ArticleGenes2018
Selective Pressures on Human Cancer Genes along the Evolution of Mammals.
Article in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- The Paipu framework enables creation of a large-scale mammalian cancer transcriptomics atlas.bioRxiv : the preprint server for biology · 2026Article
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- TRIM52 maintains cellular fitness and is under tight proteolytic control by multiple giant E3 ligases.Nature communications · 2025Article
- Positive Selection Shapes Breast Cancer Tumor Suppressor Genes: Unveiling Insights into BRCA1, BRCA2, and MDC1 Stability.Journal of molecular evolution · 2025Article
- A link between evolution and society fostering the UN sustainable development goals.Evolutionary applications · 2024Article
- The molecular evolution of cancer associated genes in mammals.Scientific reports · 2024Article
- Oncogenic BRCA1,2 Mutations in the Human Lineage-A By-Product of Sexual Selection?Biomedicines · 2023Review
- A Strategy Utilizing Protein-Protein Interaction Hubs for the Treatment of Cancer Diseases.International journal of molecular sciences · 2023Review
- The NIH Comparative Genomics Resource: addressing the promises and challenges of comparative genomics on human health.BMC genomics · 2023Review
- Long-Read Sequencing Reveals Rapid Evolution of Immunity- and Cancer-Related Genes in Bats.Genome biology and evolution · 2023Article
- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- The adaptive evolution of cancer driver genes.BMC genomics · 2023Article
- Mitochondrial DNA Repair in Neurodegenerative Diseases and Ageing.International journal of molecular sciences · 2022Review
- Article
- Cross-species identification of cancer resistance-associated genes that may mediate human cancer risk.Science advances · 2022Article
- MAST: a hybrid Multi-Agent Spatio-Temporal model of tumor microenvironment informed using a data-driven approach.Bioinformatics advances · 2022Article
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- Challenges to Building a Gene Variant Commons to Assess Hereditary Cancer Risk: Results of a Modified Policy Delphi Panel Deliberation.Journal of personalized medicine · 2021Article
- Broadening the spectrum of cancer genes under selection in human populations.FASEB bioAdvances · 2021Article
- The Burden of Post-Translational Modification (PTM)-Disrupting Mutations in the Tumor Matrisome.Cancers · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer is a disease driven by both somatic mutations that increase survival and proliferation of cell lineages and the evolution of genes associated with cancer risk in populations. Several genes associated with cancer in humans, hereafter cancer genes, show evidence of germline positive selection among species. Taking advantage of a large collection of mammalian genomes, we systematically looked for signatures of germline positive selection in 430 cancer genes available in COSMIC. We identified 40 cancer genes with a robust signal of positive selection in mammals. We found evidence for fewer selective constraints-higher number of non-synonymous substitutions per non-synonymous site to the number of synonymous substitutions per synonymous site (dN/dS)-and higher incidence of positive selection-more positively selected sites-in cancer genes bearing germline and recessive mutations that predispose to cancer. This finding suggests a potential association between relaxed selection, positive selection, and risk of hereditary cancer. On the other hand, we did not find significant differences in terms of tissue or gene type. Human cancer genes under germline positive selection in mammals are significantly enriched in the processes of DNA repair, with high presence of Fanconi anaemia/Breast Cancer A (FA/BRCA) pathway components and T cell proliferation genes. We also show that the inferred positively selected sites in the two genes with the strongest signal of positive selection, i.e.,
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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.