Year: 2020
Type: article
Abstract: The PI3K-AKT-mTOR pathway has been at the center of anti-cancer drug development 1 , 2 , but targeted inhibition of PI3K kinase activity is proven to provide a limited therapeutic effect and is often followed by the development of resistance to the drug 3 . This limitation could in part be alleviated through concurrently inhibiting multiple pathological pathways characterized by synthetic lethality relationship. For example, beneficial effects in metastatic breast cancer are observed when inhibition of PI3K is combined with BET proteins inhibition 4 . While the need for combinations of single agent targeted therapies has become clear, this approach commonly requires dose reduction of the individual agents due to additive toxicity that may compromise efficacy 5 .
Source: Cell Discovery
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,890
Funders: U.S. Department of Health and Human Services, Division of Cancer Prevention, National Cancer Institute, Tower Cancer Research Foundation, National Institutes of Health, U.S. Food and Drug Administration, National Heart, Lung, and Blood Institute, National Cancer Institute, National Institute of General Medical Sciences
Awards: G1045712244, Interdomain crosstalk in MORC3, G1488543006, G175929860, Epigenetic mechanisms for regulation of p300, G319768886, G3266081141, G4508749629, G4745612319, G5470626986, G5604825015, Development of the first-in-class novel dual PI-3K/BRD4 inhibitor SF2523, Blood Cells in Hemostasis and Thrombosis, G9000204972, G9000247249
OpenAlex ID: W3044329447