Disease relevance of Lymphoma, Mucosa-Associated Lymphoid Tissue

• To assess whether t(11;18, q21;q21), which results in a chimeric transcript between the AP12 and MLT genes, predicts lymphoma resistance to antibiotic therapy, we screened for the fusion transcript with RT-PCR in ten responsive and 12 non-responsive gastric MALT lymphomas [1].
• METHODS: H. heilmannii-induced gastritis was diagnosed histologically, by a new specific immunoglobulin G enzyme-linked immunosorbent assay, and with 16S ribosomal RNA amplification and sequencing in 5 consecutive patients with primary gastric MALT lymphoma clinical stage EI [2].
• T(14;18)(q32;q21) involving IGH and MALT1 is a frequent chromosomal aberration in MALT lymphoma [3].
• The respective frequencies of major subtypes were: small lymphocytic/lymphoplasmacytoid lymphoma (immunocytoma, SL/LPL), 28%; large cell-rich immunocytoma (LCRI), 7%; mantle cell lymphoma (MCL), 24%; mucosa-associated lymphoid tissue-lymphoma (MALT-L), 20%; other rare subtypes, 6%; and nonclassified or nonreviewed, 14% [4].
• PURPOSE: Cure of infection induces remissions in most patients with early stage Helicobacter pylori- (Hp) positive gastric MALT (mucosa-associated lymphoid tissue) lymphoma (GML) [5].

High impact information on Lymphoma, Mucosa-Associated Lymphoid Tissue

• Inactivating mutations and overexpression of BCL10, a caspase recruitment domain-containing gene, in MALT lymphoma with t(1;14)(p22;q32) [6].
• Here we show that cIAP2 is a ubiquitin ligase (E3) of BCL10 and targets it for degradation, inhibiting antigen receptor-mediated cytokine production. cIAP2-MALT1 lacks E3 activity, and concomitantly, the BCL10 protein is stabilized in MALT lymphomas harboring this fusion [7].
• A "G insertion" at nucleic acids 481 of the H. pylori fldA gene is not associated with gastric MALT lymphoma [8].
• CONCLUSIONS: In a subset of gastric MALT lymphomas, homozygous p16 deletions are acquired and may contribute to the transformation from a low-grade to a high-grade malignancy [9].
• Mucosa-associated lymphoid tissue (MALT) lymphomas are associated with overexpression and constitutive activity of bcl10, a caspase recruitment domain (CARD)-containing protein that activates NF-kappaB [10].

Chemical compound and disease context of Lymphoma, Mucosa-Associated Lymphoid Tissue

• No significant difference in clinical characteristics (sex, age, performance status, B symptoms) and biological parameters (hemoglobin [Hb] and lactate dehydrogenase levels) was observed between localized or disseminated MALT-lymphoma patients [11].
• PATIENTS AND METHODS: Twenty patients with suspected low-grade gastric MALT lymphomas were treated in a double-blinded, randomized, crossover trial with 2,250 mg of either amoxicillin or placebo, both in combination with omeprazole, for 14 days with the aim to cure H pylori infection [12].
• Phase II study of oxaliplatin for treatment of patients with mucosa-associated lymphoid tissue lymphoma [13].
• PATIENTS AND METHODS: Six patients with localised gastric MALT lymphoma underwent antibiotic treatment with clarithromycin, metronidazole, and pantoprazole [14].
• Duodenal mucosa-associated lymphoid tissue lymphoma: treatment with oral cyclophosphamide [15].

Biological context of Lymphoma, Mucosa-Associated Lymphoid Tissue

• Bcl10 and MALT1, products of distinct chromosomal translocations in mucosa-associated lymphoid tissue lymphoma, cooperate in activating NF-kappaB [16].
• The MALT lymphoma exhibited a point mutation in the splice donor region of intron 3 [17].
• In this study, we have examined the frequency of replication error (RER+) phenotype, a newly defined manifestation of genetic instability, and its relationship to p53 mutations in 40 MALT lymphomas (16 high grade and 24 low grade) [18].
• Bcl10 overexpression and nuclear translocation were originally identified in mucosa-associated lymphoid tissue lymphoma with t(1;14)(p32;q32) chromosome translocation [19].
• In summary, our data show that FAS mutations are rare in primary gastric MALT lymphomas (5.6%) but occur in a subset of primary gastric DLBCL (14.3%) and suggest that these mutations contribute to the pathogenesis of gastric lymphomas by rendering lymphocytes resistant to apoptosis [17].

Anatomical context of Lymphoma, Mucosa-Associated Lymphoid Tissue

• The human paracaspase prodomain binds Bcl10, a protein involved in the t(1;14)(p22;q32) translocation of mucosa-associated lymphoid tissue (MALT) lymphoma [20].
• Salivary gland mucosa-associated lymphoid tissue lymphoma immunoglobulin V(H) genes show frequent use of V1-69 with distinctive CDR3 features [21].
• Homing receptor expression in MALT lymphoma B cells was heterogeneous, however, in line with their memory B-cell phenotype in the majority of cases, the neoplastic B cells were alpha 4 beta 7-, CD62L+ [22].
• The infiltration of gastric mucosa with MALT lymphoma was highly significantly associated with H pylori colonisation (p < 0.0003) but neither with secretor status nor with certain ABH blood groups [23].
• Immune responses induced by immunological cross reactivity between H pylori HspB and human Hsp60 in gastric epithelium may be involved in the development of MALT lymphoma [24].

Gene context of Lymphoma, Mucosa-Associated Lymphoid Tissue

• These results correlate well with the nuclear BCL10 expression pattern in both t(1;14) and t(11;18) MALT lymphomas [25].
• Subclassification of high labeling score (>/=40) for Cdc2/Cdk1 and cyclin B1 and low labeling index (<0.6) for apoptotic cells in H. pylori-associated MALT may help in identifying a population of patients with an increased risk of developing MALT lymphoma [26].
• This study assessed the value of morphological grading and the expression of the co-stimulatory markers CD40, CD80 and CD86 and their ligands to predict clinical outcome in 23 consecutive low-grade MALT lymphoma patients treated with H. pylori eradication [27].
• In addition, in 8 of 16 MALT cases, the VH gene rearrangement of MALT lymphoma had the same bands as the CXCR3-positive B lymphocytes in PB [28].
• Frequency of chromosomal aneuploidies and deletions of the RB and TP53 genes in MALT lymphomas harboring the t(14;18)(q32;q21) [29].

Analytical, diagnostic and therapeutic context of Lymphoma, Mucosa-Associated Lymphoid Tissue

• Based on the CDR3 sequence amplified from each MALT lymphoma, individual tumor-specific primers were synthesized and used directly in the polymerase chain reaction (PCR) to analyze the sequences of their Ig heavy-chain variable region [30].
• Defined tumour cell populations from all MALT lymphoma cases were isolated by microdissection from frozen tissue sections and analysed by polymerase chain reaction-single-strand conformational polymorphism (PCR-SSCP) and direct sequencing for somatic mutations in the exon I/intron I region of the gene [31].
• We have therefore performed a retrospective analysis of t(11;18)(q21;q21) in patients undergoing chemotherapy with the nucleoside analogue cladribine (2CdA) for gastric MALT lymphoma [32].
• Sequence analysis of VH genes showed that an autoimmune mechanism may be involved in the lymphomagenesis of ocular adnexal MALT lymphoma [33].
• This study further supports the close interaction between the MALT1 and BCL10 proteins in the pathogenesis of MALT lymphomas and may indicate that BCL10 immunohistochemistry is a simple technique to identify those MALT lymphoma cases with an underlying genetic aberration [34].

References