Therefore, we examined 170 cases of B-cell chronic lymphocytic leukemia (B-CLL), 7 cases of B-cell prolymphocytic leukemia (B-PLL), 25 cases of hairy cell leukemia (HCL) and 22 cases of splenic lymphoma with villous lymphocytes (SLVL) with defined cytogenetic abnormalities by DNA blot using both 5' and 3' BCL2 probes to search for rearrangement of the BCL2 locus.
BCL2 protein levels in CLL reflect a complex interplay of transcriptional and posttranscriptional controls, but do not appear to be associated with the -938C>A promoter SNP.
However, phase III trials incorporating G3139, a phosphorothioate oligomer targeted to the initiation codon region of the bcl-2 mRNA, have recently been completed in advanced melanoma, myeloma, and chronic lymphocytic leukemia (CLL).
In this paper, we completed the structural analysis of the bcl-2/Ig lambda gene rearrangement in CLL 1446 by cloning the corresponding partner of the rearrangement.
Specific cutaneous involvement by B-CLL was confirmed by the detection of t(14;18)(q32;q21) (BCL2-IGH) using FISH in neoplastic B cells within the skin infiltrates.
Compared with samples from healthy donor controls (nonsensitive) and chronic lymphocytic leukemia (CLL) patients (highly sensitive), AML samples exhibited variable responses to BCL-2 inhibition.
The background frequency of t(14;18) (q32;q21) chromosomal translocations at the locus associated with B-cell leukemia/lymphoma-2 (BCL2) was determined from a survey of the peripheral blood lymphocytes (PBLs) of 53 living individuals and from tissues of 31 autopsies by using a nested PCR assay.
Patients who were PCR-positive for B-cell leukemia-lymphoma 2 (bcl-2) gene rearrangement [t(14;18)] were evaluated for responses to rituximab alone or combined with CHOP.
BCL2-associated X protein (BAX) and BCL2 antagonist/killer 1 (BAK1), B-cell leukemia/lymphoma 2 (BCL2) family members, mediate mitochondrial damage to generate ROS after SINV infection.
The particular translocation in follicular lymphomas (FLs) is a t(14;18)(q32;q21), recombining the immunoglobulin heavy chain (IgH) gene on chromosome 14 with the B-cell leukemia/lymphoma 2 (BCL2) gene on chromosome 18.
BCL-2 (B-cell leukemia/lymphoma 2) gene has been demonstrated to be associated with breast cancer development and a single nucleotide polymorphism (SNP; -938C > A) has been identified recently.
The BCL2 translocations were observed in 22 CLL cases, including 7 monoclonal B-cell lymphocytosis (MBL) cases re-classified according to the new International Workshop on CLL criteria, six small lymphocytic lymphoma (SLL) cases, 1 splenic marginal zone lymphoma (SMZL) case and eight cases of unclassifiable CLPD with overlapping CLL/MZL features.
The translocation in chronic lymphocytic leukemia results in the juxtaposition of the bcl-2 gene to various regions on the immunoglobulin light chain loci.
The bcl-3 pattern of expression also bears close resemblance to that of bcl-2 (Gurfinkel et al., 1987), which is frequently associated with human B follicular lymphomas [t(14; 18)] and some chronic lymphocytic leukemias (Adachi et al., 1989; 1990; Adachi & Tsujimoto, 1989).
Real-time polymerase chain reaction was used to detect expression of the mRNA encoding the apoptosis inhibition B-cell leukemia/lymphoma 2 (bcl-2) gene.
The most common translocation in non-Hodgkin lymphomas (NHL) is a t(14;18)(q32;q21) recombining the immunoglobulin heavy-chain gene (IGH) on chromosome 14 with the B cell leukemia/lymphoma 2 (BCL2) gene on chromosome 18.
Thus, based on differences in bcl-1 and bcl-2 rearrangements, molecular analysis may help to distinguish follicular lymphoma from diffuse centrocytic lymphoma and chronic lymphocytic leukemia.
This compares with the presence of these rearrangements in up to 10% of patients in other reports, and suggests that the incidence of 5' BCL2 rearrangements in CLL is considerably less than 10%.
Bcl-2 protein expression and p53 gene mutation in chronic lymphocytic leukemia: correlation with in vitro sensitivity to chlorambucil and purine analogs.
Interestingly, CLL cells from lymph node and CLL cells co-cultured on stroma expressed lower levels of CTLA4 and higher levels of c-Fos, c-Myc, and Bcl-2 compared to CLL control cells.
Given the success of venetoclax in the clinical setting thus far, it is likely that BCL-2 inhibition will take on an increasingly important role in the treatment of CLL going forward.