Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine a possible role of aberrant somatic hypermutation (ASHM) in the pathogenesis of thyroid lymphoma (TL), mutational status of genes affected by ASHM, including c-MYC, PIM-1, PAX-5 and RhoH/TTF, was analyzed. Tumor specimens from 33 patients with thyroid B-cell lymphoma and 14 with chronic lymphocytic thyroiditis (CLTH), an autoimmune thyroiditis known to provide a basis for TL development, was examined. Mutations of at least one of these genes was detected in 16 of 33 (48.5%) patients with TL and in 2 of 14 (14.3%) CLTH. Occurrence of ASHM in PIM-1, RhoH/TTF, and c-MYC was a constant finding in follicular lymphoma (FL) (all of 11 cases) but not so frequent in diffuse large B-cell lymphoma (DLBCL) (4 (33.3%) of 12 cases) and Marginal zone B-cell lymphoma (MZBCL) (1 (10.0%) of 10 cases). ASHM activity is ongoing in most of FL and DLBCL because intraclonal variants were found. FL was also unique in its lower expression level of activation-induced cytidine deaminase, a main player in DNA-modifying processes during SHM, compare to DLBCL and MZBCL.
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PMID:Aberrant somatic hypermutations in thyroid lymphomas. 1901 31

Post-transplant lymphoproliferative disorders (PTLDs) represent a frequent complication of solid organ transplantation. Although most PTLDs arise from recipient lymphoid cells, a considerable fraction of cases may arise from donor B-cells. In an attempt to clarify the histogenesis and pathogenesis of PTLDs derived from donor B-cells, monoclonal PTLDs occurring in liver transplant recipients were chosen as a model to compare donor (D-PTLDs) versus recipient PTLDs (R-PTLDs). The tumour panel included nine D-PTLDs and six R-PTLDs. D-PTLDs were early-onset, EBV-infected lymphoproliferations classified as polymorphic PTLD (P-PTLD; n = 7) or diffuse large B-cell lymphoma (DLBCL; n = 2) with tumour localization confined to the hepatic hilum. All R-PTLDs were late-onset DLBCLs and showed extrahepatic localization. A BCL-6(-)/MUM1(+)/CD138(+/-) phenotype, consistent with a post-germinal centre (GC) stage of pre-terminal B-cell differentiation, was observed in all D-PTLDs and in 2/6 R-PTLDs, whereas a BCL6(+)/MUM1(-)/CD138(-) profile, reminiscent of GC B-cells, was detected in 4/6 R-PTLDs. The presence of somatic IGHV hypermutation was observed in 6/9 D-PTLDs and in 4/6 R-PTLDs, suggesting derivation from antigen-experienced B-cells. IGHV4-39 was the IGHV gene most frequently encountered, being rearranged in 3/9 D-PTLDs. Among IGHV-mutated PTLDs, a mutational profile suggesting antigen stimulation and/or selection was observed in 4/6 D-s and in 2/4 R-PTLDs. The presence of ongoing IGHV mutations was detected in 2/4 D-PTLDs. Aberrant SHM was detected in 10/15 (66.7%) PTLDs, including 6/9 D-PTLDs and 4/6 R-PTLDs. Our findings suggest that (i) D-PTLDs show a clinical presentation distinct from R-PTLDs; (ii) immunophenotypic and genetic features of D-PTLDs are consistent with mature, GC-experienced B-cells; (iii) transformed donor-derived B-cells may experience antigen-driven stimulation and selection, and may acquire genetic lesions during neoplastic expansion in the recipient environment; and (iv) EBV infection and expression of viral oncoproteins may be relevant in the pathogenesis of D-PTLDs.
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PMID:Molecular characterization of post-transplant lymphoproliferative disorders of donor origin occurring in liver transplant recipients. 1939 Nov 28