Chapters authored
Signal Pathway in Precursor B-Cell Lymphoblastic Leukemia/Lymphoma
Stat5, c-myc, Hipk2, Fiz1, and ZFP521 to lymphomagenesis precursor B-cell lymphoblastic lymphoma/leukemia have been previously identified as a putative gene involved in the induction of B-cell lymphomagenesis. In this review, we summarize the role of ZFP521 in B-cell lymphomagenesis. Zinc finger protein 521 (Zfp521) is a novel identified gene that is responsible for pre–B-lymphoblastic lymphomagenesis through activation of pre–B-cell receptor (pre-BCR)-signaling by upregulation of adaptor genes and related kinases in the signaling downstream. The pre-BCR-signaling molecules, FLT3, CD43, and IL-7 receptor (IL-7R) were positively regulated by these genes. Stimulation of pre-BCR and/or IL-7R signaling caused aberrant upregulation of other oncogene sets such as cyclin genes, thereby inducing the growth of pre–B cells. IL-7R/Janus kinase (JAK)/STAT signaling cascade is one of the key signaling pathways that are activated in precursor B-cell lymphoblastic lymphoma/leukemia. FLT3, CD43, and pre-BCR cascades crosstalk with JAK/STAT cascade. FLT3 and CD43 cascades have the potential to enhance JAK/STAT cascade effect on pre-B cell growth. On the other hand, pre-BCR and interleukin (IL)-7 receptor exerted competitive effects on pre–B-cell growth; thus, precursor B-cell lymphoblastic lymphomagenesis is a consequence through interaction with these cascades.
Part of the book: Lymphocyte Updates