ArticleScientific reports2017
Identification of candidate genes for devil facial tumour disease tumourigenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Two kinds of evolutionary individuals: the concept of common interest as an evolutionary foundation of dualism on biological individuality.History and philosophy of the life sciences · 2026Article
- Harmonized nonhuman cancer database.bioRxiv : the preprint server for biology · 2025Article
- The evolution of two transmissible cancers in Tasmanian devils.Science (New York, N.Y.) · 2023Article
- HumanLife science alliance · 2022Article
- Spatial variation in gene expression of Tasmanian devil facial tumors despite minimal host transcriptomic response to infection.BMC genomics · 2021Article
- Article
- Curse of the devil: molecular insights into the emergence of transmissible cancers in the Tasmanian devil (Sarcophilus harrisii).Cellular and molecular life sciences : CMLS · 2020Review
- Two of a kind: transmissible Schwann cell cancers in the endangered Tasmanian devil (Sarcophilus harrisii).Cellular and molecular life sciences : CMLS · 2020Article
- Article
- The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease.Cancer cell · 2019Article
- The devil is in the details: Genomics of transmissible cancers in Tasmanian devils.PLoS pathogens · 2018Article
- Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Devil facial tumour (DFT) disease, a transmissible cancer where the infectious agent is the tumour itself, has caused a dramatic decrease in Tasmanian devil numbers in the wild. The purpose of this study was to take a candidate gene/pathway approach to identify potentially perturbed genes or pathways in DFT. A fusion of chromosome 1 and X is posited as the initial event leading to the development of DFT, with the rearranged chromosome 1 material now stably maintained as the tumour spreads through the population. This hypothesis makes chromosome 1 a prime chromosome on which to search for mutations involved in tumourigenesis. As DFT1 has a Schwann cell origin, we selected genes commonly implicated in tumour pathways in human nerve cancers, or cancers more generally, to determine whether they were rearranged in DFT1, and mapped them using molecular cytogenetics. Many cancer-related genes were rearranged, such as the region containing the tumour suppressor NF2 and a copy gain for ERBB3, a member of the epidermal growth factor receptor family of receptor tyrosine kinases implicated in proliferation and invasion of tumours in humans. Our mapping results have provided strong candidates not previously detected by sequencing DFT1 genomes.
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