[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 34 of about 34
1. Melamud A, Palekar R, Singh A: Retinoblastoma. Am Fam Physician; 2006 Mar 15;73(6):1039-44
Genetic Alliance. consumer health - Retinoblastoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Retinoblastoma, a neuroblastic tumor, is the most common primary intraocular malignancy of childhood.
  • The mean age at diagnosis is 12 months for bilateral tumors and 24 months for unilateral tumors.
  • However, new diagnostic and treatment methods allow for a high cure rate (93 percent five-year survival in the United States), therefore it is important that primary care physicians recognize the manifestations of this malignancy.
  • Treatment modalities include laser thermotherapy, cryotherapy, radioactive plaques, external beam radiotherapy, chemotherapy, and enucleation.
  • [MeSH-minor] Combined Modality Therapy. Diagnosis, Differential. Genetic Predisposition to Disease. Humans. Prognosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Am Fam Physician. 2007 Apr 1;75(7):980
  • (PMID = 16570739.001).
  • [ISSN] 0002-838X
  • [Journal-full-title] American family physician
  • [ISO-abbreviation] Am Fam Physician
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
  •  go-up   go-down


2. Ulbright TM, Hattab EM, Zhang S, Ehrlich Y, Foster RS, Einhorn LH, Cheng L: Primitive neuroectodermal tumors in patients with testicular germ cell tumors usually resemble pediatric-type central nervous system embryonal neoplasms and lack chromosome 22 rearrangements. Mod Pathol; 2010 Jul;23(7):972-80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primitive neuroectodermal tumors in patients with testicular germ cell tumors usually resemble pediatric-type central nervous system embryonal neoplasms and lack chromosome 22 rearrangements.
  • Primitive neuroectodermal tumors (PNETs) are one of the most frequent types of 'non-germ cell' tumor in patients with testicular germ cell tumors and have a guarded prognosis when present in metastatic sites after cisplatin-based chemotherapy.
  • Improved treatments, including targeted therapy, require understanding the biology of these neoplasms.
  • We therefore analyzed the morphologic, immunohistochemical and molecular biologic features of 14 PNETs from 14 patients with concurrent or previous testicular germ cell tumors; 12 tumors were from metastatic sites and 2 were primary in the testis.
  • Using standard light microscopic criteria for central nervous system and peripheral PNETs, we classified nine tumors as medulloepithelioma, three as medulloblastoma/supratentorial PNET, one as neuroblastic tumor with abundant neuropil and true rosettes and one as small cell embryonal tumor/PNET (Ewing sarcoma-like).
  • INI1 was diffusely and strongly positive in all tumors whereas the other stains, except for cytoplasmic WT1 (which showed substantial reactivity in most tumors), were mostly focal to negative, including CD99 (eight negative, six focal) and Fli-1 (all negative).
  • Only 1 tumor, classified as medulloepithelioma, was scored positive for chromosome 22 translocation (22% rearranged cells) and the remaining 13 were negative, including the one case that resembled peripheral PNET.
  • We conclude that PNETs derived from testicular germ cell tumors mostly resemble central nervous system PNETs and generally lack the chromosome 22 translocation of peripheral PNETs.
  • Future treatment strategies should take these findings into account.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / pathology. Neoplasms, Multiple Primary / pathology. Neuroectodermal Tumors, Primitive, Peripheral / pathology. Testicular Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Chromosomes, Human, Pair 22 / genetics. Gene Rearrangement. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Young Adult

  • Genetic Alliance. consumer health - Chromosome 22.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20348883.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


3. Carvalho Ade C, Parra ER, Zerbini MC, Alves VA, Capelozzi VL, Antonangelo L: Morphometric evaluation of NB84, synaptophysin and AgNOR is useful for the histological diagnosis and prognosis in peripheral neuroblastic tumors (pNTs). Clinics (Sao Paulo); 2007 Dec;62(6):731-40
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] Morphometric evaluation of NB84, synaptophysin and AgNOR is useful for the histological diagnosis and prognosis in peripheral neuroblastic tumors (pNTs).
  • OBJECTIVE: To study the importance of NB84, synaptophysin and AgNOR and explore the quantitative association of these factors with diagnosis and outcome as well as the association between NB84 and AgNOR and other tumor and stromal factors in twenty-eight peripheral neuroblastic tumors.
  • METHODS: We assessed AgNORs, NB84, synaptophysin and several other markers in tumor tissues from 28 patients with primary neuroblastic tumors.
  • The treatment included: surgery for stage 1, chemotherapy and bone marrow transplantation for most of stages 3 and 4.
  • Histochemistry, immunohistochemistry and morphometry were used to evaluate the amount of tumor staining for AgNOR, NB84 and synaptophysin; the outcome for our study was survival time until death due to recurrent neuroblastic tumors.
  • CONCLUSIONS: Determination of NB84 and synaptophysin are useful tools for the diagnosis of peripheral neuroblastic tumors The association of the evaluation of AgNOR expression by the tumor cells may provide an important contribution to the prognostic evaluation and management approach of the patients.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Clinics. 2008 Apr;63(2):291
  • (PMID = 18209916.001).
  • [ISSN] 1807-5932
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Antigens, Nuclear; 0 / Ki-67 Antigen; 0 / Synaptophysin; 0 / nucleolar organizer region associated proteins
  •  go-up   go-down


Advertisement
4. Armstrong MB, Bian X, Liu Y, Subramanian C, Ratanaproeksa AB, Shao F, Yu VC, Kwok RP, Opipari AW, Castle VP: Signaling from p53 to NF-kappa B determines the chemotherapy responsiveness of neuroblastoma. Neoplasia; 2006 Nov;8(11):964-74
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] Signaling from p53 to NF-kappa B determines the chemotherapy responsiveness of neuroblastoma.
  • Neuroblastic (N) type neuroblastoma (NB) is the predominant cell type in NB tumors.
  • Previously, we determined that activated nuclear factor kappaB (NF-kappaB) is required for doxorubicin and etoposide to kill N-type NB cells.
  • The results show that p53 protein levels increase within 15 to 30 minutes of treatment.
  • Together, these results demonstrate for the first time how NF-kappaB is activated in NB cells in response to conventional drugs.
  • Furthermore, these findings provide an explanation as to why H-Ras expression correlates with a favorable prognosis in NB and identify intermediary signaling molecules that are targets for discovering treatments for NB that is resistant to conventional agents.

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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] Cancer Res. 1973 Nov;33(11):2643-52 [4748425.001]
  • [Cites] J Natl Cancer Inst. 1983 Oct;71(4):741-7 [6137586.001]
  • [Cites] Cancer Res. 1985 Apr;45(4):1628-32 [2983884.001]
  • [Cites] Cancer Res. 1987 Mar 1;47(5):1383-9 [3028608.001]
  • [Cites] Cancer Res. 1987 Dec 15;47(24 Pt 1):6505-10 [2445473.001]
  • [Cites] Prog Clin Biol Res. 1988;271:265-76 [2900511.001]
  • [Cites] Cancer Res. 1989 Jan 1;49(1):219-25 [2535691.001]
  • [Cites] Nucleic Acids Res. 1989 Aug 11;17(15):6419 [2771659.001]
  • [Cites] Cell. 1990 Dec 21;63(6):1129-36 [2175676.001]
  • [Cites] Cancer. 1991 Sep 15;68(6):1296-302 [1873783.001]
  • [Cites] J Biol Chem. 1993 Aug 25;268(24):17676-9 [8349650.001]
  • [Cites] Cell. 1993 Sep 24;74(6):957-67 [8402885.001]
  • [Cites] FASEB J. 1995 Jun;9(9):726-35 [7601337.001]
  • [Cites] J Biol Chem. 1995 Nov 10;270(45):26770-3 [7592913.001]
  • [Cites] Curr Opin Cell Biol. 1995 Dec;7(6):798-805 [8608010.001]
  • [Cites] Am J Surg Pathol. 1996 Jun;20(6):649-55 [8651343.001]
  • [Cites] J Biol Chem. 1997 Feb 14;272(7):4252-60 [9020141.001]
  • [Cites] J Biol Chem. 1997 Aug 22;272(34):21281-8 [9261139.001]
  • [Cites] J Biol Chem. 1997 Sep 26;272(39):24113-6 [9305854.001]
  • [Cites] Biochem Pharmacol. 1998 Jan 15;55(2):185-91 [9448741.001]
  • [Cites] J Immunol. 1998 Feb 15;160(4):1875-85 [9469449.001]
  • [Cites] Adv Cancer Res. 1998;74:49-139 [9561267.001]
  • [Cites] Oncogene. 1998 Dec 17;17(24):3137-43 [9872329.001]
  • [Cites] Cell Mol Life Sci. 1999 Jan;55(1):64-75 [10065152.001]
  • [Cites] Nat Med. 1999 May;5(5):554-9 [10229233.001]
  • [Cites] Cell Mol Life Sci. 1999 Aug 15;55(10):1230-54 [10487205.001]
  • [Cites] Trends Cell Biol. 2004 Nov;14(11):639-47 [15519853.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3631-52 [10550163.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(3):468-76 [10653862.001]
  • [Cites] Trends Cell Biol. 2000 Apr;10(4):147-54 [10740269.001]
  • [Cites] Nature. 2000 Apr 20;404(6780):892-7 [10786798.001]
  • [Cites] J Neurochem. 2000 Aug;75(2):532-9 [10899928.001]
  • [Cites] J Biol Chem. 2000 Sep 8;275(36):27823-31 [10880512.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):8-13 [11196202.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):679-86 [11212268.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):37-40 [11242034.001]
  • [Cites] EMBO J. 2001 Apr 17;20(8):1931-9 [11296226.001]
  • [Cites] J Neurochem. 2001 Apr;77(2):391-8 [11299301.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):6185-93 [11507071.001]
  • [Cites] Br J Pharmacol. 2001 Nov;134(5):1055-65 [11682454.001]
  • [Cites] J Biol Chem. 2001 Dec 28;276(52):48921-9 [11679590.001]
  • [Cites] Oncogene. 2002 Jan 3;21(1):1-8 [11791171.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):7920-8 [11773061.001]
  • [Cites] Nat Immunol. 2002 Mar;3(3):221-7 [11875461.001]
  • [Cites] J Natl Cancer Inst. 2002 Mar 6;94(5):358-68 [11880474.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):12710-7 [11821415.001]
  • [Cites] J Biol Chem. 2002 Nov 1;277(44):42144-50 [12198114.001]
  • [Cites] Science. 2002 Dec 6;298(5600):1911-2 [12471242.001]
  • [Cites] Oncogene. 2003 Jan 30;22(4):477-83 [12555061.001]
  • [Cites] EMBO J. 2003 Mar 17;22(6):1289-301 [12628922.001]
  • [Cites] Science. 2003 Mar 21;299(5614):1859-63 [12649474.001]
  • [Cites] Leukemia. 2003 Jul;17(7):1263-93 [12835716.001]
  • [Cites] Cell. 2004 Jan 23;116(2):235-46 [14744434.001]
  • [Cites] J Biol Chem. 2004 Jun 18;279(25):26115-25 [15073170.001]
  • [Cites] Cancer Res. 1970 Aug;30(8):2110-8 [5459762.001]
  • (PMID = 17215959.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007622; United States / NHLBI NIH HHS / HL / 2T32HL07622; United States / NCI NIH HHS / CA / CA697276-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC1764827
  •  go-up   go-down


5. Johnson TE, Toledano SR: Ganglioneuroblastoma metastatic to the orbit. Ophthal Plast Reconstr Surg; 2003 Jul;19(4):330-3
MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Treatment with chemotherapy alone resulted in complete regression of the tumors with over 7 years of follow-up.
  • Good prognostic indicators included her young age at diagnosis, DNA index of tumor cells of 1.4, and the histologic subtype of neuroblastic tumor.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / analysis. Female. Humans. Infant. Nerve Tissue Proteins / analysis. Skull Neoplasms / diagnosis. Skull Neoplasms / drug therapy. Skull Neoplasms / secondary

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12878887.001).
  • [ISSN] 0740-9303
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Nerve Tissue Proteins
  •  go-up   go-down


6. Rodriguez-Lopez AM, Xenaki D, Eden TO, Hickman JA, Chresta CM: MDM2 mediated nuclear exclusion of p53 attenuates etoposide-induced apoptosis in neuroblastoma cells. Mol Pharmacol; 2001 Jan;59(1):135-43
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.
  • The p53 gene in neuroblastoma tumors (NB) is rarely mutated but the protein accumulates in the cytoplasm.
  • Our data show etoposide induces complete trans-location of p53 to the nucleus and activation of apoptosis in the neuroblastic NB cell line SH-SY5Y (N-type), which expresses low levels of MDM2.
  • However, in Schwann cell-like SH-EP1 cells (S-type), which have up to 10-fold higher levels of MDM2, p53 accumulates in the cytoplasm and the cells are extremely resistant to etoposide-induced apoptosis.
  • Notably, when MDM2 expression is inhibited in S-type cells, with a phosphorothioated antisense oligonucleotide (AS5), then p53 accumulates in the nucleus and the SH-EP1 cells undergo apoptosis.
  • Surprisingly, induction of p21 and G1-arrest are not attenuated in S-type cells, despite the predominantly cytoplasmic location of p53.
  • These results demonstrate for the first time that hyperactive nuclear export of p53 attenuates chemotherapy-induced apoptosis in NB cells, and our findings suggest that inhibitors of MDM2 may enhance the therapeutic efficacy of etoposide by promoting apoptosis rather than trans-differentiation.
  • [MeSH-major] Apoptosis. Etoposide / pharmacology. Neuroblastoma / pathology. Nuclear Proteins. Proto-Oncogene Proteins / physiology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Cell Nucleus / metabolism. DNA Damage. Gene Silencing. Humans. Proto-Oncogene Proteins c-mdm2. Subcellular Fractions. Transcriptional Activation. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11125034.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  •  go-up   go-down


7. Shields CL, Meadows AT, Shields JA, Carvalho C, Smith AF: Chemoreduction for retinoblastoma may prevent intracranial neuroblastic malignancy (trilateral retinoblastoma). Arch Ophthalmol; 2001 Sep;119(9):1269-72
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemoreduction for retinoblastoma may prevent intracranial neuroblastic malignancy (trilateral retinoblastoma).
  • OBJECTIVE: To evaluate whether neoadjuvant intravenous chemotherapy (chemoreduction) for retinoblastoma reduces the risk for associated intracranial neuroblastic tumor (trilateral retinoblastoma).
  • MAIN OUTCOME MEASURE: Development of associated intracranial neuroblastic tumor (trilateral retinoblastoma).
  • RESULTS: During the 54-month study period, 142 patients (66%) received chemoreduction (consisting of vincristine sulfate, etoposide phosphate, and carboplatin therapy) as part of their treatment strategy (chemoreduction group), whereas 72 (34%) were treated with nonchemoreduction methods (nonchemoreduction group).
  • In the chemoreduction group, no associated intracranial neuroblastic tumor developed during the mean 47-month follow-up.
  • Based on a recent meta-analysis of the prevalence of trilateral retinoblastoma, we would have expected the intracranial tumor to develop in 5 to 15 patients with hereditary retinoblastoma.
  • In the nonchemoreduction group, associated intracranial tumor (pinealoblastoma) developed in 1 patient, a finding consistent with the expected frequency.
  • CONCLUSION: Chemoreduction protects against the highly fatal associated intracranial neuroblastic tumor (trilateral retinoblastoma).
  • This observation is especially important in children with bilateral or familial retinoblastoma who are at greatest risk for this brain tumor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / prevention & control. Pinealoma / prevention & control. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Carboplatin / administration & dosage. Child. Child, Preschool. Drug Administration Schedule. Etoposide / administration & dosage. Female. Humans. Infant. Male. Retrospective Studies. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Retinoblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Arch Ophthalmol. 2003 Oct;121(10):1513 [14557204.001]
  • (PMID = 11545631.001).
  • [ISSN] 0003-9950
  • [Journal-full-title] Archives of ophthalmology (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
  •  go-up   go-down


8. Garcia I, Mayol G, Rodríguez E, Suñol M, Gershon TR, Ríos J, Cheung NK, Kieran MW, George RE, Perez-Atayde AR, Casala C, Galván P, de Torres C, Mora J, Lavarino C: Expression of the neuron-specific protein CHD5 is an independent marker of outcome in neuroblastoma. Mol Cancer; 2010;9:277
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The chromodomain, helicase DNA-binding protein 5 (CHD5) is a potential tumor suppressor gene located on chromosome 1p36, a region recurrently deleted in high risk neuroblastoma (NB).
  • Previous data have shown that CHD5 mRNA is present in normal neural tissues and in low risk NB, nevertheless, the distribution of CHD5 protein has not been explored.
  • With this purpose, CHD5 protein expression was analyzed in normal neural tissues and neuroblastic tumors (NTs).
  • CHD5 gene and protein expression was reexamined after induction chemotherapy in a subset of high risk tumors to identify potential changes reflecting tumor response.
  • RESULTS: We provide evidence that CHD5 is a neuron-specific protein, absent in glial cells, with diverse expression amongst neuron types.
  • The prognostic value of CHD5 was confirmed in an independent, blinded set of 32 NB tumors (P < 0.001).Reactivation of CHD5 expression after induction chemotherapy was observed mainly in those high risk tumors with induced tumor cell differentiation features.
  • Remarkably, these NB tumors showed good clinical response and prolonged patient survival.
  • Re-establishment of CHD5 expression induced by chemotherapy could be a surrogate marker of treatment response.
  • [MeSH-major] DNA Helicases / metabolism. Gene Expression Regulation, Neoplastic. Nerve Tissue Proteins / metabolism. Neuroblastoma / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cerebellum / metabolism. Cerebral Cortex / metabolism. Ganglia, Sympathetic / metabolism. Humans. In Vitro Techniques. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2007 Feb 9;128(3):459-75 [17289567.001]
  • [Cites] Genome Biol. 2006;7(9):R84 [16989664.001]
  • [Cites] Lancet. 2007 Jun 23;369(9579):2106-20 [17586306.001]
  • [Cites] Oncogene. 2008 Jan 17;27(4):441-9 [17637744.001]
  • [Cites] Oncogene. 2008 Jan 31;27(6):803-10 [17667943.001]
  • [Cites] Annu Rev Pathol. 2008;3:341-65 [18039127.001]
  • [Cites] J Natl Cancer Inst. 2008 Jul 2;100(13):940-9 [18577749.001]
  • [Cites] Epigenetics. 2008 Jul-Aug;3(4):210-5 [18698156.001]
  • [Cites] BMC Cancer. 2009;9:44 [19192278.001]
  • [Cites] Cancer Cell. 2009 Apr 7;15(4):328-40 [19345331.001]
  • [Cites] Br J Cancer. 2009 May 5;100(9):1471-82 [19401703.001]
  • [Cites] Clin Cancer Res. 2009 May 15;15(10):3244-50 [19417027.001]
  • [Cites] Clin Cancer Res. 2010 Mar 1;16(5):1532-41 [20179214.001]
  • [Cites] J Clin Oncol. 2010 Jul 20;28(21):3506-15 [20567016.001]
  • [Cites] Mamm Genome. 2002 Feb;13(2):117-9 [11889561.001]
  • [Cites] Cereb Cortex. 2002 Jul;12(7):702-9 [12050082.001]
  • [Cites] Cancer Cell. 2002 Nov;2(5):377-86 [12450793.001]
  • [Cites] Oncogene. 2003 Feb 20;22(7):1002-11 [12592387.001]
  • [Cites] Dev Neurosci. 2003 Mar-Aug;25(2-4):139-51 [12966212.001]
  • [Cites] Clin Cancer Res. 2004 Jul 1;10(13):4307-13 [15240516.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(10):3753-7 [2566996.001]
  • [Cites] Cancer Res. 1992 Mar 1;52(5):1364-8 [1737399.001]
  • [Cites] N Engl J Med. 1993 Mar 25;328(12):847-54 [8441429.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1466-77 [8336186.001]
  • [Cites] Cancer. 1995 Sep 15;76(6):1086-95 [8625212.001]
  • [Cites] Cytogenet Cell Genet. 1996;72(2-3):114-44 [8978760.001]
  • [Cites] Eur J Cancer. 1997 Oct;33(12):2090-1 [9516859.001]
  • [Cites] Cancer. 1998 Oct 15;83(8):1626-33 [9781958.001]
  • [Cites] Clin Cancer Res. 1996 Aug;2(8):1361-7 [9816308.001]
  • [Cites] Cancer. 1999 Jul 15;86(2):364-72 [10421273.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1119-28 [15709179.001]
  • [Cites] J Clin Oncol. 2006 Nov 1;24(31):5070-8 [17075126.001]
  • [Cites] Mutat Res. 2007 May 1;618(1-2):30-40 [17350655.001]
  • (PMID = 20950435.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / CHD5 protein, human
  • [Other-IDs] NLM/ PMC2992029
  •  go-up   go-down


9. Lara-Bohórquez C, González-Cámpora R, Mendoza-García E, Ríos-Martín JJ, Pareja-Megía MJ, López-Beltrán A: TP53, BCL-2, p21Waf1/Cip1 and metallothionein as markers of differentiation, response to treatment and prognosis in neuroblastic tumors. Anal Quant Cytol Histol; 2008 Apr;30(2):105-12
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] TP53, BCL-2, p21Waf1/Cip1 and metallothionein as markers of differentiation, response to treatment and prognosis in neuroblastic tumors.
  • OBJECTIVE: To identify markers of response to therapy in neuroblastic tumors.
  • STUDY DESIGN: A total of 58 patients with neuroblastic tumor (38 neuroblastomas, 13 ganglioneuroblastomas and 7 ganglioneuromas) were included in the study.
  • TP53, BCL-2, p21Waf1/Cip1 and metallothionein were included as a biologic approach to tumor differentiation, response to therapy and prognosis.
  • All patients in whom treatment failed expressed metallothionein (3 of 3).
  • CONCLUSION: TP53, BCL-2, p21Waf1/Cip1 and metallothionein had limited value reflecting tumor maturation (differentiation) or predicting response to therapy.

  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18561747.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 9038-94-2 / Metallothionein
  •  go-up   go-down


10. De Ioris MA, Fidani P, Munier FL, Serra A, Ilari I, Popovic MB, Natali G, Secco DE, Cozza R: Successful treatment of trilateral retinoblastoma with conventional and high-dose chemotherapy plus radiotherapy: a case report. J Pediatr Hematol Oncol; 2010 Nov;32(8):e343-5
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] Successful treatment of trilateral retinoblastoma with conventional and high-dose chemotherapy plus radiotherapy: a case report.
  • Trilateral retinoblastoma (TRB) is a rare condition characterized by an intracranial neuroblastic tumor associated with bilateral or unilateral retinoblastoma (RB).
  • The child, considered inoperable by 2 different neurosurgical teams, was treated with conventional chemotherapy (methotrexate, vincristine, vepeside, cyclophosphamide, and carboplatin) plus tandem transplantation (vepeside/carboplatin and thiotepa/mephalan) followed by local radiotherapy.
  • An early and aggressive treatment may improve the prognosis of TRB.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pinealoma / drug therapy. Pinealoma / radiotherapy. Retinoblastoma / drug therapy. Retinoblastoma / radiotherapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Infant. Magnetic Resonance Imaging. Prognosis. Radiation Dosage. Radiotherapy. Remission Induction

  • Genetic Alliance. consumer health - Retinoblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20881869.001).
  • [ISSN] 1536-3678
  • [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. Ito A, Uno T, Gunji Y, Yamauchi T, Egami S, Kawarasaki H, Momoi MY: Obstructive jaundice as a presentation of ganglioneuroblastoma. J Pediatr Hematol Oncol; 2005 Feb;27(2):112-4
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Obstructive jaundice is a rare symptom in the neuroblastic tumor.
  • After the histologic diagnosis with open biopsy, chemotherapy consisting of cisplatin, pirarubicin hydrochloride/doxorubicin, cyclophosphamide, and vincristine was given.
  • The treatment resulted in reduction in the tumor size and relief of the obstructive jaundice.
  • Complete resection of the tumor was possible after five courses of chemotherapy.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Child, Preschool. Cisplatin / administration & dosage. Cyclophosphamide / administration & dosage. Humans. Male. Vincristine / administration & dosage

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15701990.001).
  • [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
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; D58G680W0G / pirarubicin; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


12. Antoneli CB, Ribeiro Kde C, Sakamoto LH, Chojniak MM, Novaes PE, Arias VE: Trilateral retinoblastoma. Pediatr Blood Cancer; 2007 Mar;48(3):306-10
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.
  • BACKGROUND: Trilateral retinoblastoma (TRB) is a syndrome consisting of unilateral or bilateral hereditary retinoblastoma (Rb) associated with an intracranial neuroblastic tumor.
  • This article reports four cases of TRB and discusses the role of neuroimaging screening for early detection.
  • PROCEDURE: From January 1986 to December 2003, 470 children with Rb were admitted to the Pediatrics and Ophthalmology Departments, A C Camargo Hospital, São Paulo, Brazil.
  • Three patients had bilateral disease and all of them had one eye enucleated, followed by chemotherapy and/or external beam radiation therapy (EBRT).
  • In spite of intensive treatment, all patients died with progressive disease within 7, 8, 12, and 12 months after diagnosis of TRB.
  • CONCLUSIONS: Early diagnosis as well as new therapeutic approaches are needed to achieve better results.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Cisplatin / administration & dosage. Combined Modality Therapy. Cranial Irradiation. Cyclophosphamide / administration & dosage. Disease Progression. Etoposide / administration & dosage. Eye Enucleation. Fatal Outcome. Female. Humans. Idarubicin / administration & dosage. Ifosfamide / administration & dosage. Male. Methotrexate / administration & dosage. Neoplastic Syndromes, Hereditary / genetics. Neoplastic Syndromes, Hereditary / pathology. Prognosis. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Retinoblastoma.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for trilateral retinoblastoma .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. IFOSFAMIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16572402.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide; YL5FZ2Y5U1 / Methotrexate; ZRP63D75JW / Idarubicin
  • [Number-of-references] 27
  •  go-up   go-down


13. De Bernardi B, Gambini C, Haupt R, Granata C, Rizzo A, Conte M, Tonini GP, Bianchi M, Giuliano M, Luksch R, Prete A, Viscardi E, Garaventa A, Sementa AR, Bruzzi P, Angelini P: Retrospective study of childhood ganglioneuroma. J Clin Oncol; 2008 Apr 1;26(10):1710-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: To review a historical cohort of childhood ganglioneuroma (GN), the benign representative of the peripheral neuroblastic tumor (PNT) family.
  • Histological revision was carried out on 76 tumors.
  • RESULTS: GNs differed from other PNTs for sex, age, tumor site, stage, tumor markers, and scintigraphic results.
  • Radical tumor resection and surgery-related complication rates were comparable for GN, GNBI, and nonreviewed instances.
  • Six patients developed tumor progression but survived.
  • Two patients developed a late malignancy but survived.
  • None of the 146 patients received chemotherapy.
  • CONCLUSION: Diagnosis was changed to GNBI for approximately one third of 76 reviewed tumors.
  • Survival was not influenced by extent of tumor resection.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18375900.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


14. Moukheiber AK, Nicollas R, Roman S, Coze C, Triglia JM: Primary pediatric neuroblastic tumors of the neck. Int J Pediatr Otorhinolaryngol; 2001 Aug 20;60(2):155-61
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] Primary pediatric neuroblastic tumors of the neck.
  • Neuroblastic tumors are the third most common cause of solid tumors in early childhood.
  • Cervical tumors account for only 5% of cases.
  • In this report, we describe a series of four pediatric neuroblastic tumors of the neck.
  • Cervical computed tomography scan and/or magnetic resonance imaging depicted calcifications within the tumor in 50% of cases and allowed accurate assessment of extension.
  • Scintigraphy with [131]iodine-methyliodobenzylguanidine demonstrated selective uptake by the tumor in two cases.
  • Surgical treatment was performed in all patients.
  • Neoadjuvant chemotherapy was performed in one case.
  • [MeSH-minor] Biopsy, Needle. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Magnetic Resonance Imaging. Male. Radionuclide Imaging / methods. Tomography, X-Ray Computed. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11518594.001).
  • [ISSN] 0165-5876
  • [Journal-full-title] International journal of pediatric otorhinolaryngology
  • [ISO-abbreviation] Int. J. Pediatr. Otorhinolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  •  go-up   go-down


15. Gambini C, Sementa AR, Boni L, Marino CE, Croce M, Negri F, Pistoia V, Ferrini S, Corrias MV: Expression of HER2/neu is uncommon in human neuroblastic tumors and is unrelated to tumor progression. Cancer Immunol Immunother; 2003 Feb;52(2):116-20
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] Expression of HER2/neu is uncommon in human neuroblastic tumors and is unrelated to tumor progression.
  • Neuroblastic tumors (NT) are the most frequently occurring extracranial solid tumors during childhood.
  • Novel treatments are therefore intensively sought and tumor-targeted immuno- and chemotherapy appear promising.
  • HER2/neu over-expression is frequently detected in breast tumors and constitutes an important unfavorable prognostic factor.
  • Expression of HER2/neu has also been reported to be a negative prognostic factor in a small survey of NT tumors.
  • HER2/neu over-expression was found in 2 human cell lines and 11 tumors (14% for both types of samples).
  • No significant association was found between HER2/neu expression and stage, age, sex, ploidy, histological type or subtype.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Humans. Mice. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12594575.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


16. Duhem-Tonnelle V, Vinchon M, Defachelles AS, Cotten A, Dhellemmes P: Mature neuroblastic tumors with spinal cord compression: report of five pediatric cases. Childs Nerv Syst; 2006 May;22(5):500-5
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] Mature neuroblastic tumors with spinal cord compression: report of five pediatric cases.
  • BACKGROUND: Neuroblastic tumors cause spinal cord compression when they arise primarily in the spinal canal or invade it through the radicular foramen.
  • Whereas neuroblastomas (NB) are relatively common and are generally treated with chemotherapy, mature neuroblastic tumors (MNT), which include intermixed ganglioneuroblastomas (iGNB) and ganglioneuromas (GN), are less common and the role of surgery is more prominent.
  • REPORT OF CASES: MNT represented 10% of spinal tumors and 1.6% of all tumors of the nervous system in our pediatric neurosurgical practice.
  • The neurological and oncological outcomes were generally favorable after surgical resection, followed by orthotic treatment.
  • In one case with neurofibromatosis type 1, the tumor was inoperable and the child died of tumor progression several years later.
  • Surgery is an emergency in case of rapidly progressing paraplegia and can be challenging because the tumor is often hard and hemorrhagic.
  • In case of subtotal removal, tumor remnants can stay stable without oncological treatment.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • [Cites] Nurs Mirror Midwives J. 1975 Nov 6;141(19):48-52 [1042886.001]
  • [Cites] Cancer. 2001 May 15;91(10 ):1905-13 [11346873.001]
  • [Cites] Cancer. 1996 Jul 15;78(2):311-9 [8674009.001]
  • [Cites] Med Pediatr Oncol. 1992;20(3):215-20 [1574031.001]
  • [Cites] Pediatr Neurosurg. 2003 Dec;39(6):291-8 [14734862.001]
  • [Cites] J Child Neurol. 1998 Jul;13(7):356-8 [9701489.001]
  • [Cites] Med Pediatr Oncol. 1999 May;32(5):353-9 [10219337.001]
  • [Cites] J Clin Neurosci. 2003 Sep;10(5):579-83 [12948463.001]
  • [Cites] Radiographics. 2002 Jul-Aug;22(4):911-34 [12110723.001]
  • [Cites] Cancer. 1989 Mar 15;63(6):1211-4 [2917322.001]
  • [Cites] Cancer. 1985 Oct 1;56(7 Suppl):1837-40 [4027922.001]
  • [Cites] AJNR Am J Neuroradiol. 1995 Apr;16(4 Suppl):875-7 [7611061.001]
  • [Cites] J Clin Oncol. 2001 Feb 15;19(4):1047-55 [11181668.001]
  • (PMID = 16369850.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


17. Eberhart CG, Brat DJ, Cohen KJ, Burger PC: Pediatric neuroblastic brain tumors containing abundant neuropil and true rosettes. Pediatr Dev Pathol; 2000 Jul-Aug;3(4):346-52
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] Pediatric neuroblastic brain tumors containing abundant neuropil and true rosettes.
  • We have encountered a series of seven unusual neuroblastic pediatric central nervous system (CNS) neoplasms with a unique constellation of histologic, immunohistochemical, and ultrastructural features.
  • The tumors presented in five girls and two boys, ages 1 to 3 years.
  • The tumors consisted of small to medium-sized, round to oval, hyperchromatic cells with poorly defined cytoplasmic borders.
  • Immunohistochemically, the neuropil-like areas as well as the perinuclear cytoplasm of many embryonal tumor cells were positive for synaptophysin and neurofilament protein.
  • Ultrastructurally, the tumor cells showed microtubule-containing neuronal processes, some with neurosecretory granules.
  • The clinical outcome was poor, with five patients dead from their disease 5 to 14 months after initial presentation and one patient with recurrent disease 7 months after resection and chemotherapy.
  • These lesions present distinctive histological features within the group of primitive neuroectodermal tumors.
  • [MeSH-major] Brain Neoplasms / pathology. Neuroectodermal Tumors, Primitive / pathology
  • [MeSH-minor] Apoptosis. Brain / metabolism. Brain / pathology. Child, Preschool. Female. Glial Fibrillary Acidic Protein / analysis. Humans. Infant. Magnetic Resonance Imaging. Male. Neutrophils. Rosette Formation. 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 = 10890250.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein
  •  go-up   go-down


18. Al-Hussain TO, Dababo MA: Posterior fossa tumor in a 2 year-old girl. Brain Pathol; 2009 Apr;19(2):343-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Posterior fossa tumor in a 2 year-old girl.
  • We report a case of a 2 year-old girl who presented with three weeks' history of deterioration of walking, then became unable to walk and later she developed projectile vomiting.
  • The tumor was diagnosed as an embryonal tumor with abundant neuropil and true rosettes (ETANTR).
  • The tumor cells in the neuroblastic component were diffusely positive for synaptophysin and CD56, with scattered positive cells for glial fibrillary acidic protein.
  • Ki67 showed high index (over 90%) in the true rosettes, while the neuroblastic areas were up to 15%.
  • Our patient developed recurrent disease 6 months after resection and chemotherapy.
  • ETANTR is a very rare aggressive embryonal CNS tumor that combines features of neuroblastoma and ependymoblastoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19291003.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


19. Armstrong MB, Bian X, Liu Y, Subramanian C, Ratanaproeksa AB, Shao F, Yu VC, Kwok RP, Opipari AW Jr, Castle VP: Signaling from p53 to NF-kappaB determines the chemotherapy responsiveness of neuroblastoma. Neoplasia; 2006 Nov;8(11):967-77
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] Signaling from p53 to NF-kappaB determines the chemotherapy responsiveness of neuroblastoma.
  • Neuroblastic (N) type neuroblastoma (NB) is the predominant cell type in NB tumors.
  • Previously, we determined that activated nuclear factor kappaB (NF-kappaB) is required for doxorubicin and etoposide to kill N-type NB cells.
  • The results show that p53 protein levels increase within 15 to 30 minutes of treatment.
  • Together, these results demonstrate for the first time how NF-kappaB is activated in NB cells in response to conventional drugs.
  • Furthermore, these findings provide an explanation as to why H-Ras expression correlates with a favorable prognosis in NB and identify intermediary signaling molecules that are targets for discovering treatments for NB that is resistant to conventional agents.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. NF-kappa B / metabolism. Neuroblastoma / drug therapy. Neuroblastoma / metabolism. Signal Transduction. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Doxorubicin / pharmacology. Etoposide / pharmacology. Humans. MAP Kinase Kinase 1 / metabolism. Mutation. Prognosis. Ribosomal Protein S6 Kinases, 90-kDa / metabolism

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • (PMID = 17132229.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / 2T32HL07622; United States / NCI NIH HHS / CA / CA697276-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; EC 2.7.11.1 / RPS6KA1 protein, human; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 90-kDa; EC 2.7.12.2 / MAP Kinase Kinase 1
  •  go-up   go-down


20. Aydin GB, Kutluk MT, Buyukpamukcu M, Akyuz C, Yalcin B, Varan A: Neurological complications of neuroblastic tumors: experience of a single center. Childs Nerv Syst; 2010 Mar;26(3):359-65
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] Neurological complications of neuroblastic tumors: experience of a single center.
  • AIM: This study aims to evaluate the prevalence and clinical characteristics of neurological complications in patients with newly diagnosed neuroblastic tumors (NT).
  • PATIENTS AND METHOD: Hospital file search was performed in patients with NT, and neurological complications, clinical, and treatment features were analyzed.
  • The incidence of sequelae after laminectomy, radiotherapy, and chemotherapy were 46.2%, 66.6%, and 13.6%, respectively.
  • No differences in neurological improvement in patients with SCC were found between those treated with radiotherapy, laminectomy, or chemotherapy alone, but laminectomy and radiotherapy caused significant late sequelae.
  • [MeSH-minor] Child. Child, Preschool. Female. Follow-Up Studies. Humans. Incidence. Infant. Male. Prevalence. Retrospective Studies. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neurologic Diseases.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Neuropharmacol. 1992 Jun;15(3):186-228 [1394242.001]
  • [Cites] Med Pediatr Oncol. 2003 Dec;41(6):570-1 [14595720.001]
  • [Cites] J Clin Oncol. 2001 Jan 1;19(1):183-90 [11134211.001]
  • [Cites] Med Pediatr Oncol. 2001 Jun;36(6):612-22 [11344492.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 May-Jun;21(3):181-9 [10363850.001]
  • [Cites] Cancer Lett. 2005 Oct 18;228(1-2):275-82 [15922508.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1466-77 [8336186.001]
  • [Cites] Cancer. 2003 Jul 1;98(1):155-65 [12833468.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Mar 1;61(3):865-9 [15708267.001]
  • [Cites] Cancer. 1996 Jul 15;78(2):311-9 [8674009.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Pediatr Neurosurg. 2003 Dec;39(6):291-8 [14734862.001]
  • [Cites] Cancer Lett. 2005 Oct 18;228(1-2):283-99 [15975710.001]
  • [Cites] J Clin Oncol. 1995 Sep;13(9):2330-5 [7666091.001]
  • [Cites] Med Pediatr Oncol. 1999 May;32(5):353-9 [10219337.001]
  • [Cites] Cancer. 1980 Jun 15;45(12 ):3095-101 [7388753.001]
  • [Cites] Cancer. 1971 Feb;27(2):374-8 [5100400.001]
  • [Cites] J Pediatr Hematol Oncol. 2009 Jul;31(7):471-80 [19564739.001]
  • [Cites] Cancer. 2001 Apr 15;91(8):1510-9 [11301399.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Sep 1;57(1):177-83 [12909231.001]
  • [Cites] Med Pediatr Oncol. 2003 Feb;40(2):139 [12461808.001]
  • [Cites] Med Pediatr Oncol. 1992;20(2):149-55 [1734220.001]
  • [Cites] Childs Nerv Syst. 1998 Dec;14(12):713-8 [9881624.001]
  • [Cites] J Clin Oncol. 2001 Feb 15;19(4):1047-55 [11181668.001]
  • [Cites] Childs Nerv Syst. 2009 Jan;25(1):63-9 [18843494.001]
  • [Cites] Cancer. 1991 Nov 1;68(9):1999-2006 [1913549.001]
  • [Cites] Med Pediatr Oncol. 1997 Apr;28(4):284-8 [9078325.001]
  • (PMID = 19714340.001).
  • [ISSN] 1433-0350
  • [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


21. Oppenheimer O, Alaminos M, Gerald WL: Genomic medicine and neuroblastoma. Expert Rev Mol Diagn; 2003 Jan;3(1):39-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Neuroblastic tumors are a broad biological and clinical spectrum of neoplastic disease that has long captured the attention of clinicians and scientists alike.
  • It is the most common solid extracranial tumor in children and accounts for 8-10% of all childhood tumors.
  • Tumors are derived from neural crest cells and neural differentiation is common.
  • Stage 4 is a systemic disease with widespread metastasis that responds to chemotherapy but many develop resistance.
  • Prognosis correlates with age, stage and tumor biological profile.
  • The goal of this review is to provide an overview of the disease and highlight diagnostic, prognostic and therapeutic advances in neuroblastoma.
  • Recommendations and resources for the evaluation and treatment of this disease are outlined.
  • [MeSH-minor] Biomarkers, Tumor. Genetic Techniques. Humans. Mutation

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12528363.001).
  • [ISSN] 1473-7159
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 207
  •  go-up   go-down


22. Burattini S, Luchetti F, Battistelli M, Della Felice M, Papa S, Piersanti G, Tarzia G, Falcieri E: 5-(2-Ethyl-phenyl)-3-(3-methoxy-phenyl)-1H-[1,2,4]triazole (DL-111-IT) and related compounds induce apoptotic patterns in cultures of human tumor cell lines. J Biol Regul Homeost Agents; 2003 Oct-Dec;17(4):348-57

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 5-(2-Ethyl-phenyl)-3-(3-methoxy-phenyl)-1H-[1,2,4]triazole (DL-111-IT) and related compounds induce apoptotic patterns in cultures of human tumor cell lines.
  • Polyamine depletion has been frequently related to the induction of apoptosis and consequently we investigated DL-111-IT and analogs for this effect in myeloid (HL60), neuroblastic (SK-N-MC) and epithelial (BeWo) human tumor cell lines, by means of electron microscopy and DNA electrophoresis.
  • Our results indicate that the contragestational effect of DL-111-IT and analogs is associated with apoptotic deletion of chorionic tissue and that these molecules, due to their effect on human tumor cell lines, can be considered as antiblastic lead compounds.
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. DNA / chemistry. Electrophoresis, Agar Gel. Enzyme Inhibitors / pharmacology. Epithelial Cells. HL-60 Cells. Humans. Microscopy, Electron. Models, Chemical. Necrosis. Neoplasms / drug therapy. Ornithine Decarboxylase Inhibitors. Polyamines / chemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15065766.001).
  • [ISSN] 0393-974X
  • [Journal-full-title] Journal of biological regulators and homeostatic agents
  • [ISO-abbreviation] J. Biol. Regul. Homeost. Agents
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Immunosuppressive Agents; 0 / Ornithine Decarboxylase Inhibitors; 0 / Polyamines; 0 / Triazoles; 69095-83-6 / 3-(2-ethylphenyl)-5-(3-methoxyphenyl)-1H-1,2,4-triazole; 9007-49-2 / DNA
  •  go-up   go-down


23. Lonergan GJ, Schwab CM, Suarez ES, Carlson CL: Neuroblastoma, ganglioneuroblastoma, and ganglioneuroma: radiologic-pathologic correlation. Radiographics; 2002 Jul-Aug;22(4):911-34
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Neuroblastoma, ganglioneuroblastoma, and ganglioneuroma are tumors of the sympathetic nervous system that arise from primitive sympathogonia and are referred to collectively as neuroblastic tumors.
  • They arise wherever sympathetic tissue exists and may be seen in the neck, posterior mediastinum, adrenal gland, retroperitoneum, and pelvis.
  • The three tumors differ in their degree of cellular and extracellular maturation; immature tumors tend to be aggressive and occur in younger patients (median age, just under 2 years), whereas mature tumors occur in older children (median age, approximately 7 years) and tend to behave in a benign fashion.
  • The most benign tumor is the ganglioneuroma, which is composed of gangliocytes and mature stroma.
  • Neuroblastoma is the most immature, undifferentiated, and malignant tumor of the three.
  • Thus, these neuroblastic tumors vary widely in their biologic behavior.
  • Features such as DNA content, tumor proto-oncogenes, and catecholamine synthesis influence prognosis, and their presence or absence aids in categorizing patients as high, intermediate, or low risk.
  • Treatment consists of surgery and, usually, chemotherapy.
  • Despite recent advances in treatment, including bone marrow transplantation, neuroblastoma remains a relatively lethal tumor, accounting for 10% of pediatric cancers but 15% of cancer deaths in children.
  • [MeSH-minor] Ganglioneuroblastoma / pathology. Ganglioneuroblastoma / radiography. Humans. Magnetic Resonance Imaging. Neoplasm Staging. Prognosis. Risk Factors. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright RSNA, 2002
  • (PMID = 12110723.001).
  • [ISSN] 0271-5333
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 123
  •  go-up   go-down


24. Bourdeaut F, de Carli E, Timsit S, Coze C, Chastagner P, Sarnacki S, Delattre O, Peuchmaur M, Rubie H, Michon J, Neuroblastoma Committee of the Société Française des Cancers et Leucémies de l'Enfant et de l'Adolescent: VIP hypersecretion as primary or secondary syndrome in neuroblastoma: A retrospective study by the Société Française des Cancers de l'Enfant (SFCE). Pediatr Blood Cancer; 2009 May;52(5):585-90
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] VIP hypersecretion as primary or secondary syndrome in neuroblastoma: A retrospective study by the Société Française des Cancers de l'Enfant (SFCE).
  • BACKGROUND: Neuroblastic tumors (NTs) are occasionally associated with watery diarrhea, due to Vasoactive Intestinal Peptide (VIP) secretion.
  • In 16 cases, digestive symptoms preceded the diagnosis of the tumor ("Primary VIP secreting NTs"); 15 were localized and all showed a differentiated histology.
  • Interestingly, in another 6 patients with high-risk NT, diarrhea occurred at the time of chemotherapy or retinoic acid therapy ("Secondary VIP secreting NTs").
  • Differentiation in response to treatment was documented in 4 cases.
  • In all cases, only surgical excision of the tumor was able to control the digestive symptoms.
  • CONCLUSION: VIP secreting NTs are usually associated with differentiation; they can also secondarily arise from a high-risk tumor upon treatment.
  • Primary surgery constitutes first-line treatment.

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • 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
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19143025.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 37221-79-7 / Vasoactive Intestinal Peptide
  •  go-up   go-down


25. Bégaud-Grimaud G, Battu S, Lazcoz P, Castresana JS, Jauberteau MO, Cardot PJ: Study of the phenotypic relationship in the IMR-32 human neuroblastoma cell line by sedimentation field flow fractionation. Int J Oncol; 2007 Oct;31(4):883-92
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.
  • Neuroblastoma (NB) is the most common childhood solid tumor.
  • Cell type heterogeneity is observed either in the morphological appearance of NB tumors or in cell lines isolated from tumor specimens.
  • NB consists of two principal neoplastic cell types: i) neuroblastic or N-type (undifferentiated cells); and ii) stromal or S-type (differentiated cells).
  • As NB cells seem to have the capacity to differentiate spontaneously in vivo and in vitro, their heterogeneity could affect treatment outcome, in particular the response to apoptosis induced by chemotherapy.
  • Therefore, it is important to understand the underlying process governing changes in differentiation in order to improve treatment response and NB patient outcome and the neoplastic population in IMR-32 represented a good model for such a study.
  • The first N-phenotype forms a pool of quiescent undifferentiated cells while the second one was able to proliferate (incorporation of BrdU) and also give rise to adherent S-type cells (PSA-N-CAM+ and N-CAM+).
  • [MeSH-minor] Bromodeoxyuridine. Cell Adhesion. Cell Lineage. Cell Proliferation. Flow Cytometry. Fluorescent Antibody Technique. Humans. Kinetics. Neural Cell Adhesion Molecule L1 / metabolism. Phenotype. Sialic Acids / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • Hazardous Substances Data Bank. BROMODEOXYURIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17786321.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecule L1; 0 / Sialic Acids; 0 / polysialyl neural cell adhesion molecule; G34N38R2N1 / Bromodeoxyuridine
  •  go-up   go-down


26. Sterba J: Contemporary therapeutic options for children with high risk neuroblastoma. Neoplasma; 2002;49(3):133-40
Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Contemporary therapeutic options for children with high risk neuroblastoma.
  • Despite the use of aggressive chemotherapy, stage 4 high risk neuroblastoma still has a very poor prognosis, which is estimated at 25%.
  • Therefore, novel treatment approaches are needed.
  • Increasing number of reports has been concerned with the use of novel treatment modalities.
  • Literature regarding intensive induction, local therapy, myeloablative therapy and immunotherapy and biotherapy was reviewed in order to draw conclusions and recommendations for the management of children with high risk neuroblastic tumors.
  • [MeSH-major] Neuroblastoma / therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Bone Marrow Purging. Bone Marrow Transplantation. Child. Gangliosides / immunology. Humans. Isotretinoin / therapeutic use

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12097996.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Gangliosides; 65988-71-8 / ganglioside, GD2; EH28UP18IF / Isotretinoin
  • [Number-of-references] 64
  •  go-up   go-down


27. Pérel Y, Valteau-Couanet D, Michon J, Lavrand F, Coze C, Bergeron C, Notz A, Plantaz D, Chastagner P, Bernard F, Thomas C, Rubie H: [Prognosis of neuroblastoma in childhood. Methods of assessment and clinical use]. Arch Pediatr; 2004 Jul;11(7):834-42
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.
  • Neuroblastoma and its benign counterpart, ganglioneuroma, are pediatric neuroblastic tumors arising in the sympathetic nervous system from neural-crest cells.
  • Neuroblastoma, the most common extra-cranial solid tumour during childhood, is unique for its broad spectrum of clinical virulence from spontaneous remission to rapid and fatal progression despite intensive multimodality therapy.
  • However, a number of molecular events in neuroblastoma tumors, accounting for the variability of outcome and response to therapy, have been identified over the past decades.
  • Among these, MYCN amplification is the most relevant prognostic factor and was the first genetic marker, in paediatric oncology, to be included in clinical strategies as a guide for therapeutic decision.
  • This has allowed the most suitable intensity of therapy to be delivered according to a risk-stratified strategy, from observation to megadose chemotherapy with stem cell transplantation.
  • Recent advances in understanding the biology and genetics of neuroblastoma will ultimately allow to select poor-risk patients for appropriate future biologically based therapies.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Humans. Infant. Infant, Newborn. Patient Selection. Prognosis. Risk Factors. Stem Cell Transplantation

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15234382.001).
  • [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] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 71
  •  go-up   go-down


28. Veeramachaneni R, Herrera GA, Turbat-Herrera EA: Hepatoblastoma in a 15-month-old male: cytomorphology, electron microscopy, and differential diagnosis. Ultrastruct Pathol; 2003 Sep-Oct;27(5):369-73
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The authors describe a case of hepatoblastoma in a 15-month-old male and discuss the differential diagnosis and electron microscopic features of small round cell tumors.
  • Electron microscopic analysis performed on the liver aspirate showed features of hepatic differentiation as well as absence of neuroblastic differentiation.
  • Liver biopsy performed subsequently showed tumor cells arranged in nests, acini, and trabeculae with mitotic figures.
  • The patient underwent chemotherapy for 4 months and subsequently a partial liver resection was performed.
  • This case illustrates the important role of electron microscopy in evaluating small round cell tumors in children.
  • [MeSH-minor] Biopsy, Needle. Combined Modality Therapy. Diagnosis, Differential. Drug Therapy. Hepatomegaly / etiology. Hepatomegaly / pathology. Humans. Infant. Male. Microscopy, Electron. Neuroblastoma / diagnosis. alpha-Fetoproteins / analysis

  • Genetic Alliance. consumer health - Hepatoblastoma.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14708729.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
  •  go-up   go-down


29. Lange TS, Singh RK, Kim KK, Zou Y, Kalkunte SS, Sholler GL, Swamy N, Brard L: Anti-proliferative and pro-apoptotic properties of 3-bromoacetoxy calcidiol in high-risk neuroblastoma. Chem Biol Drug Des; 2007 Oct;70(4):302-10
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.
  • NB, predominantly a tumor of early childhood, is the most common extracranial solid tumor.
  • Despite aggressive treatments, survival for advanced stages remains low and novel treatment strategies are needed.
  • B3CD-induced apoptosis in various neuroblastic cells via caspases-3 and -9 activation.
  • Accordingly, B3CD treatment dose dependently reduced the viability of NB cells with IC50 values between 1 and 3 microm.
  • Further studies revealed that B3CD treatment inhibits the proliferation of NB cells at low concentrations (IC50 between 30 and 100 nm).
  • These results suggest that B3CD could be developed as a treatment for NB.

  • Genetic Alliance. consumer health - Neuroblastoma.
  • Genetic Alliance. consumer health - Neuroblastoma 3.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biochem. 2003 Aug 1;89(5):909-16 [12874825.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Sep 14;361(1):189-95 [17658477.001]
  • [Cites] J Clin Oncol. 1999 Jul;17(7):2264-79 [10561284.001]
  • [Cites] Nat Cell Biol. 1999 Jul;1(3):E73-9 [10559915.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(1):18-26 [10623689.001]
  • [Cites] Curr Pharm Des. 2000 May;6(7):701-16 [10828302.001]
  • [Cites] Curr Pharm Des. 2000 May;6(7):717-32 [10828303.001]
  • [Cites] Cell. 2000 Jul 7;102(1):43-53 [10929712.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4864-72 [11406564.001]
  • [Cites] Onkologie. 2001 Apr;24(2):128-33 [11441291.001]
  • [Cites] J Mol Med (Berl). 2001 Aug;79(8):428-36 [11511973.001]
  • [Cites] J Cell Biol. 2002 Apr 29;157(3):441-53 [11980919.001]
  • [Cites] Nephron. 2002 Aug;91(4):576-81 [12138257.001]
  • [Cites] Cancer Lett. 2002 Aug 8;182(1):53-9 [12175523.001]
  • [Cites] J Cell Biochem. 2003 Feb 1;88(2):267-73 [12520525.001]
  • [Cites] J Cell Biochem. 2003 Feb 1;88(2):274-81 [12520526.001]
  • [Cites] Oncologist. 2003;8(3):278-92 [12773750.001]
  • [Cites] Curr Cancer Drug Targets. 2004 Feb;4(1):65-75 [14965268.001]
  • [Cites] Acta Pol Pharm. 2003 Sep-Oct;60(5):363-6 [15005419.001]
  • [Cites] Paediatr Drugs. 2004;6(2):107-22 [15035651.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2774-84 [15077141.001]
  • [Cites] Methods Enzymol. 1975;36:374-410 [162994.001]
  • [Cites] Metab Bone Dis Relat Res. 1981;3(1):43-6 [6894958.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):3976-85 [8358726.001]
  • [Cites] J Clin Oncol. 1993 Nov;11(11):2226-33 [8229138.001]
  • [Cites] Mol Cell Biol. 1994 Jan;14(1):759-67 [8264643.001]
  • [Cites] Arch Biochem Biophys. 1996 Sep 1;333(1):139-44 [8806764.001]
  • [Cites] Science. 1996 Dec 6;274(5293):1659-64 [8939847.001]
  • [Cites] Scand J Clin Lab Invest Suppl. 1997;227:35-45 [9127467.001]
  • [Cites] Cell. 1997 Nov 14;91(4):479-89 [9390557.001]
  • [Cites] EMBO J. 1998 Jan 2;17(1):37-49 [9427739.001]
  • [Cites] EMBO J. 1998 Mar 16;17(6):1675-87 [9501089.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1256-64 [9552023.001]
  • [Cites] Nutr Rev. 1998 Feb;56(2 Pt 2):S4-10; discussion S 54-75 [9564171.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1312-6 [9721091.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1322-6 [9735050.001]
  • [Cites] Am J Kidney Dis. 1998 Oct;32(2 Suppl 2):S13-24 [9808140.001]
  • [Cites] N Engl J Med. 1999 Oct 14;341(16):1165-73 [10519894.001]
  • [Cites] Curr Opin Cell Biol. 2004 Dec;16(6):639-46 [15530775.001]
  • [Cites] Biochim Biophys Acta. 2004 Dec 10;1705(1):43-51 [15585172.001]
  • [Cites] Clin Cancer Res. 2004 Dec 1;10(23):8018-27 [15585637.001]
  • [Cites] J Biol Chem. 2005 Mar 11;280(10):9474-81 [15632181.001]
  • [Cites] Curr Cancer Drug Targets. 2005 Jun;5(4):273-83 [15975048.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):160-2 [14522248.001]
  • (PMID = 17937776.001).
  • [ISSN] 1747-0277
  • [Journal-full-title] Chemical biology & drug design
  • [ISO-abbreviation] Chem Biol Drug Des
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R21 NS051408; United States / NINDS NIH HHS / NS / NS051408-01A2; United States / NCRR NIH HHS / RR / 1-P20RR018728; United States / NINDS NIH HHS / NS / R21 NS051408-01A2; United States / NINDS NIH HHS / NS / 1R21NS051408-01A2; United States / NCRR NIH HHS / RR / P20 RR018728
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 3-bromoacetoxycalcidiol; 0 / Biomarkers; 0 / Bone Density Conservation Agents; 0 / Bromine Compounds; FXC9231JVH / Calcitriol; P6YZ13C99Q / Calcifediol
  • [Other-IDs] NLM/ NIHMS34759; NLM/ PMC2519607
  •  go-up   go-down


30. Huang D, Rutkowski JL, Brodeur GM, Chou PM, Kwiatkowski JL, Babbo A, Cohn SL: Schwann cell-conditioned medium inhibits angiogenesis. Cancer Res; 2000 Nov 1;60(21):5966-71
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.
  • Neuroblastomas are biologically heterogeneous tumors that consist of two main cell populations: neuroblastic/ganglionic cells and Schwann cells.
  • The amount of Schwannian stroma strongly impacts prognosis, and favorable outcome is associated with tumors that are Schwannian stroma rich/stroma dominant.
  • At the present time, there is controversy regarding the origin of Schwann cells in neuroblastoma tumors.
  • However, recent studies have suggested that the Schwann cells in mature neuroblastoma tumors may be normal cells that produce soluble substances that enhance the survival and differentiation of neuroblastoma cell lines.
  • In contrast, tumors with favorable histology and abundant Schwannian stroma had low tumor vascularity.
  • As a first step toward investigating whether Schwann cells also play a role in inhibiting angiogenesis in neuroblastoma tumors, we examined the ability of conditioned medium collected from normal human Schwann cells to affect basic fibroblast growth factor- and vascular endothelial growth factor-induced endothelial cell proliferation and migration and in vivo angiogenesis.
  • In vitro angiogenesis assays were also performed with conditioned medium collected from Schwann cells derived from a Schwannian stroma-dominant neuroblastoma tumor.
  • Our results indicate that Schwann cells derived from either adult nerve or tumor tissue produce a potent inhibitor(s) of angiogenesis.
  • Expression studies revealed tissue inhibitor of metalloproteinase (TIMP)-2 in conditioned medium collected from both normal and tumor-derived Schwann cells.
  • In addition, TIMP-2 was detected in the cytoplasm of Schwann cells and ganglion cells in stroma-rich/stroma-dominant neuroblastoma tumors by immunohistochemistry studies.
  • We postulate that the low level of vascularity and more benign clinical behavior of Schwannian stroma-rich/stroma-dominant neuroblastoma tumors result from the Schwann cell production of TIMP-2 and/or other inhibitors of angiogenesis.
  • [MeSH-major] Angiogenesis Inhibitors / biosynthesis. Culture Media, Conditioned. Neovascularization, Physiologic / drug effects. Schwann Cells / metabolism
  • [MeSH-minor] Adult. Animals. Cell Division / physiology. Cell Movement / physiology. Corneal Neovascularization / chemically induced. Corneal Neovascularization / drug therapy. Endothelial Growth Factors / pharmacology. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Female. Fibroblast Growth Factor 2 / pharmacology. Ganglioneuroma / blood supply. Ganglioneuroma / pathology. Humans. Lymphokines / pharmacology. Rats. Rats, Sprague-Dawley. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11085514.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA60553; United States / NCI NIH HHS / CA / CA74824
  • [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 / Angiogenesis Inhibitors; 0 / Culture Media, Conditioned; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2
  •  go-up   go-down


31. Corapcioglu F, Mutlu H, Kara B, Inan N, Akansel G, Gürbüz Y, Topcu S: Response to rituximab and prednisolone for opsoclonus-myoclonus-ataxia syndrome in a child with ganglioneuroblastoma. Pediatr Hematol Oncol; 2008 Dec;25(8):756-61
Hazardous Substances Data Bank. PREDNISOLONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Opsoclonus-myoclonus-ataxia (OMA) syndrome is a rare neurobehavioral paraneoplastic disorder in children with neuroblastic tumors.
  • Rituximab therapy was started and continued for total 8 weeks without any side effect.
  • The authors observed excellent neurologic response in the patient at the 4th week of treatment.
  • Rituximab is a new, promising, and safe therapy for OMA syndrome in children with neuroblastoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Ganglioneuroblastoma / drug therapy. Opsoclonus-Myoclonus Syndrome / drug therapy. Prednisolone / therapeutic use


32. Then C, Ebelt K, Langer A, Mayr D, Schmidmaier R, Oduncu F: Neuroblastoma in a 55-year-old patient: a case report. Case Rep Oncol; 2010 Sep;3(3):458-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Neuroblastomas account for 97% of all neuroblastic tumors and for approximately 15% of all pediatric cancer fatalities.
  • RESULTS: The patient received six cycles of a chemotherapy protocol with cisplatin, etoposide and vindesine alternating with vincristine, dacarbazine, ifosfamide and doxorubicin, but the response to treatment was insufficient (stable disease).
  • CONCLUSION: The standard chemotherapy protocols used for children are not sufficient for adult patients.
  • Different treatment approaches are needed to improve the prognosis of adult patients with neuroblastoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Lett. 2005 Oct 18;228(1-2):271-4 [15916849.001]
  • [Cites] Cancer Lett. 2005 Oct 18;228(1-2):257-66 [16024170.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2885-90 [16682723.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2891-6 [16782928.001]
  • [Cites] Health Phys. 2007 Jan;92(1):33-9 [17164597.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1019-29 [17283134.001]
  • [Cites] Paraplegia. 1989 Oct;27(5):394-401 [2601990.001]
  • [Cites] Pediatr Surg Int. 2009 Sep;25(9):789-93 [19629500.001]
  • [Cites] J Pediatr Oncol Nurs. 2009 Jul-Aug;26(4):208-16 [19726792.001]
  • [Cites] Cir Cir. 2009 Sep-Oct;77(5):397-401 [19944030.001]
  • [Cites] Oncogene. 2010 Mar 4;29(9):1249-59 [20101214.001]
  • [Cites] Cancer. 1986 Jun 15;57(12):2419-21 [3697939.001]
  • [Cites] Cancer. 1997 May 15;79(10):2028-35 [9149032.001]
  • [Cites] Zhongguo Dang Dai Er Ke Za Zhi. 2008 Aug;10(4):464-6 [18706162.001]
  • (PMID = 21611143.001).
  • [ISSN] 1662-6575
  • [Journal-full-title] Case reports in oncology
  • [ISO-abbreviation] Case Rep Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3100267
  • [Keywords] NOTNLM ; Chemotherapy / Multiple myeloma / Neuroblastoma / Response to treatment
  •  go-up   go-down


33. Arnesen T, Thompson PR, Varhaug JE, Lillehaug JR: The protein acetyltransferase ARD1: a novel cancer drug target? Curr Cancer Drug Targets; 2008 Nov;8(7):545-53
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] The protein acetyltransferase ARD1: a novel cancer drug target?
  • Triggering the induction of apoptosis or reducing the proliferative rate will potentially be helpful for cancer treatment.
  • Furthermore, hARD1 knockdown induced apoptosis or sensitized cells to drug induced apoptosis. hARD1 acts in complex with the NATH protein and catalyzes cotranslational acetylation of protein N-termini.
  • NATH was originally identified as upregulated in thyroid papillary carcinomas and has lately also been found to correlate with aggressiveness and differentiation status of neuroblastic tumours.
  • Thus, hARD1 or the hARD1-NATH complex stands out as attractive drug targets in cancer treatment.
  • [MeSH-major] Acetyltransferases / antagonists & inhibitors. Acetyltransferases / metabolism. Antineoplastic Agents / administration & dosage. Drug Delivery Systems / trends. Growth Inhibitors / administration & dosage. Neoplasms / drug therapy. Neoplasms / enzymology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Cell Line, Tumor. Enzyme Inhibitors / administration & dosage. Humans. N-Terminal Acetyltransferase A. N-Terminal Acetyltransferase E

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • 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 = 18991565.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Growth Inhibitors; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.88 / N-Terminal Acetyltransferase A; EC 2.3.1.88 / N-Terminal Acetyltransferase E; EC 2.3.1.88 / NAA10 protein, human
  • [Number-of-references] 75
  •  go-up   go-down


34. Armstrong MB, Schumacher KR, Mody R, Yanik GA, Opipari AW Jr, Castle VP: Bortezomib as a therapeutic candidate for neuroblastoma. J Exp Ther Oncol; 2008;7(2):135-45
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bortezomib as a therapeutic candidate for neuroblastoma.
  • Outcomes remain poor in neuroblastoma despite intensive treatment.
  • Agents with potential efficacy can be drawn from anti-neoplastic drugs introduced for other malignancies.
  • Bortezomib, alone and in combination with other agents, was tested across an in vitro panel of neuroblastic, stromal, and chemo-resistant neuroblastoma cell types to determine its effect on cell viability and to assess for interactions between bortezomib and other chemotherapeutic agents that either limit or increase overall response.
  • Interestingly, the different cell types exhibited varying response patterns to treatment with bortezomib alone and in combination with other drugs suggesting different mechanisms may be engaged.
  • A decision analysis, incorporating these results showing efficacy in all cell types, the synergy obtained in combination, and the available toxicity data, supports a phase II clinical trial of bortezomib in neuroblastoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology. Brain Neoplasms / drug therapy. Neuroblastoma / drug therapy. Pyrazines / pharmacology
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic. Bortezomib. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Carboplatin / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Cisplatin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Genes, p53 / drug effects. Humans. NF-kappa B / metabolism

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18771087.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / 2T32HL07622; United States / NCI NIH HHS / CA / CA697276-04
  • [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 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Boronic Acids; 0 / NF-kappa B; 0 / Pyrazines; 69G8BD63PP / Bortezomib; 7673326042 / irinotecan; 80168379AG / Doxorubicin; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
  •  go-up   go-down






Advertisement