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Fig. 1 | BMC Cancer

Fig. 1

From: A phase II study of the PI3K inhibitor copanlisib in combination with the anti-CD20 monoclonal antibody rituximab for patients with marginal zone lymphoma: treatment rationale and protocol design of the COUP-1 trial

Fig. 1

PI3K signaling pathway in physiological and malignant B-cells. PI3K activity is regulated in both a B-cell receptor (BCR) and receptor tyrosine kinase (RTK) mode. Upon RTK stimulation PI3K catalyses phosphatidylinositol 4,5-bisphosphonate (PIP2) to generate phosphatidylinositol 3,4,5-triphosphate (PIP3), resulting in recruitment of AKT (Protein kinase B) and activation of the mTOR (mechanistic target of rapamycin) pathway. On the other hand, BCR stimulation leads to the recruitment of BTK (bruton tyrosine kinase) via PIP3 with downstream activation of the MAPK (mitogen-activated protein kinase) and NFĸB (nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells) signaling pathway. Pathological triggering of both signaling pathways eventually results in increased proliferation and survival advantage of the B-cell. MZL = marginal zone lymphoma, Syk = spleen tyrosine kinase, Lyn = kinase

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BMC Cancer

ISSN: 1471-2407

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