Download PDF by Nai-Kong V. Cheung, Susan L. Cohn: Neuroblastoma

By Nai-Kong V. Cheung, Susan L. Cohn

ISBN-10: 354040841X

ISBN-13: 9783540408413

Neuroblastoma is a clinical enigma. As a formative years neoplasm coming up from neural crest cells, it truly is characterised via various medical behaviors starting from spontaneous remission to swift tumor development and dying. even if medical final result could be anticipated to a wide volume by means of the degree of affliction and the age at prognosis, an in-depth figuring out of its clinico-pathological habit, now vastly aided by way of subtle molecular genetic profiling, will enhance diagnostic precision and refine risk-based treatments. entire overseas efforts have complicated our realizing of tumor biology and more advantageous the scientific administration of kids with neuroblastoma. This booklet stories our present realizing of the genes and organic pathways that give a contribution to neuroblastoma pathogenesis, sleek risk-based therapy techniques for those sufferers, and up to date advances in biologically established treatment. It offers a concise updated reference for practitioners, scholars, and researchers.

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Med Pediatr Oncol 33:360– 361 Woods WG, Gao R, Shuster J et al. (2002) Screening of infants and mortality due to neuroblastoma. N Engl J Med 346: 1041–1046 Yamamoto K, Hayashi Y, Hanada R et al. (1995) Mass screening and age-specific incidence of neuroblastoma in Saitama Prefecture, Japan. J Clin Oncol 13:2033–2038 W. G. Woods Yamamoto K, Hanada R, Kikuchi A et al. (1998) Spontaneous regression of localized neuroblastoma detected by mass screening. J Clin Oncol 16:1265–1269 Yamamoto K, Ohta S, Ito E et al.

1 Introduction It a major tenet in cancer research that alterations in cellular genes lead to the malignant transformation of normal cells. Two major classes of cancer-related genes have been identified: (a) oncogenes, which contribute to cancer “dominantly” by positive modulation of cellular growth; and (b) tumor suppressor genes, which are thought to control normal cellular growth and differentiation and act in a “recessive” negative way, contributing to cancer through functional inactivation.

2001). 6 Conclusions There are two published studies that used classic genetic linkage methods to localize hereditary neuroblastoma predisposition genes. In a genome-wide search for linkage in seven pedigrees with at least two first-degree relatives affected with neuroblastoma, convincing evidence was discovered that a hereditary neuroblastoma predisposition gene (HNB1) is located on the distal short arm of chromosome 16 (16p12–13; Fig. 1) (Maris et al. 2002). 7 (Maris et al. 2003). Loss of heterozygosity has been observed in 13% of sporadic neuroblastomas, suggesting that somatic inactivation of a 16p tumor suppressor gene might contribute to neuroblastoma initiation or progression in at least a subset of nonfamilial cases (Furuta et al.

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Neuroblastoma by Nai-Kong V. Cheung, Susan L. Cohn


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