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Burns Lab Publications

Featured Publications and Preprints

karlow, J., et al. (2026) • biorxiv

LINE-1 retrotransposition is a recurrent cause of MET exon 14 skipping in cancer 

Here we report 9 cases in which long interspersed element-1 (LINE-1, L1)-mediated insertions within or adjacent to MET exon 14 cause exon skipping. These describe the first recurrent and clinically actionable mutations caused by LINE-1 retrotransposition in cancer. 

law, C-T., & Burns, kh. (2026) • cell genomics

Comparative genomics reveals LINE-1 recombination with diverse RNAs

These discoveries highlight the recombinatory potential of LINE-1 RNA with implications for genome evolution, TE domestication, and somatic retrotransposition.

baldwin, et. et al. (2024) • nature

Structures, functions and adaptations of the human LINE-1 ORF2 protein

We report structures of the human ORF2p reverse transcriptase by X-ray crystallography and cryo-electron microscopy in several conformational states.

taylor, M.S., et al. (2023) • Cancer Discovery

Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

To explore ORF1p as a blood-based biomarker, we engineered ultrasensitive digital immunoassays that detect mid-attomolar (10^−17 mol/L) ORF1p concentrations in plasma across multiple cancers.

Burns. (2022) • Science

Repetitive DNA in disease

Transposons become a focus of speculation and scrutiny in biomedical research

ardeljan, d., et al. (2020) • nature molecular and structural biology

Cell fitness screens reveal a conflict between LINE-1 retrotransposition and DNA replication

LINE-1 retrotransposon overexpression is a hallmark of human cancers. We identified a colorectal cancer wherein a fast-growing tumor subclone downregulated LINE-1, prompting us to examine how LINE-1 expression affects cell growth. 

rodić, N., et al. (2015) • nature medicine

Retrotransposon insertions in the clonal evolution of pancreatic ductal adenocarcinoma

We found evidence of somatic LINE-1 insertions in PDAC genomes, which were absent from corresponding normal samples. Our findings show that LINE-1 contributes to the genetic evolution of PDAC and suggest that somatic insertions are acquired discontinuously.

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