Indeed, the lack of CD5 and expression of CD10 associated with MYC rearrangement detected on interphasic nuclei could support the diagnosis of diffuse large B-cell lymphoma or Burkitt lymphoma.
Unlike DH-BCL2/MYC lymphomas, however, they are more likely to be CD10(-) but IRF4/MUM-1(+) (P=0.03) and, more like BL, only infrequently express BCL2 (P<0.001), and are cytogenetically less complex (P<0.04).
The expression of CD10 and BCL6 but not BCL2, a high Ki-67 PI (>90%) and a C-MYC rearrangement but not BCL2 or BCL6 rearrangement are the features of BL.
We evaluated 35 BLs and identified atypical immunophenotypes in 4 including SIg light chain negativity in 4, negativity for B-cell antigens in 2, lack of CD10 in 1, and CD4 expression in 1.
We suggest that, concordant with the WHO classification to be published in 2008, the diagnosis of BL should be restricted to cases with expression of CD10 and BCL6, absence or very weak expression of BCL2 protein, a homogeneously very high proliferation index and a proven IG-MYC translocation without evidence of a chromosomal translocation typical for other lymphoma entities.
We can confidently distinguish BL from DLBCL-HPSS by using histopathologic and immunohistochemical (CD10, bcl-2, bcl-6, Ki-67) methods without the aid of EBER and FISH in the great majority of cases.
Retrospective work-up of the 29-year-old tumor blocks revealed the typical histologic appearance and phenotype (CD20, CD10, BCL-6 positive) of Burkitt's lymphoma (BL) with a proliferation rate of 95%.
TIMP-1-negative cells express the phenotype associated with group I BL lines and Epstein-Barr virus (EBV)-negative, nonendemic BLs (CD10+, CD38+, sIg+, and CD77+).
A collection of in vitro EBV-converted sublines of originally EBV-negative BLs that expressed a full set of the growth transformation-associated EBV proteins maintained their CD10 and cyclin D3 expression.
BALM-13 was characterized as belonging to the Burkitt lymphoma group III cell type (CD10-, CD20+, CD23+, D39+, CD77-), and BALM-14 to the Burkitt lymphoma group I cell type (CD10+, CD20+, CD23-, CD39-, CD77+).
Unlike that observed in certain Burkitt lymphoma (BL) cell lines that share the same surface phenotype (CD10+CD38+CD23-CD39-), the c-myc-transfected cells expressed lymphocyte function-associated (LFA) 1, LFA-3, and intercellular adhesion molecule 1 and grew in large clumps rather than single-cell layers.
TP-specific transcripts were not detectable or only hardly detectable in Burkitt's lymphoma cells with the group I phenotype (CD10+ CD77+ CD21- CD23- CD30- CDw70-) as well as in P3HR1 virus-converted Burkitt's lymphoma lines.
The germinal centre specific MoAbs CD10 and CD77 (Burkitt's lymphoma antigen) displayed a heterogeneous pattern of reactivity and allowed to identify 4 subgroups: CD10+/CD77+ (44 per cent), CD10+/CD77- (15 per cent), CD10-/CD77+ (36 per cent) and CD10-/CD77- (5 per cent).
Clones retaining the original BL biopsy cell phenotype (CD10/CD77-positive, activation antigen/adhesion molecule-negative) expressed the virus-encoded nuclear antigen EBNA 1 but not any of the other known latent proteins, EBNAs 2, 3a, 3b, 3c, -LP and latent membrane protein (LMP).
Other activation antigens were unaffected by EBNA-2 expression, as were markers already expressed on the parent BL cell line, including BL markers (cALLA and BLA), proliferation markers (transferrin receptor and BK19.9), and cell adhesion-related molecules (LFA-1 and LFA-3).
In contrast with acute lymphoblastic leukemia, the common acute lymphocytic leukemia antigen (CD10) was expressed on nearly all BL cell lines of intermediate maturation stages but only on half of the pre-B ones.