title: Detection of BCL-6 rearrangements and p53 mutations in Malt-lymphomas.
abstract: 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.
authors.affiliation: Dipartimento di Scienze Mediche, Università di Torino, Novara, Italy. gaidano@med.no.unipmn.it
authors.forename: G
authors.initials: G
authors.lastname: Gaidano
authors.forename: G
authors.initials: G
authors.lastname: Volpe
authors.forename: C
authors.initials: C
authors.lastname: Pastore
authors.forename: R
authors.initials: R
authors.lastname: Chiarle
authors.forename: D
authors.initials: D
authors.lastname: Capello
authors.forename: A
authors.initials: A
authors.lastname: Gloghini
authors.forename: E
authors.initials: E
authors.lastname: Perissinotto
authors.forename: F
authors.initials: F
authors.lastname: Savinelli
authors.forename: M
authors.initials: M
authors.lastname: Bosco
authors.forename: U
authors.initials: U
authors.lastname: Mazza
authors.forename: S
authors.initials: S
authors.lastname: Pileri
authors.forename: G
authors.initials: G
authors.lastname: Palestro
authors.forename: A
authors.initials: A
authors.lastname: Carbone
authors.forename: G
authors.initials: G
authors.lastname: Saglio
mesh_terms: D015139:Blotting, Southern; D015342:DNA Probes / Q000737:chemistry; D004273:DNA, Neoplasm / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics*; D015321:Gene Rearrangement; D004854:Herpesvirus 4, Human / Q000235:genetics; D019288:Herpesvirus 8, Human / Q000235:genetics; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000235:genetics* / Q000473:pathology / Q000821:virology; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D051560:Proto-Oncogene Proteins c-bcl-6; D017422:Sequence Analysis, DNA; D014157:Transcription Factors / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D016335:Zinc Fingers / Q000235:genetics
chemical_list: D015342:DNA Probes; D004273:DNA, Neoplasm; D004268:DNA-Binding Proteins; D011518:Proto-Oncogene Proteins; D051560:Proto-Oncogene Proteins c-bcl-6; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53