Artigo Acesso aberto Revisado por pares

Human neuroblastoma cell lines that express N-myc without gene amplification

1993; Wiley; Volume: 72; Issue: 11 Linguagem: Inglês

10.1002/1097-0142(19931201)72

ISSN

1097-0142

Autores

Randal K. Wada, Robert C. Seeger, Garrett M. Brodeur, Peggy A. Einhorn, Sylvia A. Rayner, Mary M. Tomayko, C. Patrick Reynolds,

Tópico(s)

Cell death mechanisms and regulation

Resumo

CancerVolume 72, Issue 11 p. 3346-3354 ArticleFree Access Human neuroblastoma cell lines that express N-myc without gene amplification Randal K. Wada M.D., Randal K. Wada M.D. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorRobert C. Seeger M.D., Robert C. Seeger M.D. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorGarrett M. Brodeur M.D., Garrett M. Brodeur M.D. Departments of Pediatrics and Genetics, Washington University School of Medicine, St. Louis, MissouriSearch for more papers by this authorPeggy A. Einhorn B.S., Peggy A. Einhorn B.S. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorSylvia A. Rayner B.S., Sylvia A. Rayner B.S. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorMary M. Tomayko B.S., Mary M. Tomayko B.S. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorC. Patrick Reynolds M.D., Ph.D., Corresponding Author C. Patrick Reynolds M.D., Ph.D. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaDivision of Hematology/Oncology, Children's Hospital of Los Angeles, 4650 Sunset Boulevard, MS 57, Los Angeles, CA 90027===Search for more papers by this author Randal K. Wada M.D., Randal K. Wada M.D. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorRobert C. Seeger M.D., Robert C. Seeger M.D. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorGarrett M. Brodeur M.D., Garrett M. Brodeur M.D. Departments of Pediatrics and Genetics, Washington University School of Medicine, St. Louis, MissouriSearch for more papers by this authorPeggy A. Einhorn B.S., Peggy A. Einhorn B.S. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorSylvia A. Rayner B.S., Sylvia A. Rayner B.S. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorMary M. Tomayko B.S., Mary M. Tomayko B.S. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaSearch for more papers by this authorC. Patrick Reynolds M.D., Ph.D., Corresponding Author C. Patrick Reynolds M.D., Ph.D. Division of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Los Angeles and the University of Southern California School of Medicine, Los Angeles, CaliforniaDivision of Hematology/Oncology, Children's Hospital of Los Angeles, 4650 Sunset Boulevard, MS 57, Los Angeles, CA 90027===Search for more papers by this author First published: 1 December 1993 https://doi.org/10.1002/1097-0142(19931201)72:11 3.0.CO;2-ECitations: 31AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Background. About one half of aggressive neuroblastomas lack N-myc amplification. Cell lines from such tumors are needed to determine the biological basis of aggressive tumor behavior. Methods. Neuroblastoma cell lines were established from a primary tumor (SMS-LHN) and a bone marrow metastasis (LA-N-6) of two children with Stage IV neuroblastoma. Although both cell lines and their original tumors lacked N-myc genomic amplification, these patients died of progressive disease. Results. SMS-LHN and LA-N-6 can be distinguished from primitive neuroectodermal tumor (PNET) lines by cell surface antigen expression and catecholamine production. Cytogenetic analysis of each cell line revealed unique genetic rearrangements, whereas both lines showed abnormalities involving chromosome 2. Neither cell line contained double-minute chromosomes, homogeneously staining regions, a 1p chromosomal deletion, or t(11;22). The growth rates of these two new lines in vitro and in vivo (as xenografts in nude mice) are slower than N-myc amplified neuroblastoma lines. Both lines express greater amounts of N-myc RNA and protein relative to nonneuroblastoma cell lines (including PNET), although not to the extent of cell lines with N-myc genomic amplification. Conclusions. The relatively large amount of N-myc expression in these two new cell lines suggests that N-myc expression without amplification could play a role in the pathogenesis of some neuroblastomas. These cell lines should be useful for investigating mechanisms and consequences of N-myc gene activation other than genomic amplification. References 1 Brodeur GM, Seeger RC, Schwab M, Varmus HE, Bishop JM. Amplification of N-myc sequences in primary human neuroblastomas. 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