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Arch Dermatol. 1998;134:221-223.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

IT WAS the mid-1980s when the first wave of molecular biologic analysis of T-cell receptor (TCR) gene rearrangements was applied to cutaneous T-cell lymphoma (CTCL), ie, mycosis fungoides and its leukemic variant, the Sézary syndrome.¹ Initial studies involved genomic Southern blot analysis and demonstrated 2 important features: (1) each individual lesion of CTCL contained a dominant T-cell clone, and (2) multiple lesions from individual patients contained the same dominant T-cell clone in all sites of disease. These findings established that, like other forms of lymphoma, CTCL is typically a monoclonal lymphoproliferative disorder. They also formed the basis for many subsequent studies during the next decade that confirmed that the detection of monoclonal TCR gene rearrangements is a useful molecular biologic adjunct to the clinicopathologic diagnosis of this neoplasm. These more recent studies involved not only conventional genomic Southern blotting but also more sensitive clonality assays using polymerase chain . . . [Full Text of this Article]

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