Skip to main content
. Author manuscript; available in PMC: 2017 Dec 30.
Published in final edited form as: Expert Opin Investig Drugs. 2017 Oct 6;26(11):1267–1279. doi: 10.1080/13543784.2017.1384815

Figure 1.

Figure 1

(a) Upstream signals from the B cell receptor, secreted molecules (e.g. cytokines), and membrane-bound and extracellular matrix proteins stimulate the PI3K pathway. At different stages of B cell development, certain isoforms of the catalytic subunit p110 are responsible for the majority of PI3K pathway output (represented by relative size). p110β and p110γ are not included as knockout mice have no overt B cell phenotype and the role of these isoforms in B cell development is less studied. Downstream effects of PI3K activation include inhibition of IKK, FOXO, and the proapoptotic protein Bad as well as activation of mTOR. (b) A neoplastic B cell co-opts upstream signals from the microenvironment to constitutively activate the PI3K pathway. A more prominent role for p110α in aggressive NHL is hypothesized based on improved efficacy of p110α/δ combinatorial inhibitors for the treatment of these diseases. BCR – B cell receptor, NHL – Nonhodgkin Lymphoma.