Scientific Areas of Expertise: Cancer Genetics, Insertional Mutagenesis, Mouse Models of Human Cancer
For groundbreaking contributions to cancer genetics and quintessential studies involving the Sleeping Beauty transposable element system to establish various mouse models of cancer, which have been essential to the understanding of cancer initiation and progression, and for the identification of numerous candidate genes involved in carcinogenesis.
Dr. Copeland is an internationally celebrated scientist whose pioneering application of advanced genetic techniques in mouse models has transformed our understanding of the genes and pathways that govern human cancer initiation, progression, and evolution. In collaboration with his long-time research partner, Dr. Nancy Jenkins, he first applied replication-defective retroviral insertional mutagenesis screens in mice to identify genes involved in leukemia and lymphoma. This work demonstrated that no single mutation was sufficient to induce malignancy but rather mutations near multiple genes frequently co-occurred, revealing that oncogenic cooperation is essential for transformation. Building on this foundational insight, Dr. Copeland introduced the Sleeping Beauty transposon system into the field of cancer genetics, enabling high-throughput insertional mutagenesis in solid tumors. By combining unbiased, forward genetic screens with systematic mapping of transposon insertion sites, his laboratory identified thousands of candidate cancer genes implicated in carcinogenesis across a broad range of cancer types and organ systems. These data now populate the Candidate Cancer Gene Database, a widely used resource in the international cancer research community.
Dr. Copeland’s work has elucidated the gene and pathway interactions driving tumor development, particularly in gastric, colorectal, hepatic, and pancreatic cancers. His research has defined key principles of tumor evolution, including the role of truncal mutations, which are early mutational events found in all tumor cells, and the profound impact of mutation order on clonal architecture. His models underscore how initial mutations shape subsequent driver selection and branching evolution. His work with pathway analysis revealed that multiple oncogenic pathways are often mutated within the same tumor, highlighting the crosstalk and synergistic effects that support tumor progression. The work of the prolific and highly cited Drs. Copeland and Jenkins continues to produce foundational insights that bridge basic cancer biology and translational applications in drug discovery.
Selected Awards and Honors
2020 Prince Hitachi Prize for Comparative Oncology, Japanese Foundation for Cancer Research, Tokyo, Japan
2011 Elected Member, Academy of Medicine, Engineering and Science of Texas, Austin, Texas
2009 Elected Member, National Academy of Sciences, Washington, DC
2004 Burroughs Mider Lectureship Award, National Institutes of Health, Bethesda, Maryland
2004-2010 Scientific Advisory Board, Welcome Trust Sanger Institute, Saffron Walden, United Kingdom
2002-2003 Scientific Advisory Board, Zaffaroni Foundation, Menlo Park, California
1999-2000 The Harvey Lectures, The Harvey Society, New York, New York
1997-1998 Co-Chair, NCI-Mouse Genomics and Genetics Subgroup, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
1996-1997 NCI-Preclinical Models for Human Cancers Working Group, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
1991-1994 DOE-NIH Mouse Genome Advisory Committee, Bethesda, Maryland
1987-1990 Israel Cancer Research Institute Grants Review Panel, New York, New York
1987-1989 Member, Grants Panel F, National Cancer Institute of Canada, Toronto, Ontario, Canada
1977-1979 Damon Runyon Postdoctoral Fellowship, Damon Runyon Cancer Research Foundation, New York, New York
1971-1975 NIH Training Grant Award in Biochemistry, National Institutes of Health, Bethesda, Maryland
[Institutional affiliations listed for Fellows reflect those held at the time of their induction into the AACR Academy.]