Genomic Aberrations and Survival in Cutaneous T Cell Lymphomas

Information on chromosomal aberrations in cutaneous T cell lymphomas (CTCL), is scarce. In this study, comparative genomic hybridization (CGH) was used to analyze chromosomal imbalances (CI) in 32 patients with CTCL. CI were detected in 21 patients (66%). Euchromatic loss (dim) was localized most fr...

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Veröffentlicht in:Journal of investigative dermatology 2004-03, Vol.122 (3), p.579-586
Hauptverfasser: Fischer, Tanja C., Gellrich, Sylke, Marcus Muche, J., Sherev, Tumenjargal, Audring, Heike, Neitzel, Heidemarie, Walden, Peter, Sterry, Wolfram, Tönnies, Holger
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Sprache:eng
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Zusammenfassung:Information on chromosomal aberrations in cutaneous T cell lymphomas (CTCL), is scarce. In this study, comparative genomic hybridization (CGH) was used to analyze chromosomal imbalances (CI) in 32 patients with CTCL. CI were detected in 21 patients (66%). Euchromatic loss (dim) was localized most frequently (>16%) at the chromosomal regions 17p (28%), 13q (25%), 10q (16%), and 6q (19%), and gain of chromatin (enh) at 7 (25%), 8q (25%), and 17q (16%). The pattern dim6q–enh7–enh8–dim13 was the most frequent combination of CI. The number of aberrations per tumor sample varied between 0 and 19 and correlated with clinical tumor stages: from none in stage Ia to 8.75±1.8 (mean±SEM) in stage IVa. CI occurred more frequently in aggressive subtypes (9.33±2.16) than in indolent (2.88±0.8) subtypes. A high number of CI (≥5) was associated with shorter survival. Gain of chromatin in 8q and loss of 6q and 13q correlated with a significantly shorter survival, whereas the most frequently observed aberrations (loss in 17p and gain in 7) did not influence the prognosis. In summary, CGH analysis revealed a characteristic pattern of recurring chromosomal gains and losses in CTCL. The association of the imbalances with the clinical course of the disease suggests that genes encoded at these loci may influence tumor development and progression.
ISSN:0022-202X
1523-1747
DOI:10.1111/j.0022-202X.2004.22301.x