12;47(17):4151-4 [15293985.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] Mol Cancer Ther. 2005 Sep;4(9):1364-8 [16170028.001]
  • (PMID = 20978505.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / C8464/A5414; United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Indoles; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 7GR28W0FJI / Dacarbazine; 8237F3U7EH / rucaparib; 85622-93-1 / temozolomide; EC 2.4.2.30 / PARP1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2990587
  •  go-up   go-down


3. Frühwald MC, Rickert CH, O'Dorisio MS, Madsen M, Warmuth-Metz M, Khanna G, Paulus W, Kühl J, Jürgens H, Schneider P, Müller HL: Somatostatin receptor subtype 2 is expressed by supratentorial primitive neuroectodermal tumors of childhood and can be targeted for somatostatin receptor imaging. Clin Cancer Res; 2004 May 1;10(9):2997-3006
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin receptor subtype 2 is expressed by supratentorial primitive neuroectodermal tumors of childhood and can be targeted for somatostatin receptor imaging.
  • PURPOSE: Although gliomas predominate among central nervous system (CNS) neoplasms in adulthood, embryonal tumors are the most common malignant brain tumors in children.
  • Despite novel treatment approaches, including improved radiotherapy and high-dose chemotherapy, survival rates remain unsatisfactory.
  • The timely diagnosis of residual or recurrent embryonal CNS tumors and thus the earliest possible time point for intervention is often hampered by inaccuracies of conventional imaging techniques.
  • Here, we evaluated somatostatin receptor type 2 (sst(2)) expression using an antibody in an array of CNS tumors of childhood.
  • Eight high-grade gliomas, 4 atypical teratoid/rhabdoid tumors, 7 supratentorial primitive neuroectodermal tumors (stPNET), 1 medulloepithelioma (ME), and 8 ependymomas were screened.
  • Tumors positive in vitro were additionally analyzed in vivo using SRI.
  • RESULTS: Abundant expression of somatostatin receptor type 2 in stPNET, a ME, and ependymomas warranted in vivo imaging of 7 stPNET, 1 rhabdomyosarcoma, 3 ependymomas, 1 ME, and 1 glioblastoma.
  • In selected cases SRI was more sensitive in the detection of relapse than conventional imaging by magnetic resonance imaging and computed tomography.
  • CONCLUSIONS: SRI should be considered in the evaluation of residual or recurrent embryonal CNS tumors, especially stPNET.
  • The strengths of SRI lie in the differentiation of reactive tissue changes versus residual or recurrent tumor, the detection of small lesions, and possibly in the distinction of stPNET from gliomas.
  • [MeSH-major] Neuroectodermal Tumors, Primitive / pathology. Receptors, Somatostatin / biosynthesis. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Central Nervous System Neoplasms / metabolism. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / radionuclide imaging. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Tomography, Emission-Computed, Single-Photon / methods

  • Genetic Alliance. consumer health - Supratentorial primitive neuroectodermal tumors, childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15131035.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2
  •  go-up   go-down


Advertisement
4. Arcaro A, Doepfner KT, Boller D, Guerreiro AS, Shalaby T, Jackson SP, Schoenwaelder SM, Delattre O, Grotzer MA, Fischer B: Novel role for insulin as an autocrine growth factor for malignant brain tumour cells. Biochem J; 2007 Aug 15;406(1):57-66
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] Novel role for insulin as an autocrine growth factor for malignant brain tumour cells.
  • AT/RTs (atypical teratoid/rhabdoid tumours) of the CNS (central nervous system) are childhood malignancies associated with poor survival rates due to resistance to conventional treatments such as chemotherapy.
  • We characterized a panel of human AT/RT and MRT (malignant rhabdoid tumour) cell lines for expression of RTKs (receptor tyrosine kinases) and their involvement in tumour growth and survival.
  • When compared with normal brain tissue, AT/RT cell lines overexpressed the IR (insulin receptor) and the IGFIR (insulin-like growth factor-I receptor).
  • Pharmacological inhibitors, neutralizing antibodies, or RNAi (RNA interference) targeting the IR impaired the growth of AT/RT cell lines and induced apoptosis.
  • Experiments using RNAi and isoform-specific pharmacological inhibitors established a key role for the class I(A) PI3K p110alpha isoform in AT/RT cell growth and insulin signalling.
  • Taken together, our results reveal a novel role for autocrine signalling by insulin and the IR in growth and survival of malignant human CNS tumour cells via the PI3K/Akt pathway.
  • [MeSH-major] Autocrine Communication. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Growth Substances / metabolism. Insulin / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Child, Preschool. Chromosomal Proteins, Non-Histone / metabolism. Culture Media, Serum-Free. DNA-Binding Proteins / metabolism. Down-Regulation / drug effects. Down-Regulation / genetics. Enzyme Activation / drug effects. Female. Humans. Infant. Isoenzymes / metabolism. Male. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Receptor, IGF Type 1 / metabolism. Receptor, Insulin / genetics. Receptor, Insulin / metabolism. Signal Transduction / drug effects. Transcription Factors / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • MedlinePlus Health Information. consumer health - Diabetes Medicines.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2006 Apr;26(7):2661-74 [16537910.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10123-7 [16287993.001]
  • [Cites] Cell. 2006 May 19;125(4):733-47 [16647110.001]
  • [Cites] Biosci Rep. 2006 Feb;26(1):7-17 [16779663.001]
  • [Cites] J Clin Invest. 2006 Jul;116(7):1761-6 [16823473.001]
  • [Cites] Drug News Perspect. 2006 Jun;19(5):261-72 [16941048.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Int J Cancer. 2006 Dec 1;119(11):2527-38 [16988940.001]
  • [Cites] Oncogene. 2007 Apr 5;26(16):2308-17 [17016438.001]
  • [Cites] Eur J Cancer. 2007 Jul;43(10):1581-9 [17446062.001]
  • [Cites] Annu Rev Cell Dev Biol. 2001;17:615-75 [11687500.001]
  • [Cites] Annu Rev Biochem. 2001;70:247-79 [11395408.001]
  • [Cites] Annu Rev Biochem. 2001;70:535-602 [11395417.001]
  • [Cites] Nature. 2002 Jan 24;415(6870):436-42 [11807556.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(16):5975-88 [12138206.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3461-7 [12429635.001]
  • [Cites] J Immunol. 2003 Mar 1;170(5):2647-54 [12594293.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6589-97 [14528284.001]
  • [Cites] Horm Metab Res. 2003 Nov-Dec;35(11-12):778-85 [14710358.001]
  • [Cites] Nat Rev Cancer. 2004 Feb;4(2):133-42 [14964309.001]
  • [Cites] Nature. 2004 Mar 25;428(6981):427-31 [15042091.001]
  • [Cites] Cancer Cell. 2004 Mar;5(3):231-9 [15050915.001]
  • [Cites] Am J Surg Pathol. 2004 May;28(5):644-50 [15105654.001]
  • [Cites] Science. 2004 Apr 23;304(5670):554 [15016963.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):505-18 [15229476.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2877-84 [15254056.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5048-50 [15289301.001]
  • [Cites] Clin Cancer Res. 2004 Sep 1;10(17):5940-8 [15355927.001]
  • [Cites] Biochem J. 1990 Sep 1;270(2):397-400 [2205203.001]
  • [Cites] J Biol Chem. 1992 Jul 5;267(19):13488-97 [1618850.001]
  • [Cites] Annu Rev Biochem. 1992;61:307-30 [1323236.001]
  • [Cites] EMBO J. 1993 Nov;12(11):4251-9 [7901001.001]
  • [Cites] Endocrinology. 1995 Apr;136(4):1459-67 [7534700.001]
  • [Cites] Endocr Rev. 1995 Feb;16(1):3-34 [7758431.001]
  • [Cites] Genes Dev. 1996 Sep 1;10(17):2117-30 [8804307.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5370-82 [8895581.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3777-82 [9108054.001]
  • [Cites] Trends Biochem Sci. 1997 Jul;22(7):267-72 [9255069.001]
  • [Cites] Nature. 1998 Jul 9;394(6689):203-6 [9671307.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):74-9 [9892189.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4240-5 [10200246.001]
  • [Cites] Hum Mol Genet. 1999 Dec;8(13):2359-68 [10556283.001]
  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2759-63 [10914721.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13796-800 [11095756.001]
  • [Cites] Pediatr Dev Pathol. 2001 Jan-Feb;4(1):23-31 [11200487.001]
  • [Cites] Mol Cell Biol. 2001 May;21(10):3598-603 [11313485.001]
  • [Cites] J Neurooncol. 2005 Dec;75(3):309-13 [16195799.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17745-50 [16301525.001]
  • [Cites] Oncogene. 2006 Feb 2;25(5):722-34 [16302003.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):1111-7 [16186793.001]
  • [Cites] Br J Cancer. 2006 Feb 27;94(4):465-8 [16450000.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3278-88 [10207053.001]
  • [Cites] Oncogene. 1999 Apr 15;18(15):2471-9 [10229198.001]
  • [Cites] Mod Pathol. 1999 Apr;12(4):379-85 [10229502.001]
  • [Cites] Endocrinology. 2005 Feb;146(2):552-7 [15550513.001]
  • [Cites] J Pathol. 2005 Jan;205(2):145-53 [15641016.001]
  • [Cites] J Clin Oncol. 2005 Mar 1;23(7):1491-9 [15735125.001]
  • [Cites] Nat Med. 2005 May;11(5):507-14 [15834429.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Aug-Oct;16(4-5):421-39 [15936977.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1432-40 [15878979.001]
  • [Cites] Nature. 2006 May 18;441(7091):366-70 [16625210.001]
  • (PMID = 17506723.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Culture Media, Serum-Free; 0 / DNA-Binding Proteins; 0 / Growth Substances; 0 / Insulin; 0 / Isoenzymes; 0 / RNA, Small Interfering; 0 / SMARCB1 protein, human; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1948991
  •  go-up   go-down


5. Witt TC, Lo SS, Timmerman RD: Successful treatment of a skull base malignant rhabdoid tumor with surgery, chemotherapy and gamma Knife-based stereotactic radiosurgery in a young child. Stereotact Funct Neurosurg; 2007;85(6):310-3
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of a skull base malignant rhabdoid tumor with surgery, chemotherapy and gamma Knife-based stereotactic radiosurgery in a young child.
  • Most childhood rhabdoid tumors occur in the kidney or central nervous system but they can occur in other sites and they usually run an aggressive clinical course.
  • We report a case of an 8-month-old boy with a right temporal bone rhabdoid tumor treated with surgery, chemotherapy and Gamma Knife-based stereotactic radiosurgery.
  • Gamma Knife-based stereotactic radiosurgery may have a role in the management of very young children with skull base tumors.
  • [MeSH-major] Radiosurgery. Rhabdoid Tumor / drug therapy. Rhabdoid Tumor / surgery. Skull Base Neoplasms / drug therapy. Skull Base Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Humans. Infant. Magnetic Resonance Imaging. Male. Stereotaxic Techniques / instrumentation

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • [ErratumIn] Stereotact Funct Neurosurg. 2010;88(6):389
  • (PMID = 17709987.001).
  • [ISSN] 1423-0372
  • [Journal-full-title] Stereotactic and functional neurosurgery
  • [ISO-abbreviation] Stereotact Funct Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


6. Rodini CO, Suzuki DE, Nakahata AM, Pereira MC, Janjoppi L, Toledo SR, Okamoto OK: Aberrant signaling pathways in medulloblastomas: a stem cell connection. Arq Neuropsiquiatr; 2010 Dec;68(6):947-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Medulloblastoma is a highly malignant primary tumor of the central nervous system.
  • It represents the most frequent type of solid tumor and the leading cause of death related to cancer in early childhood.
  • Current treatment includes surgery, chemotherapy and radiotherapy which may lead to severe cognitive impairment and secondary brain tumors.
  • New perspectives for therapeutic development have emerged with the identification of stem-like cells displaying high tumorigenic potential and increased radio- and chemo-resistance in gliomas.
  • From the clinical viewpoint, modulation of signaling pathways such as TGFβ, regulating neural stem cell proliferation and tumor development, might be attempted as an alternative strategy for future drug development aiming at more efficient therapies and improved clinical outcome of patients with pediatric brain cancers.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Neural Stem Cells / pathology. Signal Transduction. Transforming Growth Factor beta

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21243257.001).
  • [ISSN] 1678-4227
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta
  •  go-up   go-down


7. Marachelian A, Butturini A, Finlay J: Myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue for childhood central nervous system tumors. Bone Marrow Transplant; 2008 Jan;41(2):167-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue for childhood central nervous system tumors.
  • Myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue has been evaluated in the treatment of children and young adults with brain tumors for whom conventional therapy is either too toxic (for example, radiotherapy in infants) or ineffective (for example, recurrent malignant tumors).
  • With this strategy, myeloablative chemotherapy is administered to patients after initial surgery, and standard-dose chemotherapy.
  • The success of myeloablative chemotherapy depends on the histological type of tumor, extent of disease and of surgical resection, and response to prior chemotherapy.
  • Here, we review results of myeloablative chemotherapy with hematopoietic progenitor cell rescue in brain tumors of different histologies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / methods
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy / methods. Disease-Free Survival. Humans. Myeloablative Agonists / therapeutic use. Transplantation Conditioning. Transplantation, Autologous / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18176620.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myeloablative Agonists
  • [Number-of-references] 47
  •  go-up   go-down


8. Badruddoja MA, Keir ST, King I, Zeidner J, Vredenburgh JJ, Muhlbaier LH, Bigner DD, Friedman HS: Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice. Neuro Oncol; 2007 Jul;9(3):240-4
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] Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice.
  • The current study was designed to assess the activity of VNP40101M administered at a dose of 18 mg/kg daily for five days against a panel of human adult and pediatric CNS tumors growing subcutaneously or intracranially in athymic nude mice.
  • The results demonstrated statistically significant (p < 0.05) growth delays of 15.0, 8.3, 51.0, 60+, 60+, and 60+ days in subcutaneous xenografts derived from childhood glioblastoma multiforme (D-456 MG), childhood ependymoma (D-528 EP and D-612 EP), childhood medulloblastoma (D-425 MED), and adult malignant glioma (D-245 MG and D-54 MG), respectively, with corresponding tumor regressions in 10 of 10, 4 of 10, 8 of 10, 9 of 10, 9 of 10, and 10 of 10 treated mice, respectively.
  • Delayed toxicity was seen more than 60 days after treatment, with 23 deaths in 100 treated animals, despite a median weight loss of only 0.06%.
  • In mice bearing intracranial D-245 MG xenografts, treatment with VNP40101M at a dose of 18 mg/kg daily for five days produced a 50% increase in median survival compared with controls.
  • Additional experiments conducted against subcutaneous D-245 MG xenografts by using reduced doses of 13.5 or 9.0 mg/kg daily for five days demonstrated tumor growth delays of 82.2 and 53.5 days, with corresponding tumor regressions in 8 of 9 and 9 of 10 treated mice, respectively (all values, p < 0.001), with one toxic death.
  • These findings suggest that VNP40101M is active in the treatment of a wide range of human central nervous system tumors and warrants translation to the clinic.

  • 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] Cancer Chemother Pharmacol. 1994;34(2):171-4 [8194169.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5368-72 [2164681.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2933-6 [9230204.001]
  • [Cites] Invest New Drugs. 2005 Mar;23(2):123-35 [15744588.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Biochem Pharmacol. 2000 Feb 1;59(3):283-91 [10609557.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3033-8 [11306484.001]
  • [Cites] Int J Toxicol. 2002 Jan-Feb;21(1):23-38 [11936896.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):288-95 [14685775.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2908-17 [15131024.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Neurosurgery. 1979 Apr;4(4):308-14 [450229.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4189-95 [3390813.001]
  • [Cites] J Neurooncol. 1994;20(2):111-20 [7807189.001]
  • (PMID = 17522334.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / 5P50-NS20023-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Prodrugs; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
  • [Other-IDs] NLM/ PMC1907418
  •  go-up   go-down


9. Bouhoula A, Boubaker A, Kallel J, Chikili R, Kchir N, Khaldi M: [Central nervous system medulloepithelioma. A report of three cases]. Neurochirurgie; 2010 Oct;56(5):395-400

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Central nervous system medulloepithelioma. A report of three cases].
  • [Transliterated title] Le médulloépithéliome du système nerveux central. À propos de trois cas.
  • Central nervous system medulloepithelioma is a rare, highly malignant childhood tumor.
  • It might be confused with medulloblastoma or other primitive neuroectodermal tumors, but it is quite particular by its clinical, radiological, and pathological features.
  • Only two reported cases in the literature survived beyond 4 years after treatment by gross total resection and radiotherapy without chemotherapy.
  • Two patients underwent a gross-total resection followed by radiotherapy and survived more than 4 years after treatment.
  • The third case had, however, recurred twice within the 1st postoperative month despite a complete resection each time and metastasis to the lung developed.
  • Chemotherapy was then carried out after the third procedure and the patient died 7 months later.
  • [MeSH-major] Neuroectodermal Tumors, Primitive. Supratentorial Neoplasms

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20708758.001).
  • [ISSN] 1773-0619
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


10. Norris LS, Snodgrass S, Miller DC, Wisoff J, Garvin J, Rorke LB, Finlay JL: Recurrent central nervous system medulloepithelioma: response and outcome following marrow-ablative chemotherapy with stem cell rescue. J Pediatr Hematol Oncol; 2005 May;27(5):264-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent central nervous system medulloepithelioma: response and outcome following marrow-ablative chemotherapy with stem cell rescue.
  • Medulloepithelioma is a rare primitive neuroectodermal tumor of the central nervous system usually developing in childhood, displaying highly malignant behavior, with early progression or recurrence.
  • The purpose of this study was to evaluate the efficacy of high-dose, marrow-ablative chemotherapy with autologous hemopoietic stem cell rescue in the treatment of recurrent central nervous system medulloepithelioma.
  • Three young children with recurrent central nervous system medulloepithelioma received high-dose marrow-ablative chemotherapy with thiotepa and etoposide either alone (one patient) or with the addition of carboplatin (two patients).
  • One child with residual radiographic tumor at the time of treatment could be evaluated for response and showed complete resolution of leptomeningeal disease after receiving marrow-ablative chemotherapy.
  • Two children developed tumor recurrence at 2.0 and 5.5 months after receiving marrow-ablative chemotherapy.
  • The third child continues free of tumor beyond 12 years from treatment.
  • The authors' experience with marrow-ablative chemotherapy and autologous hemopoietic stem cell rescue suggests that this treatment strategy might be beneficially incorporated into the initial treatment approach for young children with medulloepithelioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / therapy. Central Nervous System Neoplasms / therapy. Neoplasm Recurrence, Local. Stem Cell Transplantation
  • [MeSH-minor] Child, Preschool. Combined Modality Therapy. Female. Humans. Magnetic Resonance Imaging. Male. Time Factors. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15891561.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


11. Zimmerman MA, Goumnerova LC, Proctor M, Scott RM, Marcus K, Pomeroy SL, Turner CD, Chi SN, Chordas C, Kieran MW: Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor. J Neurooncol; 2005 Mar;72(1):77-84
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor.
  • Atypical teratoid/rhabdoid tumors (AT/RT) are highly malignant lesions of childhood that carry a very poor prognosis.
  • AT/RT can occur in the central nervous system (CNS AT/RT) and disease in this location carries an even worse prognosis with a median survival of 7 months.
  • In spite of multiple treatment regimens consisting of maximal surgical resection (including second look surgery), radiation therapy (focal and craniospinal), and multi-agent intravenous, oral and intrathecal chemotherapy, with or without high-dose therapy and stem cell rescue, only seven long-term survivors of CNS AT/RT have been reported, all in patients with newly diagnosed disease.
  • For this reason, many centers now direct such patients, particularly those under 5 years of age, or those with recurrent disease, towards comfort care rather than attempt curative therapy.
  • We now report on four children, two with newly diagnosed CNS AT/RT and two with progressive disease after multi-agent chemotherapy who are long term survivors (median follow-up of 37 months) using a combination of surgery, radiation therapy, and intensive chemotherapy.
  • The chemotherapy component was modified from the Intergroup Rhabdomyosarcoma Study Group (IRS III) parameningeal protocol as three of the seven reported survivors in the literature were treated using this type of therapy.
  • Our four patients, when added to the three reported survivors in the literature using this approach, suggest that patients provided this aggressive therapy can significantly alter the course of their disease.
  • More importantly, we report on the first two survivors after relapse with multi-agent intravenous and intrathecal chemotherapy treated with this modified regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Neoplasm Recurrence, Local / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant / methods. Child. Child, Preschool. Female. Humans. Infant. Male. Radiotherapy, Adjuvant / methods. Remission Induction. Survival Analysis

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • 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
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1988;412(4):393-7 [3125680.001]
  • [Cites] Childs Nerv Syst. 1993 Jun;9(3):185-90; discussion 190 [8397069.001]
  • [Cites] J Neurooncol. 2001 Mar;52(1):49-56 [11451202.001]
  • [Cites] J Neurooncol. 2003 Jan;61(2):121-6 [12622450.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jul 15;41(5):1013-9 [9719110.001]
  • [Cites] Genes Chromosomes Cancer. 2000 May;28(1):31-7 [10738300.001]
  • [Cites] Arch Ophthalmol. 1967 Dec;78(6):709-13 [4294312.001]
  • [Cites] Surg Neurol. 1992 May;37(5):410-4 [1631771.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):37-40 [7459813.001]
  • [Cites] J Neurooncol. 1995;24(1):21-8 [8523069.001]
  • [Cites] Childs Nerv Syst. 1997 Jul;13(7):418-21 [9298280.001]
  • [Cites] Surv Ophthalmol. 1994 Jan-Feb;38(4):365-70 [8160109.001]
  • [Cites] Neuroradiology. 2000 May;42(5):363-7 [10872158.001]
  • [Cites] Semin Diagn Pathol. 1986 May;3(2):151-63 [3616219.001]
  • [Cites] J Neurooncol. 1999 May;43(1):63-70 [10448873.001]
  • [Cites] Med Pediatr Oncol. 1991;19(4):310-7 [2056976.001]
  • [Cites] J Neurosurg. 1990 Nov;73(5):710-4 [2213160.001]
  • [Cites] Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1989 Sep-Oct;30(5):316-22 [2484056.001]
  • [Cites] Acta Neuropathol. 1992;83(4):445-8 [1575023.001]
  • [Cites] J Neurooncol. 2000 May;48(1):41-5 [11026695.001]
  • [Cites] Can J Neurol Sci. 1994 Aug;21(3):273-7 [8000986.001]
  • [Cites] AJNR Am J Neuroradiol. 1993 Jan-Feb;14 (1):107-15 [8427070.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Jun-Jul;24(5):337-42 [12142780.001]
  • [Cites] Surg Neurol. 1993 Nov;40(5):429-34 [8211663.001]
  • [Cites] Neuropathol Appl Neurobiol. 2003 Jun;29(3):254-61 [12787322.001]
  • [Cites] J Neurooncol. 1998 Dec;40(3):265-75 [10066100.001]
  • [Cites] J Neurooncol. 1995;25(3):193-203 [8592169.001]
  • [Cites] AJNR Am J Neuroradiol. 1995 Sep;16(8):1727-8 [7502982.001]
  • [Cites] Pediatr Neurol. 1995 Jul;13(1):65-8 [7575853.001]
  • [Cites] Acta Neuropathol. 1996;91(6):578-86 [8781656.001]
  • [Cites] J Korean Med Sci. 2002 Oct;17(5):723-6 [12378033.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1993;422(1):81-5 [7679853.001]
  • [Cites] J Neurooncol. 2003 Feb;61(3):219-25 [12675315.001]
  • [Cites] Pediatr Radiol. 2003 Apr;33(4):275-7 [12709762.001]
  • [Cites] J Neurosurg. 1996 Jul;85(1):56-65 [8683283.001]
  • [Cites] Med Pediatr Oncol. 1999 May;32(5):389-91 [10219345.001]
  • [Cites] Cancer. 1991 Apr 15;67(8):2058-61 [2004323.001]
  • [Cites] Pediatr Neurosurg. 1995;22(4):214-22 [7619723.001]
  • [Cites] Ultrastruct Pathol. 1994 Jan-Apr;18(1-2):23-8 [8191632.001]
  • [Cites] J Neurooncol. 2001 Aug;54(1):53-6 [11763423.001]
  • [Cites] Neurology. 1991 Nov;41(11):1847-8 [1944923.001]
  • [Cites] Clin Neuropathol. 1991 Jan-Feb;10(1):1-10 [2015720.001]
  • [Cites] Childs Nerv Syst. 1987;3(6):379-81 [3450389.001]
  • [Cites] J Pediatr Hematol Oncol. 1995 Feb;17(1):71-5 [7743242.001]
  • [Cites] J Comput Assist Tomogr. 1990 May-Jun;14 (3):461-3 [2335617.001]
  • [Cites] Pediatr Neurosurg. 1994;21(4):232-6 [7865408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13796-800 [11095756.001]
  • [Cites] Pediatr Pathol. 1989;9(3):307-19 [2546137.001]
  • [Cites] Childs Nerv Syst. 2003 Apr;19(4):244-8 [12682757.001]
  • [Cites] Hum Pathol. 1987 Apr;18(4):332-7 [3030922.001]
  • [Cites] Am J Surg Pathol. 1998 Sep;22(9):1083-92 [9737241.001]
  • [Cites] Postgrad Med J. 1998 Jun;74(872):369-70 [9799897.001]
  • [Cites] Childs Nerv Syst. 2000 Apr;16(4):228-34 [10855521.001]
  • [Cites] Med Pediatr Oncol. 1992;20(3):258 [1637409.001]
  • (PMID = 15803379.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 37
  •  go-up   go-down


12. Roland JT Jr, Cosetti M, Liebman T, Waltzman S, Allen JC: Cochlear implantation following treatment for medulloblastoma. Laryngoscope; 2010 Jan;120(1):139-43
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cochlear implantation following treatment for medulloblastoma.
  • OBJECTIVES/HYPOTHESIS: Medulloblastoma is the most common pediatric malignant tumor of the central nervous system in children.
  • Treatment includes surgical excision, external beam radiation, and multiagent chemotherapy.
  • Otologic sequelae are common and may result from radiation and/or chemotherapy.
  • Profound sensorineural hearing loss (SNHL) is a known complication of neuro-oncologic treatment and may render these patients eligible for cochlear implantation (CI).
  • Issues of CI in this population, including diagnosis, treatment of preoperative middle ear disease, operative and postoperative course, performance data, and long-term tumor surveillance are highlighted and reviewed.
  • METHODS: Three patients treated for pediatric medulloblastoma with surgical resection, postoperative hyperfractioned craniospinal radiotherapy, and multiagent adjuvant chemotherapy who underwent cochlear implantation were identified.
  • Details of neuro-oncologic treatment and associated otologic complications are presented and analyzed.
  • Primary outcome assessment includes treatment of middle ear pathology, perioperative cochlear implant course, and postimplantation performance data.
  • RESULTS: Each patient required surgical treatment of chronic ear disease 4 to 16 years after chemoradiation.
  • All progressed to profound SNHL and were implanted 8 to 17 years post-neuro-oncologic treatment.
  • One patient developed postoperative wound dehiscence requiring operative closure.
  • CONCLUSIONS: Patients treated for pediatric medulloblastoma develop otologic sequelae, including profound SNHL, and may require cochlear implantation.
  • [MeSH-major] Brain Neoplasms / therapy. Cochlear Implantation. Hearing Loss, Sensorineural / surgery. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Humans. Retrospective Studies. Treatment Outcome


13. Sklar CA: Childhood brain tumors. J Pediatr Endocrinol Metab; 2002 May;15 Suppl 2:669-73
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] Childhood brain tumors.
  • Primary malignant tumors of the central nervous system (CNS) account for about 16% of all childhood malignancies.
  • These tumors are the second most common type of childhood cancer and the most frequent of the solid tumors.
  • CNS tumors are diverse, representing many histological types and arising in a variety of anatomic sites.
  • The most common malignant tumors include astrocytomas (52%), medulloblastomas/primitive neuroectodermal tumors (PNETs) (21%), gliomas (19%), and ependymomas (9%).
  • The current 5-year survival rate for all pediatric CNS tumors is 67%, but rates differ considerably among tumor types.
  • Treatment modalities also differ according to histological type.
  • Currently, about 25% of patients are treated with surgery alone, 40% undergo surgery plus radiation, and 30% are treated with surgery, radiation, and chemotherapy.
  • Survivors of childhood brain tumors are at substantial risk for increased morbidity and late mortality.
  • Five-year survivors of brain tumors are 13 times more likely to die than healthy age- and sex-matched peers.
  • Neurological, neurocognitive, and endocrine disturbances are the most prevalent disabilities observed among long-term survivors of pediatric brain tumors.
  • [MeSH-major] Brain Neoplasms / epidemiology
  • [MeSH-minor] Child. Humans. Hypothalamus / pathology. Pituitary Neoplasms / pathology. Treatment Outcome

  • 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 = 12092679.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 20
  •  go-up   go-down


14. Keir ST, Hausheer F, Lawless AA, Bigner DD, Friedman HS: Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice. Cancer Chemother Pharmacol; 2001 Jul;48(1):83-7
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] Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice.
  • PURPOSE: Camptothecins have emerged as an important new class of antitumor drugs.
  • Camptothecin derivatives such as CPT-11 and topotecan are commercially available and approved for the treatment of colorectal (CPT-11) and ovarian and small-cell lung cancer (topotecan).
  • This study was designed to test the efficacy of karenitecin, a novel highly lipophilic camptothecin derivative, against a panel of human tumor xenografts derived from adult and pediatric central nervous system malignancies growing in athymic nude mice.
  • METHODS: Xenografts evaluated were derived from childhood high-grade gliomas (D-212 MG, D-456 MG), adult high-grade gliomas (D-54 MG, D-245 MG), medulloblastomas (D-341 MED, D-487 MED), and ependymomas (D-528 EP, D-612 EP), as well as sublines with demonstrated resistance to procarbazine (D-245 MG (PR)) and busulfan (D-456 (BR)).
  • CONCLUSION: These preclinical studies confirm that karenitecin is active against human central nervous system xenografts and should undergo clinical evaluation in patients with malignant central nervous system tumors.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Camptothecin / therapeutic use. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11488529.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 24R60NVC41 / cositecan; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
  •  go-up   go-down


15. Chen ML, McComb JG, Krieger MD: Atypical teratoid/rhabdoid tumors of the central nervous system: management and outcomes. Neurosurg Focus; 2005 Jun 15;18(6A):E8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical teratoid/rhabdoid tumors of the central nervous system: management and outcomes.
  • OBJECT: Atypical teratoid/rhabdoid tumors (ATRTs) represent a relatively newly categorized neoplastic entity.
  • They commonly present in childhood, and have a rapidly progressive clinical course with a survival time of less than 1 year.
  • Treatment regimens have been nonuniform.
  • In this retrospective review of patients with ATRTs who were treated at the authors' institution according to a uniform protocol, the goal was to assess the efficacy of the treatment and its outcome.
  • Tumor location was cortical in four patients, in the pineal region in four, in the posterior fossa in two, and spinal in one.
  • In one patient disseminated disease was revealed on the initial imaging study; seven patients had disseminated tumor subsequently.
  • Treatment consisted of chemotherapy in 11 patients, chemotherapy and local radiation in five, and chemotherapy and craniospinal radiation in three.
  • The mean time to death was 24 months, and ranged from 2 to 67 months.
  • The median time to progression was 3.5 months.
  • CONCLUSIONS: Atypical teratoid/rhabdoid tumors are malignant lesions with rapid progression.
  • Further study is necessary to determine the efficacy of therapy.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Magnetic Resonance Imaging / methods. Male. Retrospective Studies. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16048294.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Morgenstern DA, Gibson S, Brown T, Sebire NJ, Anderson J: Clinical and pathological features of paediatric malignant rhabdoid tumours. Pediatr Blood Cancer; 2010 Jan;54(1):29-34
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] Clinical and pathological features of paediatric malignant rhabdoid tumours.
  • BACKGROUND: Malignant rhabdoid tumours (MRT) and their central nervous system (CNS) counterparts atypical teratoid/rhabdoid tumours (ATRT) are rare, highly aggressive malignant neoplasms of childhood.
  • Although there are isolated reports of long-term survival with intensive, multimodal therapy, outcomes are generally poor.
  • PROCEDURE: We conducted a retrospective review of all patients diagnosed with MRT/ATRT at Great Ormond Street Hospital over the 20 years from 1989 to 2009.
  • There were four long-term survivors (>30 months), all of whom received chemotherapy with or without surgical resection or radiotherapy.
  • CONCLUSIONS: In view of poor outcomes, there is a clear need for new treatment strategies and the identification of novel molecular targets for MRT/ATRT.
  • [MeSH-major] Rhabdoid Tumor / pathology. Teratoma / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Child. Combined Modality Therapy. Female. Humans. Immunoenzyme Techniques. Infant. Male. Neoplasm Staging. Prognosis. Radiotherapy. Retrospective Studies. Survival Rate. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19653294.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


17. Büyükpamukçu M, Varan A, Yazici N, Akalan N, Söylemezoğlu F, Zorlu F, Akyüz C, Kutluk MT: Second malignant neoplasms following the treatment of brain tumors in children. J Child Neurol; 2006 May;21(5):433-6
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] Second malignant neoplasms following the treatment of brain tumors in children.
  • We investigated retrospectively 992 children with central nervous system tumors who were treated at our center between 1970 and 2004.
  • All of the patients were treated by surgery, chemotherapy, and/or radiotherapy.
  • Six patients developed second malignant neoplasms, and their clinical and histopathologic characteristics are reviewed in this article.
  • The second malignant neoplasms were diagnosed as non-Hodgkin lymphoma, myelodysplastic syndrome, basal cell carcinoma, malignant melanoma, Kaposi sarcoma, and high-grade neuroectodermal tumor.
  • The median latency time was 3.03 years (range 0.39-22.93 years).
  • The outcome varied according to the histopathologic type of the second tumor.
  • The patients who developed non-Hodgkin lymphoma and myelodysplastic syndrome died of progressive disease.
  • The patients with second skin neoplasms are alive as of the time of this writing.
  • The patient with Kaposi sarcoma developed one of the rare reported second malignant neoplasms following a primary brain tumor in childhood.
  • A wide spectrum of second malignant neoplasms was detected after treatment of primary brain tumors with surgery, radiotherapy, and chemotherapy.
  • Long-term follow-up is therefore necessary for the child who has survived a primary central nervous system tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / therapy. Glioma / pathology. Glioma / therapy. Neoplasms, Second Primary / pathology
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. Male. 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 = 16901454.001).
  • [ISSN] 0883-0738
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Cavazos CM, Keir ST, Yoshinari T, Bigner DD, Friedman HS: Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts. Cancer Chemother Pharmacol; 2001 Sep;48(3):250-4
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] Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts.
  • PURPOSE: The in vivo antitumor activity of a novel topoisomerase I inhibitor, J-107088, was tested in athymic nude mice bearing subcutaneous or intracranial pediatric and adult malignant CNS tumor-derived xenografts.
  • The xenografts evaluated were derived from a childhood glioblastoma multiforme (D-456 MG), a childhood medulloblastoma (D-341 MED), an adult anaplastic astrocytoma (D-54 MG), an adult glioblastoma multiforme (D-245 MG), and a procarbazine-resistant subline of D-245 MG [D-245 MG (PR)].
  • Growth delays ranged from 7.6 days with D-245 MG to 62.1 days with D-456 MG (P < 0.001).
  • CONCLUSION: These results indicate that J-107088 may be active in the treatment of childhood and adult malignant brain tumors and provide the rationale for initiation of clinical trials with this agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Carbazoles / therapeutic use. Enzyme Inhibitors / therapeutic use. Glioma / drug therapy. Glucosides / therapeutic use. Indoles. Topoisomerase I Inhibitors
  • [MeSH-minor] Adult. Animals. Child. Female. Humans. Injections, Intraperitoneal. Injections, Subcutaneous. Male. Mice. Mice, Nude. Neoplasm Transplantation. Survival Rate. Transplantation, Heterologous. Treatment Outcome. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11592348.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 2RO1-NS30245-12; United States / NINDS NIH HHS / NS / 5P50-NS-20023-17; United States / NCI NIH HHS / CA / CA11898; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / Glucosides; 0 / Indoles; 0 / Topoisomerase I Inhibitors; 1V8X590XDP / edotecarin
  •  go-up   go-down


19. Wójcik M, Dolezal-Ołtarzewska K, Kumorowicz-Czoch M, Kalicka-Kasperczyk A, Januś D, Zygmunt-Górska A, Wojtyś J, Korab-Chrzanowska E, Kwiatkowski S, Starzyk J: [Long-term endocrine complications after brain tumor treatment--own experience]. Przegl Lek; 2010;67(11):1132-5
MedlinePlus Health Information. consumer health - Endocrine Diseases.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Long-term endocrine complications after brain tumor treatment--own experience].
  • BACKGROUND: Long-term endocrine complications affect approximately 40% of childhood cancer survivors.
  • THE AIM: The retrospective analysis of parameters of the endocrine system function up to 10 years after head radiotherapy (RT) and chemotherapy (CT) due to malignant solid tumor of the central nervous system.
  • MATERIAL AND METHODS: The analysis included 30 patients (15 girls; 15 boys) followed in Endocrine Outpatient Department, University Children's Hospital of Krakow for 1-10 years (mean 5.8 years) after completion of cancer therapy.
  • Late endocrine complications after malignant brain tumor treatment affect 66% of patients followed for 1-10 years after completion of RT.
  • That points to the necessity of long-term, regular followup of the patients after cancer treatment.
  • 3. In patients after head RT and CT in childhood, there is noted secondary obesity, with complications typical for metabolic syndrome.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Endocrine System Diseases / etiology. Radiation Injuries / complications

  • 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 = 21442963.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 12629-01-5 / Human Growth Hormone
  •  go-up   go-down


20. Gow KW, Lensing S, Hill DA, Krasin MJ, McCarville MB, Rai SN, Zacher M, Spunt SL, Strickland DK, Hudson MM: Thyroid carcinoma presenting in childhood or after treatment of childhood malignancies: An institutional experience and review of the literature. J Pediatr Surg; 2003 Nov;38(11):1574-80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid carcinoma presenting in childhood or after treatment of childhood malignancies: An institutional experience and review of the literature.
  • METHODS: The authors reviewed the medical records of 8 children with PTM and 17 children with STM referred to St Jude Children's Research Hospital between February 1962 and February 2002 for evaluation and treatment of malignant thyroid carcinoma.
  • Seventeen patients had thyroid carcinoma as a second malignant neoplasm after treatment for acute lymphoblastic leukemia (n = 6), Hodgkin's disease (n = 5), central nervous system tumor (n = 2), Wilms' tumor (n = 1), retinoblastoma (n = 1), non-Hodgkin's lymphoma (n = 1), or neuroblastoma (n = 1).
  • Twelve of the 17 patients (70.6%) had received radiation to the thyroid gland during therapy for the primary cancer.
  • At the time of this report, all 17 patients are alive and in continue to be free of disease.
  • CONCLUSIONS: Pediatric thyroid carcinoma is uncommon and responds well to current therapy.
  • Given the limited period of follow-up of our cohort of secondary malignant thyroid tumors that arise after childhood cancer, these lesions appear to have similar presentations and outcomes when compared with primary carcinomas and can therefore be managed in the same manner.
  • [MeSH-major] Adenocarcinoma, Follicular / epidemiology. Carcinoma, Papillary / epidemiology. Neoplasms, Second Primary / epidemiology. Thyroid Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Child. Cohort Studies. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / therapeutic use. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Neoplasms / drug therapy. Neoplasms / radiotherapy. Neoplasms, Radiation-Induced / epidemiology. Retrospective Studies. Tennessee / epidemiology. Thyroidectomy. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14614703.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
  • [Number-of-references] 49
  •  go-up   go-down


21. Hurwitz CA, Strauss LC, Kepner J, Kretschmar C, Harris MB, Friedman H, Kun L, Kadota R: Paclitaxel for the treatment of progressive or recurrent childhood brain tumors: a pediatric oncology phase II study. J Pediatr Hematol Oncol; 2001 Jun-Jul;23(5):277-81
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paclitaxel for the treatment of progressive or recurrent childhood brain tumors: a pediatric oncology phase II study.
  • PURPOSE: To assess the efficacy and define the toxicity of paclitaxel given at a dosage of 350 mg/m2 every 3 weeks as a 24-hour continuous infusion to children with recurrent or progressive primary brain tumors.
  • PATIENTS AND METHODS: Seventy-three eligible patients, ages 4 months to 19 years, with progressive or recurrent primary brain tumors were treated according to a Pediatric Oncology Group (POG) phase II protocol with paclitaxel (POG 9330).
  • Tumor histologic strata included: astrocytoma (n = 4), malignant glioma (n = 13), medulloblastoma (n = 16), brain stem glioma (n = 15), ependymoma (n = 13), and miscellaneous histologies (n = 12).
  • All patients had previous histologic confirmation of a primary intracranial or spinal cord tumor with magnetic resonance imaging or computed tomography documentation of unequivocally measurable progressive or recurrent disease.
  • All patients had received previous therapy including surgery, radiation therapy, and/or chemotherapy, but no patient had been previously treated on more than one phase II trial.
  • Patients were allowed to continue therapy for a total of 18 cycles in the absence of progressive disease or unacceptable toxicity.
  • RESULTS: Seventy-five patients were enrolled onto the POG 9330 protocol; two ineligible patients were removed from the study before receiving any therapy.
  • Toxicities included mild nausea, central nervous system toxicity, myelosuppression, and febrile neutropenia, including one septic death.
  • CONCLUSION: Paclitaxel is well tolerated in children with recurrent or progressive brain tumors at this dosage and schedule and may result in short-term disease stabilization in this patient population.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy. Paclitaxel / therapeutic use
  • [MeSH-minor] Adolescent. Astrocytoma / drug therapy. Astrocytoma / pathology. Child. Child, Preschool. Dexamethasone / therapeutic use. Disease Progression. Drug Hypersensitivity / prevention & control. Ependymoma / drug therapy. Ependymoma / pathology. Female. Glioma / drug therapy. Glioma / pathology. Humans. Immunosuppressive Agents / therapeutic use. Infant. Infratentorial Neoplasms / drug therapy. Infratentorial Neoplasms / pathology. Infusions, Intravenous. Male. Medulloblastoma / drug therapy. Medulloblastoma / pathology. Nausea / chemically induced. Neoplasm Recurrence, Local. Neutropenia / chemically induced. Remission Induction. Salvage Therapy. Treatment Failure

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11464982.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA03161; United States / NCI NIH HHS / CA / CA07431; United States / NCI NIH HHS / CA / CA15525; etc
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Immunosuppressive Agents; 7S5I7G3JQL / Dexamethasone; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


23. Leal-Leal CA, Rivera-Luna R, Flores-Rojo M, Juárez-Echenique JC, Ordaz JC, Amador-Zarco J: Survival in extra-orbital metastatic retinoblastoma:treatment results. Clin Transl Oncol; 2006 Jan;8(1):39-44
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] Survival in extra-orbital metastatic retinoblastoma:treatment results.
  • INTRODUCTION: Retinoblastoma (RB) is the most frequent malignant eye tumor in childhood.
  • The purpose of this paper is to present our 21-year clinical experience with metastatic extra ocular RB patients treated with 5 different chemotherapy schemas at a single Mexican Pediatric referral center.
  • The information analyzed included the delay in diagnosis after first symptoms, age, sex, ocular staging, and anatomic site of metastases, treatment scheme, initial response and status at the last contact or date of death.
  • The most common site of metastasis was central nervous system (83.9%).
  • From those patients treated with chemotherapy (n = 74), 89.2% presented a complete initial response (n = 66).
  • Early mortality occurred in 7 cases before any treatment.
  • Fifty-six received treatment and died with progressive disease.
  • All patients without radiotherapy died with tumor activity (n = 15).
  • The prevalent cause of death was tumor progression.
  • CONCLUSIONS: In our experience, metastatic RB has a very high mortality rate in spite of the use of different chemotherapy regimens.
  • [MeSH-major] Eye Neoplasms / mortality. Retinoblastoma / secondary
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / mortality. Bone Neoplasms / radiotherapy. Bone Neoplasms / secondary. Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / mortality. Central Nervous System Neoplasms / radiotherapy. Central Nervous System Neoplasms / secondary. Child. Child, Preschool. Cisplatin / administration & dosage. Cobalt Radioisotopes / therapeutic use. Combined Modality Therapy. Cranial Irradiation. Disease Progression. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Life Tables. Liver Neoplasms / drug therapy. Liver Neoplasms / mortality. Liver Neoplasms / secondary. Male. Mexico / epidemiology. Neoadjuvant Therapy. Proportional Hazards Models. Remission Induction. Retrospective Studies. Skull Neoplasms / drug therapy. Skull Neoplasms / mortality. Skull Neoplasms / radiotherapy. Skull Neoplasms / secondary. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Retinoblastoma.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3742-51 [15923571.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1847-50 [10561224.001]
  • [Cites] Med Pediatr Oncol. 2003 Mar;40(3):158-61 [12518344.001]
  • [Cites] Arch Dis Child. 1999 Feb;80(2):171-4 [10325735.001]
  • [Cites] S Afr Med J. 1997 Jul;87(7):885-9 [9259725.001]
  • [Cites] J Clin Oncol. 1995 Apr;13(4):902-9 [7707117.001]
  • [Cites] Cancer. 1994 Jul 15;74(2):722-32 [8033054.001]
  • [Cites] Cancer. 1988 Dec 1;62(11):2301-3 [3052786.001]
  • [Cites] Br J Cancer. 2001 Mar 2;84(5):604-10 [11237379.001]
  • [Cites] Ophthalmic Genet. 1999 Sep;20(3):189-91 [10520239.001]
  • [Cites] J Oral Maxillofac Surg. 1991 Oct;49(10):1120-3 [1890525.001]
  • [Cites] J Clin Oncol. 1996 May;14(5):1532-6 [8622068.001]
  • [Cites] Ann N Y Acad Sci. 1964 Apr 2;114(2):958-62 [5220131.001]
  • [Cites] Baillieres Best Pract Res Clin Haematol. 1999 Mar-Jun;12(1-2):247-59 [11000997.001]
  • [Cites] Pediatr Clin North Am. 1972 Nov;19(4):1141-55 [4343068.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):3956-62 [10632325.001]
  • [Cites] Am J Ophthalmol. 2002 May;133(5):716-8 [11992879.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1991 Fall;13(3):315-9 [1793158.001]
  • [Cites] Hematol Oncol Clin North Am. 1987 Dec;1(4):721-35 [3323180.001]
  • [Cites] Ophthalmology. 2003 Jun;110(6):1237-40 [12799253.001]
  • [Cites] Pediatr Hematol Oncol. 2003 Sep;20(6):473-6 [14631622.001]
  • [Cites] Ophthalmology. 1991 Feb;98(2):136-41 [2008269.001]
  • [Cites] Drugs. 1999 Dec;58(6):983-96 [10651386.001]
  • (PMID = 16632438.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cobalt Radioisotopes; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 24
  •  go-up   go-down


24. Schiavetti A, Clerico A, De Pasquale MD, Bernardini L, Moleti ML: Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2003 Jul;25(7):562-4
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] Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia.
  • Malignant brain tumors have been reported to occur in survivors of childhood acute lymphoblastic leukemia (ALL) more frequently than in the noncancer control population.
  • The strongest risk factor seems to be cranial radiotherapy, used as central nervous system (CNS) prophylaxis.
  • We report the case of a 9-year-old girl affected with metastatic medulloblastoma that developed 6 years after a diagnosis of acute lymphoblastic leukemia.
  • CNS prophylaxis for ALL consisted of intrathecal methotrexate plus cytarabine (20 administrations) and 4 courses of high-dose methotrexate (5g/m2).
  • The child, in first complete remission, was well until the occurrence of a second tumor.
  • She was treated for medulloblastoma with craniospinal radiotherapy and chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebellar Neoplasms / radiotherapy. Medulloblastoma / radiotherapy. Neoplasms, Second Primary / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Medulloblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12847325.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


25. Sun XF, Jiang WQ, Liu DG, Xia ZJ, Huang HQ, Zhang L, Li YH, Zhou ZM, Zhen ZJ, Xia Y, He YJ, Guan ZZ: [Efficacy of modified BFM-90 regimen on children and adolescents with T cell lymphoblastic lymphoma: a report of 20 cases]. Ai Zheng; 2004 Dec;23(12):1687-91
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Efficacy of modified BFM-90 regimen on children and adolescents with T cell lymphoblastic lymphoma: a report of 20 cases].
  • BACKGROUND & OBJECTIVE: T-cell lymphoblastic lymphoma in childhood and adolescence is an aggressive malignant disease with higher mortality.
  • METHODS: A total of 20 naive children and adolescents with T cell lymphoblastic lymphoma were enrolled, 7 in stage III, and 13 in stage IV.
  • All patients received modified BFM-90 regimen consisting of induction, consolidation and central nervous system prophylaxis, reinduced alleviation, and maintenance therapy.
  • Total treatment duration was 2 years.
  • The 2 patients with PR or PD died of tumor progression.
  • Of 2 patients at CR1 received APBSC, 1 relapsed after transplantation, but achieved CR and survived after salvage chemotherapy;1 survived all along.
  • Of other patients achieved CR, 5 relapsed; of these 5 patients, 1 survived after allogeneic stem cell transplantation, 1 survived after autologous stem cell transplantation, 3 died of progressive disease after chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Adolescent. Asparaginase / therapeutic use. Child. Child, Preschool. Cyclophosphamide / therapeutic use. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Female. Follow-Up Studies. Humans. Male. Methotrexate / therapeutic use. Neoplasm Recurrence, Local. Neoplasm Staging. Prednisone / therapeutic use. Remission Induction. Stem Cell Transplantation. Survival Rate. Treatment Outcome. Vincristine / therapeutic use

  • Genetic Alliance. consumer health - Lymphoblastic lymphoma.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15601561.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; AIEOP acute lymphoblastic leukemia protocol
  •  go-up   go-down


26. Indolfi P, Casale F, Carli M, Bisogno G, Ninfo V, Cecchetto G, Bagnulo S, Santoro N, Giuliano M, Di Tullio MT: Pleuropulmonary blastoma: management and prognosis of 11 cases. Cancer; 2000 Sep 15;89(6):1396-401
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Pleuropulmonary blastoma (PPB) is a rare and aggressive malignant tumor that affects children and adults.
  • This neoplasm is histologically characterized by primitive blastema and a malignant mesenchymal stroma that often demonstrates multidirectional differentiation.
  • Despite the introduction of multimodal therapy, the prognosis of patients with PPB remains poor.
  • METHODS: In the current study the authors reported on PPB cases from a national retrospective search performed in 18 Italian Associations for Pediatric Hematology and Oncology centers.
  • Clinical data, surgical notes, pathologic findings, and summaries of chemotherapy and radiotherapy were obtained from reports and correlated with outcome by standard statistical methods.
  • In three patients the PPB developed from other primary dysplastic diseases: cystic adenomatoid malformation in one case and congenital lung cysts in the other two cases.
  • Five patients experienced disease recurrences (local recurrence in three patients and distant metastasis in two patients, within the central nervous system and an intraocular location, respectively).
  • Patients with a type 2 histologic pattern and/or pleural involvement were found to have a worse outcome compared with patients without such features.
  • Event free survival at 2 years from the time of diagnosis was 45% for all patients.
  • CONCLUSIONS: PPB is an aggressive neoplasm of early childhood and to the authors' knowledge no adequate therapy has been defined to date for patients with PPB.
  • After making the diagnosis, the main goal of therapy should be radical surgery, even in patients with microscopic residual disease.
  • Because the response to chemotherapy is poor, the authors' experience suggests that chemotherapy should be given with local radiotherapy in the majority of patients.
  • [MeSH-major] Lung Neoplasms / therapy. Pleural Neoplasms / therapy. Pulmonary Blastoma / therapy
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Infant. Male. Prognosis. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Pleuropulmonary blastoma.
  • Genetic Alliance. consumer health - Blastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 11002236.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  •  go-up   go-down


27. Rossi A, Caracciolo V, Russo G, Reiss K, Giordano A: Medulloblastoma: from molecular pathology to therapy. Clin Cancer Res; 2008 Feb 15;14(4):971-6
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] Medulloblastoma: from molecular pathology to therapy.
  • Medulloblastoma is the most common malignant tumor of central nervous system in children.
  • Currently, multimodality treatment, including surgery, radiotherapy, and chemotherapy is considered as the most effective strategy against these malignant cerebellar tumors of the childhood.
  • Attempts to further reduce the morbidity and mortality associated with medulloblastoma have been restricted by the toxicity of conventional treatments and the infiltrative nature of the disease.
  • Over the past decade, new discoveries in molecular biology have revealed new insights in signaling pathways regulating medulloblastoma tumor formation.
  • Recent advances in the molecular biology of medulloblastoma indicate that the classification of these embryonal tumors, solely based on histology and clinical criteria, may not be adequate enough.
  • Better understanding of the growth control mechanisms involved in the development and progression of medulloblastoma will allow a better classification, leading to the improvement of the existing therapies, as well as to the development of new therapeutic approaches.

  • Genetic Alliance. consumer health - Medulloblastoma.
  • 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
  • [Cites] Cancer Res. 1996 Jan 15;56(2):377-83 [8542595.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jan;50(1):163-6 [16724315.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2085-8 [9187099.001]
  • [Cites] Cancer Res. 1999 Feb 1;59(3):711-9 [9973222.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):832-45 [10071274.001]
  • [Cites] Int J Clin Oncol. 2004 Dec;9(6):471-4 [15616877.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):978-86 [15758008.001]
  • [Cites] Oncogene. 2005 Jun 2;24(24):3923-31 [15806170.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):4975-8 [15958535.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):903-10 [15959507.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4215-22 [16618744.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 Sep;58(3):343-7 [16408203.001]
  • [Cites] J Clin Oncol. 1999 Jul;17(7):2127-36 [10561268.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):269-79 [10661332.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):383-9 [10667591.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):433-7 [10666372.001]
  • [Cites] Genes Chromosomes Cancer. 2000 May;28(1):77-81 [10738305.001]
  • [Cites] Genes Dev. 2000 Apr 15;14(8):994-1004 [10783170.001]
  • [Cites] Nat Med. 2000 Jul;6(7):826-31 [10888935.001]
  • [Cites] J Clin Oncol. 2000 Aug;18(16):3004-11 [10944134.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(23):9055-67 [11074003.001]
  • [Cites] J Clin Oncol. 2001 May 15;19(10):2696-704 [11352962.001]
  • [Cites] Mol Pathol. 2001 Oct;54(5):331-7 [11577176.001]
  • [Cites] Nat Genet. 2001 Oct;29(2):143-52 [11544480.001]
  • [Cites] Oncogene. 2002 Aug 29;21(38):5897-905 [12185589.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1559-61 [12202832.001]
  • [Cites] Int J Cancer. 2002 Sep 10;101(2):198-201 [12209999.001]
  • [Cites] Genes Dev. 2002 Nov 1;16(21):2743-8 [12414725.001]
  • [Cites] Development. 2003 Jan;130(1):15-28 [12441288.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):140-8 [12517790.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1581-91 [12697884.001]
  • [Cites] Pediatr Neurosurg. 2003 Dec;39(6):299-304 [14734863.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):984-93 [14970185.001]
  • [Cites] Lancet Oncol. 2004 Apr;5(4):209-18 [15050952.001]
  • [Cites] Neoplasia. 2004 Jul-Aug;6(4):310-22 [15256053.001]
  • [Cites] J Neurosurg. 1994 Nov;81(5):690-8 [7931615.001]
  • [Cites] J Neurooncol. 1994;19(2):169-73 [7964993.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5220-7 [16936740.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5263-7 [16936746.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5294-301 [16936750.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5333-40 [16936755.001]
  • [Cites] J Clin Oncol. 2006 Sep 1;24(25):4202-8 [16943538.001]
  • [Cites] Lancet Oncol. 2006 Oct;7(10):813-20 [17012043.001]
  • [Cites] J Cell Physiol. 2007 Jan;210(1):183-91 [16998811.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(17):3004-14 [16956759.001]
  • [Cites] Indian J Pathol Microbiol. 2006 Oct;49(4):535-9 [17183845.001]
  • [Cites] Lab Invest. 2007 Feb;87(2):97-103 [17211410.001]
  • [Cites] Nat Clin Pract Oncol. 2007 May;4(5):295-304 [17464337.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1814-23 [9164190.001]
  • (PMID = 18281528.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095518-08; United States / NCI NIH HHS / CA / R01 CA095518; United States / NCI NIH HHS / CA / R01 CA095518-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 50
  • [Other-IDs] NLM/ NIHMS279562; NLM/ PMC3222918
  •  go-up   go-down


28. Marchetti D, Mrak RE, Paulsen DD, Sinnappah-Kang ND: Neurotrophin receptors and heparanase: a functional axis in human medulloblastoma invasion. J Exp Clin Cancer Res; 2007 Mar;26(1):5-23
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) is the most common malignant brain tumor of childhood.
  • Although modern therapy has produced five-year survival rates as high as 70% for some MB patients, this resulted in significant long-term treatment-related morbidity.
  • Neurotrophins (NT) comprise a family of structurally and functionally related neurotrophic factors that are critical for central nervous system (CNS) development with nerve growth factor (NGF) being the prototypic NT.
  • NT acts through two groups of structurally unrelated neurotrophin receptors (NTR): a family of receptor tyrosine kinases (Trks, mainly TrkA, TrkB, and TrkC) and a tumor necrosis factor receptor (TNFR)-like molecule called p75NTR TrkC expression is a good prognostic indicator for MB.
  • Importantly, little is known about the biological functions of p75 in primitive neuroectodermal tumors such as MB.
  • In contrast, NT-regulated heparanase (HPSE) is a unique extracellular matrix-degrading enzyme known to be associated with tumor progression in a wide variety of cancers.
  • We provide evidence of a differential expression of HPSE in newly-developed medulloblastoma cell lines.
  • Finally, by using antibodies specific to TrkC and immunohistochemistry (IHC) we prove that IHC scores reveal a significant expression of HPSE in 76% of MB tissues from children aged 3 years and older.
  • Taken together, our data provide evidence that HPSE functionality, in a context linked to TrkC and p75NTR activation, may play critical roles in medulloblastoma tumor invasion and progression.
  • [MeSH-major] Cerebellar Neoplasms / metabolism. Glucuronidase / metabolism. Medulloblastoma / metabolism. Meningeal Neoplasms / metabolism. Receptors, Nerve Growth Factor / metabolism
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Infant. Male. NF-kappa B / metabolism. Neoplasm Invasiveness. Nerve Tissue Proteins / metabolism. Neurotrophin 3 / metabolism. Neurotrophin 3 / pharmacology. Phosphorylation. Prognosis. Receptor, trkC / metabolism

  • 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 = 17550129.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA086832; United States / NCI NIH HHS / CA / CA103955
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / NGFR protein, human; 0 / Nerve Tissue Proteins; 0 / Neurotrophin 3; 0 / Receptors, Nerve Growth Factor; EC 2.7.10.1 / Receptor, trkC; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
  •  go-up   go-down


29. Albert A, Cruz O, Montaner A, Vela A, Badosa J, Castañón M, Morales L: [Congenital solid tumors. A thirteen-year review]. Cir Pediatr; 2004 Jul;17(3):133-6
MedlinePlus Health Information. consumer health - Wilms Tumor.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Congenital solid tumors. A thirteen-year review].
  • Tumors diagnosed during the first month of life are infrequent: 0.5 to 2% of all childhood neoplasms.
  • This is an interesting group of tumors because their type, relative incidence, natural history and response to treatment differ from those seen in older children.
  • AIM: To contribute the experience of our institution in congenital tumors the last 13 years.
  • MATERIAL AND METHODS: The records of all neonates (< 31 days old) diagnosed with solid tumors since January 1990 to December 2002 have been retrospectively reviewed.
  • RESULTS: Twenty-seven neonates have been diagnosed with tumors in the last 13 years.
  • Neuroblastoma was the commonest tumor (10 cases, 37%), of which 4 were stage I, 4 stage IV-S and 2 stage III.
  • There were 8 teratomas (3 sacrocoxigeal, 1 retroperitoneal, 1 in the CNS, 1 orbitary and two oronasal), two hepatic tumors (1 hepatoblastoma, 1 hemangioendothelioma, two CNS tumors, two giant nevus (one on a hamartoma), and one each Wilms tumor, infantile fibrosarcoma and myofibroblastic tumor.
  • Treatment was surgical resection alone in 17 cases (68%) and surgery + chemotherapy in 8 (32%) (5 neuroblastomas, one CNS tumor, one Wilms tumor and one presacral teratoma who developed a yolk sac tumor); 3 patients died (11%): one at surgery, one of tumoural airway obstruction at birth and one with craniopharyngioma.
  • Among the 14 tumors that were initially not malignant, two can be locally agressive, one was an immature teratoma, the giant nevus with hamartoma developed in situ melanoma, the other nevus had meningeal melanosis with hydrocephalus, and one mature presacral teratoma developed a yolk sac tumor.
  • CONCLUSIONS: Diagnosis of congenital tumors is performed earlier in recent years due to the wide use of prenatal ultrasound.
  • Their natural history is more benign than in other age groups, except for CNS tumors and very large or obstructing tumors.
  • Complete surgical excision is the treatment of choice, most cases not need adjuvant chemotherapy.
  • [MeSH-major] Central Nervous System Neoplasms / congenital. Kidney Neoplasms / congenital. Liver Neoplasms / congenital. Neuroblastoma / congenital. Skin Neoplasms / congenital. Soft Tissue Neoplasms / congenital. Teratoma / congenital. Wilms Tumor / congenital
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Infant, Newborn. Male. Neoplasm Recurrence, Local. Postoperative Complications. Pregnancy. Prenatal Diagnosis. Time Factors

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15503950.001).
  • [ISSN] 0214-1221
  • [Journal-full-title] Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
  • [ISO-abbreviation] Cir Pediatr
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down






Advertisement