AHR
Overview
AHR (aryl hydrocarbon receptor) is a ligand-activated transcription factor involved in xenobiotic metabolism, immune regulation, and cell proliferation. In cancer genomics, AHR expression has been identified as a pharmacogenomic biomarker: elevated AHR expression correlates with enhanced sensitivity to MEK inhibitors in NRAS-mutant cancer cell lines, and shRNA knockdown confirmed a functional dependency. AHR also regulates CYP1A1 expression, and both genes are suppressed by MEK inhibitor treatment in NRAS-mutant melanoma.
Alterations observed in the corpus
- Elevated AHR expression correlates with MEK inhibitor (PD-0325901) sensitivity in NRAS-mutant cancer cell lines; functional dependency confirmed by shRNA knockdown PMID:22460905
- Expression correlates with APOBEC-signature mutation load in muscle-invasive bladder cancer (MIBC); AHR is identified as part of the broader mutagenic landscape driven by APOBEC activity PMID:28988769
Cancer types (linked)
- Melanoma (NRAS-mutant): AHR expression is a mechanistic stratifier within NRAS-mutant lines predicting MEK inhibitor response; MEK inhibition reduces AHR and CYP1A1 expression PMID:22460905
Co-occurrence and mutual exclusivity
- AHR expression co-varies with CYP1A1 expression (a transcriptional target of AHR) in NRAS-mutant melanoma cell lines PMID:22460905
- AHR expression further stratifies MEK inhibitor sensitivity within NRAS-mutant lines in the CCLE dataset PMID:22460905
Therapeutic relevance
- AHR expression may serve as a biomarker for enhanced MEK inhibitor sensitivity in NRAS-mutant cancers; data derived from the Cancer Cell Line Encyclopedia (CCLE) profiling of 947 cell lines PMID:22460905
Open questions
- Whether AHR expression as a biomarker for MEK inhibitor sensitivity translates from cell line models to clinical settings in NRAS-mutant patients remains to be demonstrated PMID:22460905
Sources
- PMID:22460905 — Cancer Cell Line Encyclopedia (CCLE) pharmacogenomic profiling of 947 cancer cell lines
- PMID:28988769
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