Mutation alters chromatin changes during injury response to drive cancer

Vassiliadis, Dane; Dawson, Mark A.

doi:10.1038/d41586-021-00211-y

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03 February 2021
Correction 08 February 2021

Mutation alters chromatin changes during injury response to drive cancer

Cancer-associated mutations promote the formation of pancreatic tumours after tissue injury, but how this occurs is unclear. Changes to chromatin in injured cells with such mutations explain this predisposition to malignancy.

Dane Vassiliadis⁰ &
Mark A. Dawson¹

Dane Vassiliadis
1. Dane Vassiliadis is at the Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, Australia, and in the Sir Peter MacCallum Department of Oncology, University of Melbourne.
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Mark A. Dawson
1. Mark A. Dawson is at the Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, Australia, in the Sir Peter MacCallum Department of Oncology, University of Melbourne, and at the University of Melbourne Centre for Cancer Research.
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It is increasingly clear that, as humans age, many, if not most, of our tissues become composed of populations of cells, termed clones, that often harbour genetic mutations found in the malignant tumours that arise from the same type of tissue. Although these clonal populations seem to be normal cellular lineages apart from the cancer-associated mutations, little is known about how these cells respond to damage caused by exposure to ultraviolet light or toxic chemicals, for example. A process called metaplasia — the replacement of one cell type with another after tissue damage — increases the risk of cancer formation¹. Why abnormal repair during metaplasia predisposes cells to form cancer is mainly unknown. Writing in Nature, Alonso-Curbelo et al.² report a study of pancreatic cancer in mice that reveals how a mutation biases the outcome of metaplasia towards the development of cancer.

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Nature 590, 557-558 (2021)

doi: https://doi.org/10.1038/d41586-021-00211-y

Updates & Corrections

Correction 08 February 2021: This article incorrectly described KRAS as a type of enzyme termed a kinase. It is a GTPase.

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Competing Interests

M.A.D. has been a member of advisory boards for GlaxoSmithKline, CTx CRC, Storm Therapeutics, Celgene and Cambridge Epigenetix. The Dawson lab receives research funding from CTx CRC.