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Localisation of a novel region of recurrent amplification in follicular lymphoma to an ∼6.8 Mb region of 13q32‐33
Author(s) -
Neat Michael J.,
Foot Nicola,
Jenner Michael,
Goff Lindsey,
Ashcroft Kevin,
Burford Deborah,
Dunham Andy,
Norton Andrew,
Lister T. Andrew,
Fitzgibbon Jude
Publication year - 2001
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.1187
Subject(s) - metaphase , follicular lymphoma , biology , lymphoma , chromosome , gene duplication , microbiology and biotechnology , comparative genomic hybridization , cytogenetics , dna , malignancy , genetics , gene , immunology
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.