Anton Berns studied biochemistry at the University of Nijmegen and received his Masters degree in 1969 and his PhD in 1972 from that same University, both with honors. He did his postdoctoral training in the group of Rudolf Jaenisch at the Salk Institute in La Jolla, CA., where he studied the role of retroviruses in causing lymphomas in mice. In 1976 he returned to the University of Nijmegen where he became junior staff member. His group explored proviral insertional mutagenesis as a means to identify new oncogenes. In 1985 he was appointed as staff scientist at the Netherlands Cancer Institute and in 1986 he became head of the Division of Molecular Genetics of the Institute. In 1999 he was appointed as Director of Research and Chairman of the Board of Directors of The Netherlands Cancer Institute – Antoni van Leeuwenhoek Hospital. He retired from that position at the end of 2011. He is member of several academies: The Netherlands and European Academy of Sciences, The European Academy of Cancer Science, he is EMBO member, and fellow of the AACR. He has received a number of prestigious prizes for his research.

Research Interests

My laboratory is interested in defining the genetic aberrations that are critical for lung tumor development. Genetically engineered mouse models are used to unravel the specific mechanisms of action of the various lesions found in lung cancer in man. The tumor subtypes we are focusing on are: small cell lung cancer, squamous cell carcinoma, and mesothelioma. We induce tumor development by genetic activation of oncogenes and/or inactivation of tumor suppressor genes. The specific questions we try to answer: 1. What is the cell-of-origin of these tumors? Can different cell types in lung give rise to similar tumors? Do they retain specific features of their cell-of-origin? 2. Can we identify better intervention strategies? Do genetic screens in cell lines in vitro (transposon and Crisp/Cas9 mutagenesis) yield actionable targets that subsequently can be validated in autochthonous mouse models? 3. To what extent does the genetic background influence tumor development? Can we identify alleles of unaltered germline genes that synergize with oncogenic lesions in facilitating tumor development? 4. Do the observations made in the mouse models have a corollary in cognate human tumors and can this information be used for designing better intervention strategies?

Membership Type

International Member

Election Year


Primary Section

Section 41: Medical Genetics, Hematology, and Oncology

Secondary Section

Section 22: Cellular and Developmental Biology