CHARACTERIZATION OF T(2-5) RECIPROCAL TRANSCRIPTS AND GENOMIC BREAKPOINTS IN CD30(+) CUTANEOUS LYMPHOPROLIFERATIONS

NPM-ALK chimeric transcripts, encoded by the t(2;5), lead to an aberra nt expression of ALK by CD30(+) systemic lymphomas. To determine if t( 2;5) is involved in cutaneous lymphoproliferative disorders, we studie d 37 CD30(+) cutaneous lymphoproliferations, 27 mycosis fungoides (MF) , and 16 benign inflammatory disorders (BID). NPM-ALK transcripts were detected by nested reverse transcription-polymerase chain reaction (R T-PCR) in 1 of 11 lymphomatoid papulosis (LyP), 7 of 15 CD30(+) primar y cutaneous T-cell lymphoma (CTCL), 3 of 11 CD30(+) secondary cutaneou s lymphoma, 6 of 27 MF, and 1 of 16 BID. However, the expression of NP M-ALK transcripts was not associated with ALK1 immunoreactivity in MF, LyP, or BID cases. Only 1 CD30(+) primary CTCL and 3 CD30(+) secondar y cutaneous lymphoma were ALK1 immunoreactive. The ALK1(+) cases were also characterized by amplification of tumor-specific genomic breakpoi nts on derivative chromosome 5. These cases, except for 1 secondary cu taneous lymphoma, were also characterized by reciprocal breakpoints on derivative chromosome 2, leading to the expression of reciprocal ALK- NPM transcripts. Amplification of chromosomal breakpoints on both deri vative chromosomes could represent an alternative to conventional cyto genetics for the diagnosis of t(2;5) and seems to be more reliable tha n the detection of cryptic NPM-ALK transcripts by nested RT-PCR. (C) 1 998 by The American Society of Hematology.