overexpression of BCL2A1 in cell lines has been shown to mediate resistance to etoposide,88 stauros- porine89 or cisplatin.90 Conversely, silencing of BCL2A1 by gene knockdown was found to sensitize malignant B-cell lines to apoptosis induced by chemotherapy or the therapeutic antibody rituximab....
Genetic rearrangements and constitutively active B-cell receptor and NFκB signaling are common oncogenic drivers in the lymphomagenesis [2, 3]. The most frequent first line therapy is a combination of the chimeric monoclonal antibody rituximab that targets the B-lymphocyte antigen CD20 with the ...
We previously demonstrated that pretreatment with obinutuzumab, an anti-CD20 antibody13 and ibrutinib18 was able to counteract microenvironment-dependent resistance to venetoclax in MCL, mostly through the downregulation of NF-κB–dependent BCLXL expression. This rationale was involved in the design of ...
Acute A1 knockdown leads to mature B-cell loss. Single-cell suspensions from mice kept for 17 days on doxycycline were stained with specified antibodies and B-cell distribution was assessed in the GFP++fraction of cells. (a) Cells were gated on forward and side scatter profiles, then on viab...
A rabbit IgG isotype antibody was used as negative isotype control for the immunoprecipitation. For immunoprecipitation, the anti-IgG and anti-pSTAT3 antibodies were used (Cell Signaling Technology). We also included a nontemplate control in the PCR reaction (Table S2). The following formula was ...