Expression of cell cycle regulating proteins in an unusual transformation of mantle cell lymphoma

Citation
J. Tamaru et al., Expression of cell cycle regulating proteins in an unusual transformation of mantle cell lymphoma, LEUK LYMPH, 36(1-2), 1999, pp. 129-137
Citations number
62
Categorie Soggetti
Hematology,"Onconogenesis & Cancer Research
Journal title
LEUKEMIA & LYMPHOMA
ISSN journal
10428194 → ACNP
Volume
36
Issue
1-2
Year of publication
1999
Pages
129 - 137
Database
ISI
SICI code
1042-8194(199912)36:1-2<129:EOCCRP>2.0.ZU;2-U
Abstract
We describe here two patients with mantle cell lymphoma (MCL) who after a f ew years, developed to the diffuse large cell lymphoma (DLCL)( anaplastic c entrocytic lymphoma) growing in a diffuse sheets without the classical MCL component. In both the initial and second biopsy specimens, in each case, t umor cells were positive for cyclin D1, sIgM, sIgD, and CD5, but were negat ive for CD10 and CD23. In a study of immunoglobulin heavy chain (IgH) gene rearrangement, using the polymerase chain reaction (PCR) method, the produc ts obtained from each paired biopsy tissue sample were the same size, and i n one case had an identical sequence to the non-mutated VH gene. Immunohistochemistry was used to examine the expression of p53, p27(Kip1) a nd cyclin E. Interestingly, there was clear overexpression of p53 protein i n case 1 but not in case 2, compared with other typical MCL cases. The expr ession of p27(Kip1) in the second biopsies of each case was decreased compa red with those in the initial biopsies. In case 2, however, p27(Kip1) was c learly expressed in the first and second biopsies, in contrast to other typ ical MCL cases. Thus these 2 cases demonstrate not only that the variant fo rm of MCL may arise de novo, but also that MCL may transform to DLCL at the time of relapse. Although the mechanism of tumor progression/transformatio n is still poorly understood, the overexpression of p53 or p27(Kip1) may be linked to a cellular mechanism involved in the development of the variant form of MCL.