Fig. 8: Proposed mechanism of 177Lu-lilotomab action. | Leukemia

Fig. 8: Proposed mechanism of 177Lu-lilotomab action.

From: The therapeutic effectiveness of 177Lu-lilotomab in B-cell non-Hodgkin lymphoma involves modulation of G2/M cell cycle arrest

Fig. 8

Beta particles emitted by 177Lu cause DNA double strand breaks that are recognized by the ATM/ATR sensor proteins. In Burkitt’s lymphoma (BL) and mantle cell lymphoma (MCL) cells, this leads to CHK1 phosphorylation and activation and consequently to phosphorylation of WEE-1 and MYT-1. This subsequently induces CDK1 phosphorylation at Tyr15 and Thr14, and G2/M cell cycle arrest to allow DNA repair. Conversely in follicular lymphoma (FL) cells, phosphorylation of CDK1 at Thr161 by CDK7 promotes G2/M cell cycle progression. Unrepaired DNA lesions lead to apoptosis.

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