Matthew G.K. Benesch

TL;DR: This review is intended to present an up-to-date understanding of the physiological and pathological consequences of changing the activities of the different LPPs, especially in relation to cell signaling by LPA and S1P.

TL;DR: Current knowledge on autotaxin‐mediated disease processes including cancer, and recent advancements in the development of autotAXin‐targeting strategies are summarized, and new insights into autOTaxin as an inflammatory mediator in the tumor microenvironment that promotes cancer progression and therapy resistance are provided.

TL;DR: It is shown for the first time that inhibiting autotaxin decreases initial tumor growth and subsequent lung metastatic nodules both by 60% compared with vehicle‐treated mice.

TL;DR: It is demonstrated that accumulation of LPA in the circulation decreases ATX production, but this feedback regulation can be overcome by the inflammatory cytokines, TNF-α or interleukin 1β, which enables high LPA and ATX levels to coexist in inflammatory conditions.

TL;DR: It is shown that concentrations of tamoxifen and its metabolites, which accumulate in tumors of patients, killed both ER α-positive and ERα-negative breast cancer cells, and overcoming tamoxIFen-induced activation of the anti-oxidant response element (ARE) could increase the efficacy of tamxifen in treating breast cancer.