ArticleGenome biology and evolution2018
The Genomic Basis of Tumor Regression in Tasmanian Devils (Sarcophilus harrisii).
Article in Genome biology and evolution, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Boost or Bust? The Impact of Supplementation on Functional Genetic Diversity and Selective Processes in Tasmanian Devils.Molecular ecology · 2025Article
- The devil in more detail: Eco-evolutionary genomics of Tasmanian devil persistence despite range-wide spread of a fatal, transmissible cancer.PLoS pathogens · 2025Article
- When Do Tumours Develop? Neoplastic Processes Across Different Timescales: Age, Season and Round the Circadian Clock.Evolutionary applications · 2024Review
- Translating genomic advances into biodiversity conservation.Nature reviews. Genetics · 2024Review
- Intergenomic signatures of coevolution between Tasmanian devils and an infectious cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- In vitro competition between two transmissible cancers and potential implications for their host, the Tasmanian devil.Evolutionary applications · 2024Article
- Complex associations between cancer progression and immune gene expression reveals early influence of transmissible cancer on Tasmanian devils.Frontiers in immunology · 2024Article
- Transmissible cancer and longitudinal telomere dynamics in Tasmanian devils (Sarcophilus harrisii).Molecular ecology · 2022Article
- Article
- Restoring faith in conservation action: Maintaining wild genetic diversity through the Tasmanian devil insurance program.iScience · 2022Article
- Disruption of Metapopulation Structure Reduces Tasmanian Devil Facial Tumour Disease Spread at the Expense of Abundance and Genetic Diversity.Pathogens (Basel, Switzerland) · 2021Article
- Spatial variation in gene expression of Tasmanian devil facial tumors despite minimal host transcriptomic response to infection.BMC genomics · 2021Article
- Contemporary and historical selection in Tasmanian devils (Proceedings. Biological sciences · 2021Article
- Quantifying 25 years of disease-caused declines in Tasmanian devil populations: host density drives spatial pathogen spread.Ecology letters · 2021Article
- Darwin, the devil, and the management of transmissible cancers.Conservation biology : the journal of the Society for Conservation Biology · 2021Article
- Applied ecoimmunology: using immunological tools to improve conservation efforts in a changing world.Conservation physiology · 2021Article
- Article
- The ecology and evolution of wildlife cancers: Applications for management and conservation.Evolutionary applications · 2020Article
- 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
- Disease swamps molecular signatures of genetic-environmental associations to abiotic factors in Tasmanian devil (Sarcophilus harrisii) populations.Evolution; international journal of organic evolution · 2020Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Understanding the genetic basis of disease-related phenotypes, such as cancer susceptibility, is crucial for the advancement of personalized medicine. Although most cancers are somatic in origin, a small number of transmissible cancers have been documented. Two such cancers have emerged in the Tasmanian devil (Sarcophilus harrisii) and now threaten the species with extinction. Recently, cases of natural tumor regression in Tasmanian devils infected with the clonally contagious cancer have been detected. We used whole-genome sequencing and FST-based approaches to identify the genetic basis of tumor regression by comparing the genomes of seven individuals that underwent tumor regression with those of three infected individuals that did not. We found three highly differentiated candidate genomic regions containing several genes related to immune response and/or cancer risk, indicating that the genomic basis of tumor regression was polygenic. Within these genomic regions, we identified putative regulatory variation in candidate genes but no nonsynonymous variation, suggesting that natural tumor regression may be driven, at least in part, by differential host expression of key loci. Comparative oncology can provide insight into the genetic basis of cancer risk, tumor development, and the pathogenicity of cancer, particularly due to our limited ability to monitor natural, untreated tumor progression in human patients. Our results support the hypothesis that host immune response is necessary for triggering tumor regression, providing candidate genes that may translate to novel treatments in human and nonhuman cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.