Direct Ras G12C inhibitors: crossing the rubicon

Colin R Lindsay; Fiona H Blackhall

doi:10.1038/s41416-019-0499-1

Direct Ras G12C inhibitors: crossing the rubicon

Br J Cancer. 2019 Jul;121(3):197-198. doi: 10.1038/s41416-019-0499-1. Epub 2019 Jun 26.

Authors

Colin R Lindsay^{1

2

3}, Fiona H Blackhall^{4

5

6}

Affiliations

¹ Division of Molecular and Clinical Cancer Sciences, University of Manchester, Manchester, UK. colin.lindsay@manchester.ac.uk.
² Department of Medical Oncology, The Christie NHS Foundation Trust, Wilmslow Road, Manchester, M20 4BX, UK. colin.lindsay@manchester.ac.uk.
³ Cancer Research UK Lung Cancer Centre of Excellence, London and Manchester, Manchester, UK. colin.lindsay@manchester.ac.uk.
⁴ Division of Molecular and Clinical Cancer Sciences, University of Manchester, Manchester, UK.
⁵ Department of Medical Oncology, The Christie NHS Foundation Trust, Wilmslow Road, Manchester, M20 4BX, UK.
⁶ Cancer Research UK Lung Cancer Centre of Excellence, London and Manchester, Manchester, UK.

Abstract

Despite its status as the most commonly mutated oncogene in cancer, Ras has long been considered 'undruggable'. In 2019, we will see the first clinical trial results for direct mutant Ras inhibitors, a result of persistent cross-disciplinary research that has been informed by a number of previous clinical and biological failures.

Publication types

Editorial
Research Support, Non-U.S. Gov't

MeSH terms

Benzimidazoles
Humans
Mutation*
Proto-Oncogene Proteins p21(ras) / antagonists & inhibitors*
Proto-Oncogene Proteins p21(ras) / genetics*
ras Proteins / antagonists & inhibitors*

Substances

AZD 6244
Benzimidazoles
KRAS protein, human
Proto-Oncogene Proteins p21(ras)
ras Proteins

Abstract

Publication types

MeSH terms

Substances

Grants and funding