B cells predominate in a quiescent state until an antigen is encountered, which results in
rapid growth, proliferation and differentiation of the B cells. These distinct cell states are …

Chronic myeloid leukemia (CML) is induced by the oncogenic BCR-ABL1 tyrosine kinase
and can be effectively treated for many years with tyrosine kinase inhibitors (TKIs). However, …

BCL6 protects germinal center (GC) B cells against DNA damage–induced apoptosis during
somatic hypermutation and class-switch recombination. Although expression of BCL6 was …

The Sox4 transcription factor mediates early B-cell differentiation. Compared with normal pre-B
cells, SOX4 promoter regions in Ph + ALL cells are significantly hypomethylated. Loss …

Initial cell surface expression of the pre-B cell receptor induces proliferation. After 2 to 5
divisions, however, large pre-BII (Fraction C') cells exit cell cycle to become resting, small pre-BII …

Germinal center (GC) B cells surge in their proliferative capacity, which poses a direct risk for
B cell malignancies. G1- to S-phase transition is dependent on the expression and stability …

Somatic mutations in cancer cells may influence tumor growth, survival, or immune interactions
in their microenvironment. The tumor necrosis factor receptor family member HVEM (…

The PI3K pathway is integral for the germinal center (GC) response. However, the contribution
of protein kinase B (AKT) as a PI3K effector in GC B cells remains unknown. Here, we …

… Ramezani-Rad performed and analyzed the calcium flux and proliferation assays. CF Ware,
P. Ramezani-Rad, … Ramezani-Rad, and E. Kao provided assistance with experiments. M. …

Highlights • The mutational landscape in B-NHL can be mechanistically assessed in murine
models. • Murine models can mimic the etiology and evolution of human B-NHL in vivo. • …