ARID1A mutations in lung cancer: biology, prognostic role, and therapeutic implications
Mutations in the AT-interacting domain-rich protein 1A (ARID1A) gene, a critical component of the switch/sucrose nonfermentable (SWI/SNF) complex, are frequently found in most human cancers. Approximately 5-10% of lung cancers carry ARID1A mutations. ARID1A loss in lung cancer correlates with clinic...
Saved in:
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
11 May 2023
|
| In: |
Trends in molecular medicine
Year: 2023, Volume: 29, Issue: 8, Pages: 646-658 |
| ISSN: | 1471-499X |
| DOI: | 10.1016/j.molmed.2023.04.005 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.molmed.2023.04.005 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S1471491423000758 |
| Author Notes: | Fukang Jin, Zhiguang Yang, Jingbo Shao, Jianxin Tao, Christoph Reißfelder, Sonja Loges, Lei Zhu and Sebastian Schölch |
| Summary: | Mutations in the AT-interacting domain-rich protein 1A (ARID1A) gene, a critical component of the switch/sucrose nonfermentable (SWI/SNF) complex, are frequently found in most human cancers. Approximately 5-10% of lung cancers carry ARID1A mutations. ARID1A loss in lung cancer correlates with clinicopathological features and poor prognosis. Co-mutation of ARID1A and epidermal growth factor receptor (EGFR) results in the limited efficacy of EGFR tyrosine kinase inhibitors (EGFR-TKIs) but increases the clinical benefit of immune checkpoint inhibitors (ICIs). ARID1A gene mutation plays a role in cell cycle regulation, metabolic reprogramming, and epithelial-mesenchymal transition. We present the first comprehensive review of the relationship between ARID1A gene mutations and lung cancer and discuss the potential of ARID1A as a new molecular target. |
|---|---|
| Item Description: | Online verfügbar 11 May 202323 Gesehen am 05.10.2023 |
| Physical Description: | Online Resource |
| ISSN: | 1471-499X |
| DOI: | 10.1016/j.molmed.2023.04.005 |