Five (27.8%) of the 18 patients showed different IgH gene rearrangements in the two components and three (60%) of these five patients had differential response of MALToma and DLBCL to HPET.
The chromosomal translocation t(8;14)(q24;q32) with juxtaposition of MYC to enhancer elements in the immunoglobulin heavy chain (IGH) gene locus is the genetic hallmark of the majority of Burkitt lymphoma and a subset of Diffuse large B-cell lymphoma patients.
Tissue microarray sections from 78 DLBCLs were evaluated for BCL3 protein expression using immunohistochemistry and for BCL3 and IGH rearrangement using Fluorescent in situ hybridisation (FISH) with split-apart probes.
Although these findings suggest that t(14;18)/IGH-MALT1 is a rare molecular event in gastrointestinal MALT lymphomas and DLBCLs, further studies to elucidate the role of this genetic alteration in these diseases are indicated.
Somatically mutated immunoglobulin IGHV@ genes without intraclonal heterogeneity indicate a postgerminal centre origin of primary intraocular diffuse large B-cell lymphomas.
B-cell lymphomas with concurrent IGH-BCL2 and MYC rearrangements are aggressive neoplasms with clinical and pathologic features distinct from Burkitt lymphoma and diffuse large B-cell lymphoma.
The variable region of the IgH gene of secondary DLBCL (CD5+ two cases and CD5- two cases) exhibited a 0.5-9.0% somatic mutation range and no intraclonal microheterogeneity.
We tested empirically clonality rearrangements of IGH and incomplete IGH D-J, on formalin-fixed, paraffin embedded (FFPE) tissue of patients with diffuse large B cell lymphoma (DLBCL).
NOTCH1 mutation increased the risk of transformation to diffuse large B-cell lymphoma independently from IGHV, with this being validated in resampling tests of replicability.
We have therefore investigated somatic mutation of the lg heavy chain (IgH) genes among 17 cases of B-ALCL to clarify whether there is a difference in characteristic and origin of tumor cells between B-ALCL, B-HD and DLBCL.
Non-IGH gene was the preferential partner of rearrangement in those diffuse large B-cell lymphoma showing MYC heteroclonality (P=0.016) and/or non-classical FISH breakpoints (P=0.058).
To clarify this issue, 12 HIV-related DLBCL from 11 patients were analysed for the presence of clonally rearranged and somatically mutated immunoglobulin heavy chain (IgH) genes and their association with EBV was determined.
The t(14;18)(q32;q21) involving the IGH and the MALT1 gene has previously been described in PCMZL, whereas the t(14;18)(q32;q21)IGH/BCL2 seems to be restricted to follicular lymphoma and diffuse large B-cell lymphoma.
We have comprehensively investigated the incidence and clinical significance of lymphoma-associated chromosomal translocations, particularly those involving the immunoglobulin heavy chain (IGH) gene locus, in a large series of gastric DLBCL.
While they share similarities with extracerebral DLBCL with respect to the presence of IGH translocations, they appear to differ in the usage of translocation partner genes, which remain to be identified.
This study was performed on samples from 70 patients with B-NHL, including two cases of follicular lymphoma (FL), 20 cases of diffuse large B-cell lymphoma (DLBCL), one case of mantle cell lymphoma (MCL), and 47 cases of B-cell neoplasm (non-classified), which had been previously assessed for complete IGH clonality, and failure to clarify gene rearrangements.
These findings suggest that EBV(+) DLBCL and EBV(-) DLBCL were both derived from germinal center (GC) or post-GC B cells, and EBV(+) DLBCL frequently have a non-functional IgH gene owing to crippling mutation.
Similarly, the translocation involving at least one of the IGs (IGH, IGK and/or IGL) was associated with more favorable prognosis in DLBCLs or even in DLBCL, NOS.