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Biology subjects

Baker, T. M.

Publications and source records attributed to Baker, T. M..

3 recordsLinked to original sources

Genome-wide classification of tumor-derived reads from bulk long-read sequencing

DNA extracted from tissue samples typically derives from a complex mixture of cell types. Without single cell analysis, it has been generally impossible to determine the cell type of origin for most molecules. One clear example of this is in the complex milieu of a human neoplasm. Here, we develop ROCIT (https://github.com/tobybaker/rocit), a transformer-based model to classify the tumor or non-tumor origin of individual reads from bulk tumor samples sequenced with long-read whole genome sequencing. Using somatic mutations to derive training data, ROCIT uses read-level methylation patterns to accurately classify reads from any-where in the genome without requiring the adjacent normal tissue or the explicit identification of tumor differentially methylated regions. We apply ROCIT to a cohort of prostate and ovarian tumors and demonstrate high classification accuracy across the entire genome. We then demonstrate the potential of ROCIT predictions to improve somatic variant calling. ROCIT represents a major step forward in the analysis of bulk tumors with long-reads, enabling the accurate and sensitive identification of reads with specific cell types of origin genome-wide.

bioinformatics↗

Synchronous L1 retrotransposition events promote chromosomal crossover early in human tumorigenesis

L1 retrotransposition is a significant source of genomic variation in human epithelial tumours, which can contribute to tumorigenesis. However, fundamental questions about the causes and consequences of L1 activity in cancer genomes remain unresolved, primarily due to the limitations of short-read sequencing technologies. Here, we employ multiplatform sequencing, with an emphasis on long reads, to analyse a fine selection of 10 tumours exhibiting high rates of somatic retrotransposition, encompassing over 6000 events. The analysis of L1 locus-specific single-nucleotide variants reveals a novel panorama of L1 loci activity. Furthermore, examination of the internal structure of somatic L1s uncovers the mechanisms behind their inactivation. A hidden landscape of chromosomal aberrations emerges in the light of long reads, where reciprocal translocations mediated by L1 insertion represent frequent events. Resolution of L1 bridges configuration elucidates the mechanisms of their formation, where typically two independent, but synchronous, somatic L1 insertions drive the reciprocal exchange between non-homologous chromosomes. Timing analyses indicate that L1 retrotransposition is an early driver of chromosomal instability, active before the first whole-genome doubling event. Overall, these findings highlight L1 activity as a more significant contributor to tumour genome plasticity than previously recognized, extending its impact beyond simple insertional mutagenesis.

cancer biology↗

The history of chromosomal instability in genome doubled tumors

Tumors frequently display high chromosomal instability (CIN) and contain multiple copies of genomic regions. Here, we describe GRITIC, a generic method for timing genomic gains leading to complex copy number states, using single-sample bulk whole-genome sequencing data. By applying GRITIC to 5,656 tumors, we found that non-parsimonious evolution is frequent in the formation of complex copy number states in genome-duplicated tumors. We measured CIN before and after genome duplication in human tumors and found that late genome doubling was followed by an increase in the rate of copy number gain. Copy number gains often accumulate as punctuated bursts, commonly after genome duplication. We infer that genome duplications typically affect the selection landscape of copy number losses, while only minimally impacting copy number gains. In summary, GRITIC is a novel copy number gain timing framework that permits the analysis of copy number evolution in chromosomally unstable tumors. Statement of significanceComplex genomic gains are associated with whole-genome duplications, which are frequent across tumors, span a large fraction of their genomes, and are linked to poorer outcomes. GRITIC infers when these gains occur during tumor development, which will help to identify the genetic events that drive tumor evolution.

genomics↗