Signalling input from divergent pathways subverts B cell transformation.

ABSTRACT: Malignant transformation of cells typically involves several genetic lesions, whose combined activity gives rise to cancer¹. Here we analyse 1,148 patient-derived B-cell leukaemia (B-ALL) samples, and find that individual mutations do not promote leukaemogenesis unless they converge on one single oncogenic pathway that is characteristic of the differentiation stage of transformed B cells. Mutations that are not aligned with this central oncogenic driver activate divergent pathways and subvert transformation. Oncogenic lesions in B-ALL frequently mimic signalling through cytokine receptors at the pro-B-cell stage (via activation of the signal-transduction protein STAT5)^2-4 or pre-B-cell receptors in more mature cells (via activation of the protein kinase ERK)^5-8</

SUBMITTER: Chan LN 

PROVIDER: S-EPMC7394729 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature