New insights into lung cancer development uncovered by NIH study
Researchers identified that mobile DNA LINE-1 (L1) activity and specific mutational signatures contribute to the aggressiveness of lung cancers, with KRAS mutations driving rapid clonal evolution and EGFR mutations leading to more diverse tumor architectures, informing future therapeutic strategies.
The National Institutes of Health (NIH) has announced results from a study that could broaden our understanding of aggressive lung cancers and how they develop, according to an announcement.
The researchers, led by the NIH, used whole-genome sequencing to identify 542 lung adenocarcinomas with diverse clonal architectures. Upon analyzing them, they noticed “a collection of aggressive tumors enriched with the ID2 mutational signature, characterized by a single base pair deletion.” They discovered a connection between the signature and mobile DNA LINE-1 (L1). The scientists noted that this could be why lung cancer is so aggressive in these patients. L1 was reborn in these tumors and can insert “many copies of itself in different places across the genome.”
Another discovery from this study is that KRAS mutations cause “rapid clonal evolution,” and EGFR mutations have “more sub-clonal architecture.” The researchers hope these findings will lead to early diagnosis, less treatment resistance, and personalized care.
