Mutual exclusion of t(11;18)(q21;q21) and numerical chromosomal aberrations in the development of different types of primary gastric lymphomas.
until further notice
SourceBritish Journal of Haematology, 123, 4, (2003), pp. 590-599
Article / Letter to editor
Display more detailsDisplay less details
British Journal of Haematology
SubjectUMCN 1.2: Molecular diagnosis, prognosis and monitoring; UMCN 1.3: Tumor microenvironment; UMCN 5.1: Genetic defects of metabolism
Gastric non-Hodgkin's lymphomas can be divided histologically into mucosa-associated lymphoid tissue (MALT) lymphoma (ML) and diffuse large cell lymphoma (DLCL) with or without evidence of preceding/accompanying ML (DLCL + ML). We studied the incidence of the most frequent structural chromosomal aberration in ML, t(11;18)(q21;q21), and numerical aberrations of seven chromosomes in 36 ML, 39 DLCL + ML and ten gastric DLCL cases, by dual-colour interphase fluorescence in situ hybridization (FISH) and reverse transcriptase polymerase chain reaction (RT-PCR). t(11;18)(q21;q21) was exclusively detected in ML (FISH 22%; RT-PCR 24%), being completely absent in DLCL + ML and DLCL. No other translocations involving 11q21 or 18q21 and other partner chromosomes were detected by FISH. In lymphomas harbouring t(11;18)(q21;q21), this translocation was the sole genetic abnormality. In contrast, 45% of the t(11;18)(q21;q21)-negative ML showed trisomies, especially of chromosome 3 and 18. In DLCL + ML with separate small and large cell components, trisomies were either detected in both components or occurred exclusively in large tumour cells. Our results suggest that ML can be divided in lymphomas characterized by the t(11;18)(q21;q21), which are unlikely to transform into high-grade tumours, and t(11;18)(q21;q21)-negative ML that may develop into DLCL + ML after the acquisition of additional genetic aberrations.
Upload full text
Use your RU credentials (u/z-number and password) tolog in with SURFconextto upload a file for processing by the repository team.