It remains elusive how mutations that may promote tumour formation are tolerated in young human tissues but less so in tissues of the elderly.

At the molecular level, ageing and cancer are similar, and parallels can be drawn between the classical ‘hallmarks of cancer’, i.e. genetic mutations, changes to mitochondria, the epigenome, metabolome, accumulation of senescent cells, inflammation, and immune changes taking place, and molecular changes that also underlie ageing.

In this timely thematic issue of Molecular Oncology, Ageing and Cancer, readers can browse through a series of articles that aim to document the complexity of mechanisms underlying ageing and cancer and catalyse the formation of new hypotheses and research insight into this fascinating and important topic. Indeed, an array of avenues via which aging may facilitate cancer are discussed in this Issue:

James DeGregori & colleagues consider how cells deal with mutational burden which may resemble ageing or cancer, Masashi Narita & team examine dysregulated autophagy and its links to inflammation, and Laura Greaves’ group focus on the role of a declining mitochondrial function in ageing and cancer. Ana Gomes et al discuss how an ever-changing ‘ageing’ metabolic program may facilitate tumour establishment and maintenance.

Rugang Zhang and group members well as Naoko Ohtani and colleagues review ways in which senescence can act as a reservoir of chronic inflammation ‘wearing down’ tissues and weakening T cell activity. Raul Mostoslavsky and coworkers elaborate on how deficiencies in DNA repair participate in progressing ageing and cancer whilst Lea Harrington and team expand on telomere dysfunction limiting cell proliferative capacity driving genomic instability.

A comprehensive summary of the Review articles included can be found in this Editorial or to find the individual articles in the Thematic Issue, read more here: https://febs.onlinelibrary.wiley.com/toc/18780261/2022/16/18