AI Article Synopsis
- - The RAS gene family includes genes like KRAS that control cell growth, and mutations in KRAS are commonly associated with various cancers, leading to unchecked tumor growth.
- - Recent clinical trials have shown that many NSCLC patients are resistant to treatments targeting KRAS mutations, particularly G12C, due to factors like co-mutations and secondary resistance.
- - The paper reviews recent findings on KRAS resistance mechanisms and how KRAS interacts with the tumor microenvironment, highlighting the potential of immune checkpoint inhibitors.
Article Abstract
The RAS gene family comprises genes that regulate cell growth and differentiation. KRAS, a member of this family, is often mutated in different cancers, resulting in uncontrolled cell growth and tumor development. Recent clinical trial results on KRAS inhibition in NSCLC have defined the presence of a significant proportion of patients resistant to direct G12C inhibition. The presence of co-mutations and the occurrence of secondary resistance phenomena observed in preclinical and clinical settings partly justify these poor results. In addition, all other non-G12C mutations currently remain without specific strategies. Evidence of interactions between KRAS signaling and the TME suggests potential efficacy of immune checkpoint inhibitors. In this short paper, we have reviewed the most relevant data from recent conferences, with a focus on KRAS inhibitors resistance mechanisms and interactions with the peri-tumor immune system. Commentary.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11061671 | PMC |
| http://dx.doi.org/10.1016/j.heliyon.2024.e29739 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!