Disease Models & Mechanisms (DMM) is an Open Access biomedical research journal advancing novel insight into the mechanism, diagnosis and therapy of human disease.
DMM is committed to publishing rigorously peer-reviewed research in disease biology that has significant translational impact at the interface of basic and clinical science. Our content is freely available to our communities of basic and clinical researchers, health professionals, patients and their advocates and families. DMM is interdisciplinary in scope, and covers a diverse range of diseases. We also publish cutting-edge techniques and resources that advance the disease biology field.
DMM is led by an international team of expert research-active Editors, including Editor-in-Chief Liz Patton and Deputy Editor-in-Chief Elaine Mardis, and supported by an outstanding Editorial Advisory Board.
Call for Papers – Translating Multiscale Research in Rare Disease
We are pleased to invite submissions for our upcoming Special Issue: Translating Multiscale Research in Rare Disease. The deadline for submitting articles to the special issue has been extended to Monday 6 November 2023.
You might be able to publish in this special issue without paying an APC. DMM is included in many of the Read & Publish agreements offered by The Company of Biologists. This enables discounted or fee-free publication of an uncapped number of Open Access Research Articles in DMM for corresponding authors at participating institutions. Find out whether your institute is included.
2024 DMM Journal Meeting - Register Now!
Pre-clinical Modelling of Human Genetic Disease and Therapy
Registration is now open for the 2024 DMM Journal Meeting 'Pre-clinical Modelling of Human Genetic Disease and Therapy', organised by Wendy Bickmore, Luke Boulter, Sara Brown, Pleasantine Mill, Liz Patton and Owen Sansom. View our fantastic line up of speakers and find out more.
Editor's choice
Acetaldehyde and defective mismatch repair increase colonic tumours in a Lynch syndrome model with Aldh1b1 inactivation by Guia Cerretelli, Ying Zhou, Mike Müller, David Adams and Mark Arends
In this month’s Editor’s choice Research Article, Mark Arends and colleagues show that, in a mouse model of Lynch syndrome with defective mismatch repair, ALDH1B1 loss leads to increased acetaldehyde levels and DNA damage that accelerate colonic tumour formation.
Additionally, David Church highlights this study in the context of increased colon cancer risk associated with alcohol consumption in individuals with Lynch syndrome.
