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Common gene mutations in 103 authenticated colorectal cancer cell lines
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  • Published: 27 January 2026

Common gene mutations in 103 authenticated colorectal cancer cell lines

  • Christian Kranjec  ORCID: orcid.org/0000-0001-9713-74061 na1,
  • Ina A. Eilertsen1 na1,
  • Luís Nunes  ORCID: orcid.org/0000-0002-3391-16071,
  • Seyed H. Moosavi  ORCID: orcid.org/0000-0002-0533-74761,
  • Kaja C. G. Berg1,
  • Mette Eknæs1,
  • Merete Hektoen1,
  • Barbara Niederdorfer1,
  • Guro E. Lind1,2,
  • Rolf I. Skotheim  ORCID: orcid.org/0000-0002-5609-40481,3,
  • Anita Sveen  ORCID: orcid.org/0000-0001-8219-62511,4 &
  • …
  • Ragnhild A. Lothe  ORCID: orcid.org/0000-0002-1693-10321,4 

Oncogenesis , Article number:  (2026) Cite this article

We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Cancer genetics
  • Cancer models
  • Gene amplification
  • Genomic instability

Abstract

Colorectal cancer (CRC) cell lines represent the main molecular subtypes of tumors and are valuable models for preclinical investigations. However, cell lines can diverge over time and careful selection of models based on their molecular features is key. We have authenticated 103 commonly used CRC cell lines and present the mutation profiles of 20 CRC-relevant genes sequenced to an average depth of 575 times coverage. The cell lines reflected the distinct mutation patterns of hypermutation phenotypes associated with microsatellite instability and pathogenic POLE mutations. Hypermutated cell lines appeared to have a stronger mutational divergence and more frequent subclonal mutations, while mutations not associated with hypermutation were more frequently homozygous or hemizygous, classified as pathogenic, and subject to stronger selection pressure. Loss of heterozygosity at mutated loci was primarily observed in tumor suppressor genes. Genetic interactions based on co-occurring mutations identified cell lines representative of particularly aggressive subtypes of CRC, including concurrent BRAF p.V600 and truncating APC mutations, as well as APC/TP53/RAS triple mutations with double hits of APC. This study provides a resource to guide the selection of cell lines for functional studies of CRC, and detailed mutation data including classifications of pathogenicity, variant allele frequencies and illustrations of the mutation distribution along the length of encoded proteins are included.

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Data availability

All mutations (processed data) and STR profiles are available in the supplementary material.

Code availability

The MiniCN R package, including source code, example data, and documentation, is freely available at https://github.com/SveenLab/miniCN. Additional computer code and supporting information used for data processing and plotting are accessible on Zenodo: https://doi.org/10.5281/zenodo.17357561.

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Acknowledgements

Co-115, COLO 320, EB, FRI, HT-29, Isreco-1, Isreco-3, LS1034, LS174T, TC71, SW480, and VACO 9P cells were kindly provided by Dr. Richard Hamelin (National Institute for Health and Medical Research (INSERM), France). The study was funded by grants from the South-Eastern Norway Regional Health Authority (project number 2023101 to A.S. and project numbers 2024108; 2021058 to R.A.L.), the Norwegian Cancer Society (project number 208336 to A.S. and project number 223319-2021 to R.A.L.), and the Research Council of Norway (project number 287899 to A.S.).

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Author notes

  1. These authors contributed equally: Christian Kranjec, Ina A. Eilertsen.

Authors and Affiliations

  1. Department of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway

    Christian Kranjec, Ina A. Eilertsen, Luís Nunes, Seyed H. Moosavi, Kaja C. G. Berg, Mette Eknæs, Merete Hektoen, Barbara Niederdorfer, Guro E. Lind, Rolf I. Skotheim, Anita Sveen & Ragnhild A. Lothe

  2. Department of Biosciences, The Faculty of Mathematics and Natural Sciences, University of Oslo, Oslo, Norway

    Guro E. Lind

  3. Department of Informatics, The Faculty of Mathematics and Natural Sciences, University of Oslo, Oslo, Norway

    Rolf I. Skotheim

  4. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway

    Anita Sveen & Ragnhild A. Lothe

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Contributions

KCGB, AS, and RAL designed the gene panel. BN, ME, IAE, and MH performed the experiments. CK, IAE, LN, GEL, RIS, RAL, and AS analyzed/interpreted the STR and mutational data. CK, IAE, and AS wrote the manuscript. SHM extracted data on mutations’ pathogenicity from public databases. AS and RAL provided supervision, conceptualizationn and acquired funding. All authors reviewed and approved the manuscript.

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Correspondence to Christian Kranjec or Ina A. Eilertsen.

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Kranjec, C., Eilertsen, I.A., Nunes, L. et al. Common gene mutations in 103 authenticated colorectal cancer cell lines. Oncogenesis (2026). https://doi.org/10.1038/s41389-026-00599-0

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  • Received: 16 June 2025

  • Revised: 11 December 2025

  • Accepted: 15 January 2026

  • Published: 27 January 2026

  • DOI: https://doi.org/10.1038/s41389-026-00599-0

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