A proposed staging for children with neuroblastoma.Children's cancer study group A

Evans, Audrey E.; D’Angio, Giulio J.; Randolph, Judson G.

doi:10.1002/1097-0142(197102)27:2<374::aid-cncr2820270221>3.0.co;2-g

Cited by 902 publications

(265 citation statements)

References 8 publications

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“…Thus, classification of a tumor as stage 1 indicates a tumor mass that is completely confined to the organ or structure in which it originated. Stages 2, 3, and 4 indicate progressive degrees of metastatic spread of tumor cells beyond the orimary site (Evans et al, 1971). Analysis of tumor DNAs from patients having different stages of neuroblastoma disease has clearly shown that genomic amplification of the N-myc gene is more frequent in the more advanced stages of disease (Brodeur et al, 1984;Seeger et al, i985).…”

Section: Discussionmentioning

confidence: 99%

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

Bernards

Dessain

Weinberg

1986

Cell

262

151

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Section: Discussionmentioning

confidence: 99%

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

Bernards

Dessain

Weinberg

1986

Cell

262

151

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“…The clinical stages in NB patients were according to Evan's staging system. 31 All patients were in stage IV and N-myc amplification ranged from 20 to 50 copies. Histologic sections of tumors from NB specimens were evaluated for stromal cells, neuroblastic differentiation and categorized as having favorable or unfavorable histology.…”

Section: Cam Assaymentioning

confidence: 99%

Inhibition of neuroblastoma-induced angiogenesis by fenretinide

et al. 2001

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Retinoids are a class of natural or synthetic compounds that participate in the control of cell proliferation, differentiation and fetal development. The synthetic retinoid fenretinide (HPR) inhibits carcinogenesis in various animal models. Retinoids have also been suggested to be effective inhibitors of angiogenesis. The effects of HPR on certain endothelial cell functions were investigated in vitro, and its effects on angiogenesis was studied in vivo, by using the chorioallantoic membrane (CAM) assay. HPR inhibited vascular endothelial growth factor-(VEGF-) and fibroblast growth factor-2-(FGF-2)-induced endothelial cell proliferation without affecting endothelial motility; moreover, HPR inhibited growth factor-induced angiogenesis in the CAM assay. Furthermore, a significant antiangiogenic potential of HPR has also been observed in neuroblastoma (NB) biopsy-induced angiogenesis in vivo. We previously demonstrated that supernatants derived from NB cell lines stimulated endothelial cell proliferation. In the present study, we found that this effect was abolished when NB cells were incubated in the presence of HPR. VEGF-and FGF-2-specific ELISA assays, performed on both NB cells derived from conditioned medium and cellular extracts, indicated no consistent effect of HPR on the level of these angiogenic cytokines. Moreover, RT-PCR analysis of VEGF and FGF-2 gene expression confirmed the above lack of effect. HPR was also able to significantly repress the spontaneous growth of endothelial cells, requiring at least 48 -72 hr of treatment with HPR, followed by a progressive accumulation of cells in G 1 at subsequent time points. Finally, immunohistochemistry experiments performed in the CAM assay demonstrated that endothelial staining of both VEGF receptor 2 and FGF-2 receptor-2 was reduced after implantation of HPR-loaded sponges, as compared to control CAMs. These data suggest that HPR exerts its antiangiogenic activity through both a direct effect on endothelial cell proliferative activity and an inhibitory effect on the responsivity of the endothelial cells to the proliferative stimuli mediated by angiogenic growth factors.

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“…The ages of the patients at the time of operation ranged from 6 months to 8 years. They were staged according to Evans' classification (Evans et al, 1971). Primary sites of NB were as follows: 37 from adrenal gland, 12 from retro-peritoneum and five from mediastinum.…”

Section: Patients With Nb Analysedmentioning

confidence: 99%

Detailed deletion mapping of chromosome band 14q32 in human neuroblastoma defines a 1.1-Mb region of common allelic loss

et al. 2000

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Neuroblastoma (NB) is a well-known malignant disease in infants, but its molecular mechanisms have not yet been fully elucidated. To investigate the genetic contribution of abnormalities on the long arm of chromosome 14 (14q) in NB, we analysed loss of heterozygosity (LOH) in 54 primary NB samples using 12 microsatellite markers on 14q32. Seventeen (31%) of 54 tumours showed LOH at one or more of the markers analysed, and the smallest common region of allelic loss was identified between D14S62 and D14S987. This region was estimated to be 1-cM long from the linkage map. Fluorescence in situ hybridization also confirmed the loss. There was no statistical correlation between LOH and any clinicopathologic features, including age, stage, amplification of MYCN and ploidy. We further constructed a contig spanning the lost region using bacterial artificial chromosome and estimated this region to be approximately 1.1-Mb by pulsed-field gel electrophoresis. Our results will contribute to cloning and characterizing the putative tumour-associated gene(s) in 14q32 in NB. © 2000 Cancer Research Campaign

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A proposed staging for children with neuroblastoma.Children's cancer study group A

Cited by 902 publications

References 8 publications

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

Inhibition of neuroblastoma-induced angiogenesis by fenretinide

Detailed deletion mapping of chromosome band 14q32 in human neuroblastoma defines a 1.1-Mb region of common allelic loss

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