Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS

Erin Sheffels; Robert L. Kortum

doi:10.1021/acs.jmedchem.1c00698

Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS

Erin Sheffels
, Robert L. Kortum^*

^*Corresponding author for this work

Pharmacology and Molecular Therapeutics

Research output: Contribution to journal › Review article › peer-review

20 Scopus citations

Abstract

In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.

Original language	English
Pages (from-to)	6566-6568
Number of pages	3
Journal	Journal of Medicinal Chemistry
Volume	64
Issue number	10
DOIs	https://doi.org/10.1021/acs.jmedchem.1c00698
State	Published - 27 May 2021

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10.1021/acs.jmedchem.1c00698

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title = "Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS",

abstract = "In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.",

author = "Erin Sheffels and Kortum, \{Robert L.\}",

note = "Publisher Copyright: {\textcopyright} Not subject to U.S. Copyright. Published 2021 by American Chemical Society.",

year = "2021",

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doi = "10.1021/acs.jmedchem.1c00698",

language = "English",

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TY - JOUR

T1 - Breaking Oncogene Addiction

T2 - Getting RTK/RAS-Mutated Cancers off the SOS

AU - Sheffels, Erin

AU - Kortum, Robert L.

N1 - Publisher Copyright: © Not subject to U.S. Copyright. Published 2021 by American Chemical Society.

PY - 2021/5/27

Y1 - 2021/5/27

N2 - In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.

AB - In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.

UR - https://www.scopus.com/pages/publications/85106456220

U2 - 10.1021/acs.jmedchem.1c00698

DO - 10.1021/acs.jmedchem.1c00698

M3 - Review article

C2 - 33961431

AN - SCOPUS:85106456220

SN - 0022-2623

VL - 64

SP - 6566

EP - 6568

JO - Journal of Medicinal Chemistry

JF - Journal of Medicinal Chemistry

IS - 10

ER -

Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS

Abstract

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