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Blood, Vol. 95 No. 9 (May 1), 2000:
pp. 2937-2942
Loss of heterozygosity on 10q and microsatellite instability in
advanced stages of primary cutaneous T-cell lymphoma and possible
association with homozygous deletion of PTEN
Julia J. Scarisbrick,
Alison J. Woolford,
Robin Russell-Jones, and
Sean J. Whittaker
From the Skin Tumour Unit, St John's Institute Dermatology, St
Thomas' Hospital, London, United Kingdom.
Previous cytogenetic studies of primary cutaneous T-cell lymphoma
(CTCL) were based on limited numbers of patients and seldom showed
consistent nonrandom chromosomal abnormalities. In this study, 54 tumor
DNA samples from patients with CTCL were analyzed for loss of
heterozygosity on 10q. Allelic loss was identified in 10 samples, all
of which were from the 44 patients with mycosis fungoides (10/44
patients; 23%). Of the patients with allelic loss, 3 were among the 29 patients with early-stage myosis fungoides (T1 or
T2) (3/29 patients; 10%), whereas the other 7 were among the 15 patients with advanced cutaneous disease (T3 or
T4) (7/15 patients; 47%). The overlapping region of
deletion was between 10q23 and 10q24. In addition, microsatellite
instability (MSI) was present in 13 of the 54 samples (24%), 12 from
patients with mycosis fungoides and 1 from a patient with Sezary
syndrome. There was also an association between MSI and disease
progression in patients with mycosis fungoides, with 6 of 15 (40%)
patients with MSI having advanced cutaneous disease and only 6 of 29 (21%) having early-stage disease. Samples with allelic loss on 10q
were analyzed for abnormalities of the tumor suppressor gene
PTEN (10q23.3). No tumor-specific mutations were detected, but
homozygous deletion was found in 2 patients. Thus, we found loss of
heterozygosity on 10q and MSI in advanced cutaneous stages of mycosis
fungoides. These findings indicate that a tumor suppressor gene or
genes in this region may be associated with disease progression.
Furthermore, abnormalities of PTEN may be important in the
pathogenesis of mycosis fungoides, but our data imply that this gene is
rarely inactivated by small deletions or point mutations.
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