Expression of CD44 splice variant v10 in Hodgkin's disease is associated with aggressive behaviour and high risk of relapse

Citation
C. Beham-schmid et al., Expression of CD44 splice variant v10 in Hodgkin's disease is associated with aggressive behaviour and high risk of relapse, J PATHOLOGY, 186(4), 1998, pp. 383-389
Citations number
48
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
186
Issue
4
Year of publication
1998
Pages
383 - 389
Database
ISI
SICI code
0022-3417(199812)186:4<383:EOCSVV>2.0.ZU;2-6
Abstract
Expression of CD44 isoforms has been shown to correlate with the progressio n and prognosis of some malignant tumours, The aim of this study was to inv estigate the expression of CD44 standard (CD44s) and CD44 splice variants ( CD44v) v5, v6, and v10 in lymph node specimens from patients with nodular s clerosing Hodgkin's disease (NSHD), with or without initial bone marrow inv olvement and with or without relapse, Specimens were studied by immunohisto chemistry to determine CD44s and CD44v in Hodgkin- and Reed-Sternberg (HRS) cells, For validation of the immunohistochemical detection of CD44v10 in p araffin-embedded samples, selected cases mere analysed in parallel immunohi stochemically using fresh frozen material and by reverse transcription-poly merase chain reaction (RT-PCR), There was high expression of CD44 isoforms containing the variant exon v10 selectively in HRS cells of patients with r elapse within 2-3 years or with initial bone marrow involvement. In patient s without relapse, however, no or only very few HRS cells were positive. Th ese differences were statistically highly significant (p less than or equal to 0.001), whereas evaluation of CD44s, CD44v5, and v6 expression revealed no marked differences, It is concluded that evaluation of CD14v10 expressi on could serve as a new prognostic marker in NSHD. These results are consid ered to be of sufficient importance to initiate a large multi-institutional study for confirmation; furthermore, they might suggest causal involvement of CD44v10 in the progression of NSHD. (C) 1998 John Wiley & Sons, Ltd.