Efficacy of the combination of MEK and CDK4/6 inhibitorsin vitroandin vivoin KRAS mutant colorectal cancer models | Zendy

Michael S. Lee | Zendy; Timothy L. Helms | Zendy; Ningping Feng | Zendy; Jason Gay | Zendy; Qing Chang | Zendy; Feng Tian | Zendy; Ji Yuan Wu | Zendy; Carlo Toniatti | Zendy; Timothy P. Heffernan | Zendy; Garth Powis | Zendy; Lawrence N. Kwong | Zendy; Scott Kopetz | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Efficacy of the combination of MEK and CDK4/6 inhibitorsin vitroandin vivoin KRAS mutant colorectal cancer models

Author(s) -

Michael S. Lee,

Timothy L. Helms,

Ningping Feng,

Jason Gay,

Qing Chang,

Feng Tian,

Ji Yuan Wu,

Carlo Toniatti,

Timothy P. Heffernan,

Garth Powis,

Lawrence N. Kwong,

Scott Kopetz

Publication year - 2016

Publication title -

oncotarget

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.373

H-Index - 127

ISSN - 1949-2553

DOI - 10.18632/oncotarget.9153

Subject(s) - palbociclib , kras , mek inhibitor , trametinib , in vivo , cancer research , mapk/erk pathway , colorectal cancer , medicine , selumetinib , cell cycle , cancer , kinase , biology , microbiology and biotechnology , breast cancer , metastatic breast cancer

Though the efficacy of MEK inhibitors is being investigated in KRAS-mutant colorectal cancers (CRC), early clinical trials of MEK inhibitor monotherapy did not reveal significant antitumor activity. Resistance to MEK inhibitor monotherapy developed through a variety of mechanisms converging in ERK reactivation. Since ERK increases cyclin D expression and increases entry into the cell cycle, we hypothesized that the combination of MEK inhibitors and CDK4/6 inhibitors would have synergistic antitumor activity and cause tumor regression in vivo.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research