Universität zu Köln

Schleiermacher, G., Mosseri, V., London, W. B., Maris, J. M., Brodeur, G. M., Attiyeh, E., Haber, M., Khan, J., Nakagawara, A., Speleman, F., Noguera, R., Tonini, G. P., Fischer, M., Ambros, I., Monclair, T., Matthay, K. K., Ambros, P., Cohn, S. L. and Pearson, A. D. J. (2012). Segmental chromosomal alterations have prognostic impact in neuroblastoma: a report from the INRG project. Br. J. Cancer, 107 (8). S. 1418 - 1423. LONDON: NATURE PUBLISHING GROUP. ISSN 0007-0920

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Abstract

BACKGROUND: In the INRG dataset, the hypothesis that any segmental chromosomal alteration might be of prognostic impact in neuroblastoma without MYCN amplification (MNA) was tested. METHODS: The presence of any segmental chromosomal alteration (chromosome 1p deletion, 11q deletion and/ or chromosome 17q gain) defined a segmental genomic profile. Only tumours with a confirmed unaltered status for all three chromosome arms were considered as having no segmental chromosomal alterations. RESULTS: Among the 8800 patients in the INRG database, a genomic type could be attributed for 505 patients without MNA: 397 cases had a segmental genomic type, whereas 108 cases had an absence of any segmental alteration. A segmental genomic type was more frequent in patients > 18 months and in stage 4 disease (P < 0.0001). In univariate analysis, 11q deletion, 17q gain and a segmental genomic type were associated with a poorer event-free survival (EFS) (P < 0.0001, P = 0.0002 and P < 0.0001, respectively). In multivariate analysis modelling EFS, the parameters age, stage and a segmental genomic type were retained in the model, whereas the individual genetic markers were not (P < 0.0001 and RR = 2.56; P = 0.0002 and RR = 1.8; P = 0.01 and RR = 1.7, respectively). CONCLUSION: A segmental genomic profile, rather than the single genetic markers, adds prognostic information to the clinical markers age and stage in neuroblastoma patients without MNA, underlining the importance of pangenomic studies. British Journal of Cancer (2012) 107, 1418-1422. doi:10.1038/bjc.2012.375 www.bjcancer.com Published online 13 September 2012 (c) 2012 Cancer Research UK

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Schleiermacher, G. UNSPECIFIED UNSPECIFIED UNSPECIFIED Mosseri, V. UNSPECIFIED UNSPECIFIED UNSPECIFIED London, W. B. UNSPECIFIED UNSPECIFIED UNSPECIFIED Maris, J. M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Brodeur, G. M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Attiyeh, E. UNSPECIFIED UNSPECIFIED UNSPECIFIED Haber, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Khan, J. UNSPECIFIED UNSPECIFIED UNSPECIFIED Nakagawara, A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Speleman, F. UNSPECIFIED UNSPECIFIED UNSPECIFIED Noguera, R. UNSPECIFIED UNSPECIFIED UNSPECIFIED Tonini, G. P. UNSPECIFIED UNSPECIFIED UNSPECIFIED Fischer, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ambros, I. UNSPECIFIED UNSPECIFIED UNSPECIFIED Monclair, T. UNSPECIFIED UNSPECIFIED UNSPECIFIED Matthay, K. K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ambros, P. UNSPECIFIED UNSPECIFIED UNSPECIFIED Cohn, S. L. UNSPECIFIED UNSPECIFIED UNSPECIFIED Pearson, A. D. J. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-481084
DOI:	10.1038/bjc.2012.375
Journal or Publication Title:	Br. J. Cancer
Volume:	107
Number:	8
Page Range:	S. 1418 - 1423
Date:	2012
Publisher:	NATURE PUBLISHING GROUP
Place of Publication:	LONDON
ISSN:	0007-0920
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language CLINICAL-RELEVANCE; HIGHER RISK; GAIN; AMPLIFICATION; RELAPSE; TUMORS; 1P; HETEROZYGOSITY; ACCUMULATION; PROGRESSION Multiple languages Oncology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/48108