How epigenomics broke the mold: an interview with Peter W Laird

Epigenomics. 2022 Mar;14(6):303-308. doi: 10.2217/epi-2022-0066. Epub 2022 Mar 24.

Abstract

In this interview, Professor Peter W Laird speaks with Storm Johnson, Commissioning Editor for Epigenomics, on his work to date in the field of cancer epigenetics. Dr Peter W Laird is a Professor at Van Andel Institute (VAI) in Grand Rapids, Michigan. He earned his B.S. and M.S., Cum Laude, from the University of Leiden, The Netherlands. He trained for his PhD with Dr Piet Borst, The Netherlands Cancer Institute, and as a postdoc with Dr Anton Berns, The Netherlands Cancer Institute, and with Dr Rudolf Jaenisch, at the Whitehead Institute for Biomedical Research in Cambridge, MA, USA. He joined the faculty at the University of Southern California in 1996, where he served as the Founding Director of the USC Epigenome Center and also as the Leader of the Epigenetics and Regulation Program of the Norris Comprehensive Cancer Center. In 2014, he relocated to VAI to join Dr Peter Jones in building an internationally acclaimed research center focused on Epigenetics. Dr Laird published the first demonstration of the causal role for DNA methylation in oncogenesis (Cell, 1995) [1]. He served as the Principal Investigator for all DNA methylation data production for the Cancer Genome Atlas (TCGA) and led many TCGA analysis efforts. He has been awarded 10 patents related to DNA methylation technology by the United States Patent and Trademark Office, one of which is the basis for the first US FDA-approved blood-based DNA methylation assay for cancer (Epi proColon). His research findings include the report of a close link between DNA methylation and BRAF mutation in colorectal cancer (Nature Genetics, 2006) [2], the discovery that embryonic stem cell polycomb repressor targets are predisposed to abnormal DNA methylation in cancer (Nature Genetics, 2007) [3], the identification of a novel epigenetic subtype of glioma (G-CIMP), tightly associated with IDH1 mutation (Cancer Cell, 2010) [4], and the connection between nuclear architecture, late replication, and domains of epigenetic instability (Nature Genetics, 2011) [5], later showing a link with mitotic cell division, thus providing a mechanistic explanation for the loss of DNA methylation in aging and cancer first described four decades ago (Nature Genetics, 2018) [6].

Keywords: DNA methylation; TCGA; The Cancer Genome Atlas; cancer epigenetics; mouse models; polycomb repressor.

Publication types

  • Interview

MeSH terms

  • DNA Methylation
  • Epigenesis, Genetic
  • Epigenome
  • Epigenomics*
  • Humans
  • Male
  • Neoplasms* / genetics
  • United States