Evidence for an Age Cutoff Greater Than 365 Days for Neuroblastoma Risk Group Stratification in the Children's Oncology Group

London, Wendy B.; Castleberry, Robert P.; Matthay, Katherine K.; Look, A. Thomas; Seeger, Robert C.; Shimada, Hiroyuki; Thorner, Paul; Gm, Brodeur; Maris, John M.; Reynolds, C. Patrick; Cohn, Susan L.

doi:10.1200/jco.2005.05.571

Cited by 497 publications

(395 citation statements)

References 31 publications

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“…As has been shown with other important DUSPs, we present evidence that DUSP26 is overexpressed in neuroblastoma cell lines and in high-risk neuroblastoma tissue samples. The highrisk tissue samples represent patients with high-risk features such as age 41 year of age, MYCN amplification, poorly differentiated histopathologic characteristics and poor prognosis (London et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma

Shang

Vasudevan

et al. 2010

Oncogene

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Section: Discussionmentioning

confidence: 99%

Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma

Shang

Vasudevan

et al. 2010

Oncogene

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“…In this study, established clinical factors were of prognostic significance, such as tumour stage and age at diagnosis. We used an age cut-off of 12 months, rather than the age of 18 months suggested recently (London et al, 2005), as the treatment protocols according to which patients were treated were based on the 12-month cut-off. Furthermore, nearly all genetic markers have been shown to be of prognostic significance in univariate analysis.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal CGH identifies patients with a higher risk of relapse in neuroblastoma without MYCN amplification

et al. 2007

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Whereas neuroblastoma (NB) with MYCN amplification presents a poor prognosis, no single marker allows to reliably predict outcome in tumours without MYCN amplification. We report here an extensive analysis of 147 NB samples at diagnosis, without MYCN amplification, by chromosomal comparative genomic hybridisation (CGH), providing a comprehensive overview of their genomic imbalances. Comparative genomic hybridisation profiles showed gains or losses of entire chromosomes (type 1) in 71 cases, whereas partial chromosome gains or losses (type 2), including gain involving 17q were observed in 68 cases. Atypical profiles were present in eight cases. A type 1 profile was observed more frequently in localised disease (Po0.0001), and in patients of less than 12 months at diagnosis (Po0.0001). A type 2 genomic profile was associated with a higher risk of relapse in the overall population (logrank test; Po0.0001), but also in the subgroup of patients with localised disease (log-rank test, P ¼ 0.007). In multivariate analysis, the genomic profile was the strongest independent prognostic factor. In conclusion, the genomic profile is of prognostic impact in patients without MYCN amplification, making it a help in the management of low-stage NB. Further studies using higher-resolution CGH are needed to better characterise atypical genomic alterations.

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“…No overall sex predominance has been reported. 12 All were presented with suprarenal or retroperitoneal mass & pain. Uncommon manifestations of NB related to unusual clinical behavior or to paraneoplastic syndromes were not seen in any case.…”

Section: Discussionmentioning

confidence: 99%

Pediatric Genitourinary Tumors-Clinicopathological Experience

Consultant¹,

Gite²,

Maruti³

2016

Nephrol Open J

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Objective: To document general baseline data on the patterns of childhood genitourinary tumors. Design, Setting and Participants: This is a retrospective analysis of 28 cases of pediatric genitourinary tumors (Age group 0-12 years) in surgical pathology in a tertiary care hospital encountered over a period of 5 years. Results: In the genitourinary system tumors of the kidney, bladder, prostate, testis, and adrenal were included. A total of 3149 pediatric surgical specimen presented over a five years. Of this, 28 were diagnosed with genitourinary tumors. In the renal tumors only Wilm's tumors (WTs) (9 cases) was seen, with classical triphasic tumors were more common. The mean age of presentation is 3 year with commonest age group of presentation (8 cases out of 9) in the age group 1-5 years. Three of them had showed unfavorable histology. Among the gonadal germ cell tumors, there were noted four mature teratoma, one immature teratoma, two yolk sac tumors of ovary & one yolk sac tumour in testis was seen. In the adrenal gland, adrenal medullary tumors were more common than adrenal cortex with neuroblastoma (4 of 10 cases) as common individual tumor. Conclusion: Different types of genitourinary tumors seen in the childhood. A high index of suspicion should be maintained with an aim of surgical treatment to avoid the poor management. Histological type is important for understanding etiology and progression of disease. The likelihood of a given type of tumor being present in a particular age or sex group or particular site may heighten the index of suspicion and ultimately influences etiology, biology, and natural history, relative incidence and distribution frequency, clinical presentation and manifestations, and response to therapy and outcome."

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Evidence for an Age Cutoff Greater Than 365 Days for Neuroblastoma Risk Group Stratification in the Children's Oncology Group

Abstract: The prognostic contribution of age to outcome is continuous in nature. Within clinically relevant risk stratification, statistical support exists for an age cutoff of 460 days.

Cited by 497 publications

References 31 publications

Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma

Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma

Chromosomal CGH identifies patients with a higher risk of relapse in neuroblastoma without MYCN amplification

Pediatric Genitourinary Tumors-Clinicopathological Experience

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