Burgeoning interest in the tumour suppressor p53 in the Australasian region provoked the birth of the first Australian p53 Workshop, held at the Peter MacCallum Cancer Centre in Melbourne, 19–21 November 2012 and attended by over 130 international and national delegates. The Workshop was organized by Ygal Haupt, Andreas Strasser, Sue Haupt, Antony Braithwaite and Paul Neilsen: 33 oral presentations and 23 posters communicated exciting new p53 findings.

Defining targets that are transcriptionally activated by stress-primed p53 has largely eclipsed the study of the targets it represses. However, a revolutionary study presented by Andrei Gudkov (Buffalo, NY, USA) has indicated that the transcriptional repression function of p53 is fundamental to genomic stability. Concerted cooperation between p53 transcriptional repression and DNA methylation was found to be critical for silencing non-coding DNA repeats. Unsilenced DNA repeats generate dsRNA elements that mimic viral infection and consequently trigger an interferon (IFN)-mediated apoptotic response. This phenomenon (coined as ‘transcription of repeats activates interferon’ (TRAIN)) was defined in mouse cancer models and it reveals a new tumour-suppressive role for the IFN response and may provide an explanation for its frequent inactivation in cancers and the observation that defects in the IFN response and loss of p53 cooperate in lymphoma development in genetically modified mice.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account
Continue with Google
Continue with ORCiD