Cited by 102Protein Kinase Regulation and GTPase SignalingLung Cancer Treatments and MutationsProtein Tyrosine Phosphatases

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A RAS Renaissance: Emerging Targeted Therapies for KRAS-Mutated Non–Small Cell Lung Cancer

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Vasan, Neil, Boyer, Julie L., Herbst, Roy S.·2014·Clinical Cancer Research

DOI 10.1158/1078-0432.ccr-13-1762PMC PMC5369356

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Abstract

Of the numerous oncogenes implicated in human cancer, the most common and perhaps the most elusive to target pharmacologically is RAS. Since the discovery of RAS in the 1960s, numerous studies have elucidated the mechanism of activity, regulation, and intracellular trafficking of the RAS gene products, and of its regulatory pathways. These pathways yielded druggable targets, such as farnesyltransferase, during the 1980s to 1990s. Unfortunately, early clinical trials investigating farnesyltransferase inhibitors yielded disappointing results, and subsequent interest by pharmaceutical companies in targeting RAS waned. However, recent advances including the identification of novel regulatory enzymes (e.g., Rce1, Icmt, Pdeδ), siRNA-based synthetic lethality screens, and fragment-based small-molecule screens, have resulted in a “Ras renaissance,” signified by new Ras and Ras pathway–targeted therapies that have led to new clinical trials of patients with Ras-driven cancers. This review gives an overview of KRas signaling pathways with an emphasis on novel targets and targeted therapies, using non–small cell lung cancer as a case example. Clin Cancer Res; 20(15); 3921–30. ©2014 AACR.

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See all 102

Authors: Vasan, N., Boyer, J. L., & Herbst, R. S.
Affiliations: Massachusetts General Hospital (US)
Cornell University (US)
Yale Cancer Center (US)
Corresponding author: Herbst, Roy S.
ORCID: Vasan, Neil
Herbst, Roy S.
Venue: Clinical Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2014-07-31
Volume: 20
Issue: 15
Pages: 3921-3930
ISSN: 1078-0432 (ISSN-L)
1557-3265
DOI: 10.1158/1078-0432.ccr-13-1762
PMC: PMC5369356
OpenAlex: W1982288880
Cited by: 102
References: 79
Citations by year: 2026: 3 · 2025: 8 · 2024: 5 · 2023: 3 · 2022: 8 · 2021: 6 · 2020: 7 · 2019: 9 · 2018: 10 · 2017: 14 · 2016: 13 · 2015: 14 · 2014: 2
FWCI: 1.35
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Clinical Cancer Research (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R01CA155196)
National Institute of General Medical Sciences (T32GM007205)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Keywords: KRAS mutation, non-small cell lung cancer, oncogenic Ras, targeted therapy, Ras signaling, farnesyltransferase inhibitors, RCE1, IcmT, PDEδ, synthetic lethality, siRNA screen, RAS-driven cancers
MeSH terms: Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Prognosis, Proto-Oncogene Proteins, Signal Transduction, Proto-Oncogene Proteins p21(ras), ras Proteins, Molecular Targeted Therapy

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A RAS Renaissance: Emerging Targeted Therapies for KRAS-Mutated Non–Small Cell Lung Cancer

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