Molecular characterisation of the t(1;15)(p22;q22) translocation in the prostate cancer cell line LNCaP

Vol. 112, No. 1-2, 2006

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Original Article

Molecular characterisation of the t(1;15)(p22;q22) translocation in the prostate cancer cell line LNCaP
J.C. Strefford^a, T.M. Lane^a, A. Hill^a, L. LeRoux^a, N.J. Foot^a, J. Shipley^b, R.T.D. Oliver^c, Y.-J. Lu^a, B.D. Young^a

^aCancer Research UK Medical Oncology Unit, Queen Mary and Westfield College, Charterhouse Square, London;
^bMolecular Cytogenetics, Institute of Cancer Research, Sutton, London;
^cDepartment of Medical Oncology, Cancer Services Directorate, St Bartholomew's Hospital, London (UK)

Address of Corresponding Author

Cytogenet Genome Res 2006;112:45-52 (DOI: 10.1159/000087512)

Abstract.

Although chromosome translocations are well-documented recurrent events in hematological malignancies and soft tissue sarcomas, their significance in carcinomas is less clear. We report here the molecular characterization of the reciprocal translocation t(1;15)(p22;q22) in the prostate carcinoma cell line, LNCaP. The chromosome 1 breakpoint was localized to a single BAC clone, RP11-290M5, by sequential FISH analysis of clones selected from the NCBI chromosome 1 map. This was further refined to a 580-bp region by Southern blot analysis. A 2.85-kb fragment spanning the der(1) breakpoint was amplified by long-range inverse PCR. The breakpoint on chromosome 1 was shown to lie between the CYR61 and the DDAH1 genes with the der(1) junctional sequence linking the CYR61 gene to the TSPAN3 (TM4SF8) gene on chromosome 15. Confirmatory PCR and FISH mapping of the der(15) showed loss of chromosome material proximal to the breakpoint on chromosome 15, containing the PSTPIP1 and RCN2 genes. On the available evidence we conclude that this translocation does not result in an in-frame gene fusion. Comparative expressed sequence hybridization (CESH) and comparative genomic hybridization (CGH) analysis, showed relative down-regulation of gene expression surrounding the breakpoint, but no gross change in genomic copy number. Real-time quantitative RT-PCR for genes around the breakpoint supported the CESH data. Therefore, here we may have revealed a gene down-regulation mechanism associated with a chromosome translocation, either through small deletion at the breakpoint or through another means of chromosome domain related gene regulation.

Author Contacts

Request reprints from Dr Jon Strefford
Leukaemia Research Fund Cytogenetics Group
Cancer Sciences Division, MP822 Duthie Building
Southampton General Hospital, Southampton SO16 6YD (UK)
telephone: 023 8079 8403; fax: 023 8079 6432; e-mail: jcs@soton.ac.uk

Article Information

Supported by The Orchid Cancer Appeal and Cancer Research UK.

Manuscript received 9 November 2004;
accepted in revised form for publication by P. Lichter, 27 April 2005.
Number of Print Pages : 8
Number of Figures : 2, Number of Tables : 2, Number of References : 61

Medline Abstract (ID 16276089)

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