Cited by 186Melanoma and MAPK PathwaysProtein Kinase Regulation and GTPase SignalingProtein Tyrosine Phosphatases

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Targeting the Mitogen-Activated Protein Kinase Pathway: Physiological Feedback and Drug Response

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Pratilas, Christine A., Solit, David B.·2010·Clinical Cancer Research

DOI 10.1158/1078-0432.ccr-09-3064PMC PMC2912210

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Abstract

Mitogen-activated protein kinase (MAPK) pathway activation is a frequent event in human cancer and is often the result of activating mutations in the BRAF and RAS oncogenes. Targeted inhibitors of BRAF and its downstream effectors are in various stages of preclinical and clinical development. These agents offer the possibility of greater efficacy and less toxicity than current therapies for tumors driven by oncogenic mutations in the MAPK pathway. Early clinical results with the BRAF-selective inhibitor PLX4032 suggest that this strategy will prove successful in a select group of patients whose tumors are driven by V600E BRAF. Relief of physiologic feedback upon pathway inhibition may, however, attenuate drug response and contribute to the development of acquired resistance. An improved understanding of the adaptive response of cancer cells to MAPK pathway inhibition may thus aid in the identification of those patients most likely to respond to targeted pathway inhibitors and provide a rational basis for tailored combination strategies. Clin Cancer Res; 16(13); 3329–34. ©2010 AACR.

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Authors: Pratilas, C. A., & Solit, D. B.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
Corresponding author: Solit, David B.
ORCID: Pratilas, Christine A.
Solit, David B.
Venue: Clinical Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2010-06-30
Volume: 16
Issue: 13
Pages: 3329-3334
ISSN: 1078-0432 (ISSN-L)
1557-3265
DOI: 10.1158/1078-0432.ccr-09-3064
PMC: PMC2912210
OpenAlex: W2079576402
Cited by: 183
References: 74
Citations by year: 2026: 5 · 2025: 7 · 2024: 2 · 2023: 7 · 2022: 7 · 2021: 6 · 2020: 5 · 2019: 9 · 2018: 9 · 2017: 9 · 2016: 14 · 2015: 9 · 2014: 17 · 2013: 21 · 2012: 20
FWCI: 2.13
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Clinical Cancer Research (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R01CA127240, K08CA127350, P30CA008748, P50CA092629)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Keywords: MAPK signaling, BRAF V600E mutation, RAS mutations, BRAF inhibitors, vemurafenib, physiological feedback, acquired drug resistance, targeted therapy, combination therapy, predictive biomarkers
MeSH terms: Antineoplastic Agents, Humans, Neoplasms, Genes, ras, Signal Transduction, Drug Delivery Systems, Mitogen-Activated Protein Kinases, Feedback, Physiological, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf

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Targeting the Mitogen-Activated Protein Kinase Pathway: Physiological Feedback and Drug Response

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