Dr Seth Cheetham

Honorary Fellow

Mater Research Institute-UQ
Faculty of Medicine

Overview

Dr Seth Cheetham is a NHMRC Early Career Fellow and holds a postdoctoral position in the Genome Plasticity and Disease research group lead by Professor Geoff Faulkner at Mater Research.

Seth is a molecular biologist and biochemist with a focus on molecular mechanisms of gene regulation. He has a long-term interest in the functions of the so-called ‘junk’ DNA—noncoding DNA regions scattered randomly throughout the genome with no obvious function— and its role in human biology.

Seth’s research is uncovering new mechanisms by which this “junk” DNA could contribute to the onset and spreading of cancer, and he is particularly interested in understanding how a type of noncoding mobile DNA, known as L1 retrotransposon, is activated in cancer. He believes understanding the role of ‘junk’ DNA, including mobile DNA, noncoding RNAs and pseudogenes, will be key to improving cancer diagnosis and identifying novel therapeutic targets.

Seth conducted his Honours project with Professor John Mattick at the Institute for Molecular Bioscience at UQ focussed on differentiating human protein-coding and noncoding RNA transcripts. For his PhD, he joined the group of Professor Andrea Brand at the University of Cambridge, on a Herchel Smith Studentship. He studied the functions of long noncoding RNAs (lncRNAs) in neural development and the mechanisms through which they act. One of Seth’s most important achievements was the development of a powerful technique to map interactions between lncRNA and the DNA genome in vivo . He was the first to identify cell-type-specific lncRNA binding sites in vivo.

Seth was awarded an NHMRC Peter Doherty Early Career Fellowship to identify key factors that control mobile DNA in cancer. These factors may be potential biomarkers for cancer diagnosis and prognosis. Seth also investigates the functions of “pseudogenes”, which are dysfunctional copies of genes, which he believes play important roles in cancer. He has authored nine publications, including five as first author. He has published in influential journals including Science and Nature Structural and Molecular Biology (NSMB).

"The discovery that 'junk' DNA regions have important roles in biology has revolutionised our understanding of the human genome. My research applies cutting-edge approaches to understand the mechanisms through which mobile DNA and pseudogenes impact tumour initiation and progression. My ultimate research goal is to translate our growing understanding of 'junk' DNAs functions to clinically relevant information”.

Publications

View all Publications

Available Projects

  • In cancer, but not healthy cells, ~100 L1 “jumping genes” can copy and paste themselves into the human genome. L1s can contribute to cancer initiation by activating oncogenes and inactivating tumour suppressor genes and can drive tumour evolution, underpinning resistance to chemotherapy. This project aims to determine the cause of L1 activation in cancer. This project will identify novel factors that regulate L1 expression in cancer, transforming our understanding of the mechanism of L1 activation. As L1 expression is highly correlated with cancer severity, these factors may hold important prognostic and diagnostic value.

View all Available Projects

Publications

Featured Publications

Journal Article

Grants (Administered at UQ)

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • In cancer, but not healthy cells, ~100 L1 “jumping genes” can copy and paste themselves into the human genome. L1s can contribute to cancer initiation by activating oncogenes and inactivating tumour suppressor genes and can drive tumour evolution, underpinning resistance to chemotherapy. This project aims to determine the cause of L1 activation in cancer. This project will identify novel factors that regulate L1 expression in cancer, transforming our understanding of the mechanism of L1 activation. As L1 expression is highly correlated with cancer severity, these factors may hold important prognostic and diagnostic value.