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a Department of
Dermatology, Columbia University, College of Physicians & Surgeons, New
York, NY, USA, b Department of Pathology, Columbia
University, College of Physicians & Surgeons, New York, NY, USA
Correspondence to: Dr Peacocke, 630 West 168th Street, VC-1526, New York, NY 10032, USA, mp231{at}columbia.edu
Revised version received 17 April 2000;
Accepted for publication 1 May 2000
CONTEXT
PTEN,
a tumour suppressor gene located on chromosome 10q23, develops somatic
mutations in various tumours and tumour cell lines including brain,
endometrium, prostate, breast, kidney, thyroid, liver, and melanoma.
OBJECTIVESTo investigate the
mutational profile of this gene further, as well as its role in tumour
progression in melanoma.
DESIGN, SETTINGSWe examined 21 metastatic melanoma samples for 10q23 allelic losses and
PTEN sequence alterations. Additionally, we
screened these samples for mutations in
CDKN2A, a gene in which alterations are well
documented in primary melanoma as well as in the germline of familial melanoma.
RESULTSLoss of heterozygosity
(LOH) at 10q23 was observed in 33% (7/21) of the samples tested. We
identified four sequence alterations in PTEN
(19%) and two in CDKN2A (9.5%). Of
interest, only one case showed mutations in both genes.
CONCLUSIONSThese data support the
notion that PTEN alterations occur in some
metastatic melanomas, and that mutation of this gene plays a role in
the progression of some forms of melanoma.
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