Volume 32, Issue 3 pp. 236-243
Research Article

Localisation of a novel region of recurrent amplification in follicular lymphoma to an ∼6.8 Mb region of 13q32-33

Michael J. Neat

Corresponding Author

Michael J. Neat

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London EC1M 6BQ, England, UK.Search for more papers by this author
Nicola Foot

Nicola Foot

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

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Michael Jenner

Michael Jenner

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

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Lindsey Goff

Lindsey Goff

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

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Kevin Ashcroft

Kevin Ashcroft

The Sanger Centre, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK

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Deborah Burford

Deborah Burford

The Sanger Centre, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK

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Andy Dunham

Andy Dunham

The Sanger Centre, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK

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Andrew Norton

Andrew Norton

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

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T. Andrew Lister

T. Andrew Lister

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

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Jude Fitzgibbon

Jude Fitzgibbon

ICRF Medical Oncology Unit, St. Bartholomew's Hospital, Charterhouse Square, London, UK

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First published: 25 September 2001
Citations: 38

Abstract

Follicular lymphoma (FL) is characterised by the presence of the t(14;18)(q32;q21) and represents ∼25% of new cases of non-Hodgkin's lymphoma. While the t(14;18) is a well-documented rearrangement, the role of secondary cytogenetic abnormalities in the development and progression of these tumours remains unclear. Comparative genomic hybridisation was used to characterise changes in DNA copy number in tumour DNA from patients with this malignancy. The mean numbers of deletion and amplification events found in each of the 45 samples studied were 1.8 and 2.3, respectively. Regions of recurrent (>10% tumour samples) gain involved chromosomes 2p13-16 (16%), 7 (20%), 12 (16%), 13q21-33 (18%), 18 (27%), and X (36%) and frequent losses localised to 6q (29%) and 17p (20%). Amplification of chromosome 13 represents a novel finding in FL. The minimal amplified region was refined to a 6.8-Mb interval of 13q32-33 between the BAC clones 88K16 and 44H20 by fluorescence in situ hybridisation studies using metaphase chromosomes derived from tumour material. There are a number of reports in the literature suggesting that amplification of chromosome 13 also occurs in other human cancers. The location of the putative oncogene on 13q described here in follicular and transformed lymphoma may also be important in the evolution of many other malignancies. © 2001 Wiley-Liss, Inc.

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