Targeting the mitogen-activated protein kinase pathway: physiological feedback and drug response
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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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ERK phosphorylates CRAF to inhibit its activity, and the MAPK pathway induces DUSP phosphatases to dephosphorylate ERK and Sprouty and SPRED proteins to inhibit Ras activation.
“For example, ERK can phosphorylate CRAF to inhibit its activity; MAPK pathway can induce the expression of DUSP phosphatases to dephosphorylate ERK and Sprouty and SPRED proteins to inhibit Ras activation (41).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [41]
Acute inhibition of KRAS or MAPK in KRAS and BRAF mutant cells often results in a bi-phasic response: initial pathway shutdown, then rebound to a new steady state with increased RTK and PI3K/AKT activation.
“As a result, acute inhibition of KRAS or MAPK in KRAS and BRAF mutant cells often results in a bi-phasic response. Initially, the pathway is effectively shut down by the inhibitor. This, however, also diminishes the activity of the negative feedback loops. Consequently, the activity of the MAPK pathway gradually rebounds to a new steady state level despite the continuous presence of the inhibitor,”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [41]
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- Authors
- Pratilas, C. A., & Solit, D. B.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Solit, David B.
- Venue
- Clinical Cancer Research
- Published
- 2010-06-30
- Volume
- 16
- Issue
- 13
- Pages
- 3329-3334
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- 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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