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The mutational and clonality profile of high-grade serous ovarian cancer is established early in tumour development and conserved throughout therapy resistance


The diversity of high-grade serous ovarian cancer (HGSOC) makes tracking tumour evolution challenging. Oxford Nanopore sequencing successfully phased ultra-long SVs, revealing that tumour evolution is driven by early clonal events rather than therapy-induced mutations. Despite shared mutational mechanisms, each person develops unique somatic mutations, supporting the need for a personalised medicine approach to cancer treatment.

Key points:

  • Tumour heterogeneity is believed to be a key feature of recurrence and resistance in HGSOC tumours

  • In matched primary and recurrent HGSOC tumours from 32 patients, Diaz and Gull et al. found that somatic mutation profiles remained largely conserved through disease progression

  • Chemoresistance likely arises from pre-existing clones rather than new mutations

  • Ultra-long reads generated by Oxford Nanopore sequencing validated SVs detected by short-read sequencing, but also uncovered novel SVs including large insertions, deletions, and complex rearrangements

  • SV analysis identified three distinct tumour subtypes, providing potential biomarkers for targeted treatment strategies in the future

Sample type: human ovarian cancer tumours

Kit: Ultra-Long DNA Sequencing Kit

Authors: Michael Diaz, Nicole Gull, Pei-Chen Peng, Kruttika Dabke, Jessica Baker, Jennifer Sun, Juan Alvarado, Benjamin Bastin, Nimisha Mazumdar, Chintda Santiskulvong, Andrew J. Li, Beth Y. Karlan, BJ Rimel, Sarah J. Parker, Simon A. Gayther, Michelle R. Jones

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