Detection of BCL ‐6 rearrangements and p53 mutations in malt‐lymphomas

Twenty‐seven lymphomas of mucosa‐associated lymphoid tissue (MALT) derived from distinct anatomical sites were tested for the presence of genetic lesions commonly involved in B‐cell lymphomagenesis, including activation of proto‐oncogenes ( BCL ‐1, BCL ‐2, BCL ‐6, and c‐ MYC ), disruption of tumor suppressor loci ( p53 , 6q), and infection by viruses [Epstein‐Barr virus (EBV), and Kaposi's sarcoma‐herpesvirus/human herpesvirus‐8 (KSHV/HHV‐8)]. Sixteen low‐grade and 11 high‐grade MALT‐lymphomas were included in the study. The presence of genetic lesions was tested by a combination of molecular approaches, including Southern blot hybridization, polymerase chain reaction (PCR), and PCR‐single strand conformation polymorphism followed by DNA direct sequencing. Alterations of BCL ‐1, BCL ‐2, or c‐ MYC , as well as infection by KSHV/HHV‐8, scored negative in all MALT‐lymphomas analysed. Conversely, rearrangements of BCL ‐6 and mutations of p53 clustered with a fraction of high‐grade MALT‐lymphomas. Deletions of 6q occurred in selected cases of both low‐ and high‐grade MALT‐lymphomas, whereas a monoclonal infection by EBV was restricted to one single patient. These data corroborate the notion that the molecular pathogenesis of MALT‐lymphomas differs substantially from that of nodal B‐cell lymphomas. Occasionally, however, a proportion of high‐grade MALT‐lymphomas may harbor selected genetic lesions among the ones commonly involved in nodal B‐cell lymphomagenesis. Am. J. Hematol. 56:206–213, 1997. © 1997 Wiley‐Liss, Inc.