Two patients with FSCCL, 22 patients with DSCCL, and all of the patients with MZL had a phenotype of mantle zone (MZ) B-lymphocytes (SIgD+, Leu-1+, Leu-8+, positive alkaline phosphatase [ALPase+], and negative common acute lymphoblastic leukemia antigen [CALLA-]), and all the tested patients (2 patients with FSCCL, 13 patients with DSCCL, and 4 patients with MZL) had germlines of bcl-2 gene.
Two patients with FSCCL, 22 patients with DSCCL, and all of the patients with MZL had a phenotype of mantle zone (MZ) B-lymphocytes (SIgD+, Leu-1+, Leu-8+, positive alkaline phosphatase [ALPase+], and negative common acute lymphoblastic leukemia antigen [CALLA-]), and all the tested patients (2 patients with FSCCL, 13 patients with DSCCL, and 4 patients with MZL) had germlines of bcl-2 gene.
As opposed to FCCL and MZL, all WDLL and all but one of the ILL (associated only with DRC-1+, OKB7+, and desmoplakin+ DRC) did not show any DRC as identifiable with the antibody panel used.
As opposed to FCCL and MZL, all WDLL and all but one of the ILL (associated only with DRC-1+, OKB7+, and desmoplakin+ DRC) did not show any DRC as identifiable with the antibody panel used.
As opposed to FCCL and MZL, all WDLL and all but one of the ILL (associated only with DRC-1+, OKB7+, and desmoplakin+ DRC) did not show any DRC as identifiable with the antibody panel used.
Statistical associations with FAB subtypes were found: aCLL and trisomy 12 (P < 0.00001); mantle zone lymphoma (MZL) and t(11;14) (P < 0.00001) and del(6)(q) (P < 0.0001); CLL/mixed cell type and del(6)(q) (P < 0.002); follicular lymphoma and t(14;18) (P < 0.00001); splenic lymphoma with villous lymphocytes and del(7)(q) (P < 0.0004); leukemic lymphoma (LL) with rearrangements in chromosome 9q (P < 0.0001) and trisomy of 3 (P < 0.001).
The present study for the first time demonstrates the occurrence of t(3;14)/BCL6 gene rearrangement in MZBCL, thus suggesting a role of the BCL6 proto-oncogene in the pathogenesis of MZBCL.
Karpas1106P was derived from mediastinal lymphoblastic B-cell lymphoma and exhibited the immunophenotype characteristic of marginal-zone B-cell lymphoma (MZL): smIg+, pan-B antigen+, CD5-, CD10- and CD23-.
Karpas1106P was derived from mediastinal lymphoblastic B-cell lymphoma and exhibited the immunophenotype characteristic of marginal-zone B-cell lymphoma (MZL): smIg+, pan-B antigen+, CD5-, CD10- and CD23-.
Expression analyses confirmed that PAX-5 transcription was upregulated due to efficient initiation at the Smicro promoter in the malignant B lymphocytes of patient MZL-1.
Strong CXCR3 expression was also seen in splenic marginal zone lymphoma (14 of 14 cases) and in the monocytoid and plasmacytic cells in extranodal marginal zone lymphoma (15 of 16 cases).
In B cell non-Hodgkin's lymphoma (NHL), MUM1 expression was observed in 73.2% (30/41) of diffuse large B cell lymphoma (DLBCL), 20% (1/5) of marginal zone lymphoma (MZL) and 43% (3/7) of small lymphocytic lymphoma (SLL) cases, whereas it was not seen in any cases of mantle cell lymphoma (MCL) or follicle center lymphoma (FCL).
In B cell non-Hodgkin's lymphoma (NHL), MUM1 expression was observed in 73.2% (30/41) of diffuse large B cell lymphoma (DLBCL), 20% (1/5) of marginal zone lymphoma (MZL) and 43% (3/7) of small lymphocytic lymphoma (SLL) cases, whereas it was not seen in any cases of mantle cell lymphoma (MCL) or follicle center lymphoma (FCL).
The BCL6 proto-oncogene, located on 3q27, which is rearranged in some MZBCL and a high proportion of large cell B-cell lymphomas with extranodal localization, represents one of the candidate genes residing in these critical regions.
We conclude that deletions of the analyzed tumor suppressor genes are relatively rare in MZBCL, which contrasts with the findings in some other subtypes of NHL.
The translocation of chromosome 11, long arm, region 2, band 1, to chromosome 18, long arm, region 2, band 1 (t(11;18)(q21;q21)) represents a recurrent chromosomal abnormality in extranodal marginal zone B-cell lymphoma (MZBCL) of mucosa-associated lymphoid tissue (MALT) type and leads to a fusion of the apoptosis inhibitor-2 (API2) gene on chromosome 11 and the MALT lymphoma-associated translocation (MLT) gene on chromosome 18.
The translocation of chromosome 11, long arm, region 2, band 1, to chromosome 18, long arm, region 2, band 1 (t(11;18)(q21;q21)) represents a recurrent chromosomal abnormality in extranodal marginal zone B-cell lymphoma (MZBCL) of mucosa-associated lymphoid tissue (MALT) type and leads to a fusion of the apoptosis inhibitor-2 (API2) gene on chromosome 11 and the MALT lymphoma-associated translocation (MLT) gene on chromosome 18.
i) Besides +3 and 7q-, 13q14 deletion, total/partial +12, BCL6 rearrangement, and deletions at 6q21, 11q22-23, and 17p13.3 are relatively frequent events in MZBCL; ii) unlike in mantle cell lymphoma, 9p21 deletion occurred infrequently in MZBCL; iii) a switch into high grade histology is usually associated with complex chromosome defects, including 6q-, 11q-, +12, and 17p.
Fourteen cases of MZBCL diagnosed according to the REAL classification were studied by conventional chromosome analysis (CCA) and by interphase fluorescence in situ hybridization (FISH) using the following probes: 3q27/BCL6, 6q21, 7q31, 9p21/p16, 11q22/ATM, 13q14, 17p13, centromeres of #3, #7, #12.Pertinent clinical data were collected.
The observed pattern of V(H) mutations suggested that nodal MZL, formerly deemed a malignancy of memory B cells, may arise from different subsets of marginal zone B cells-the naive B cells that express unmutated V(H) genes-from memory B cells showing somatic mutations without intraclonal variation, and from germinal center B cells defined by their capacity to undergo the somatic hypermutation process.(Blood.2001;98:781-786)