ArticleProceedings. Biological sciences2016
Size, longevity and cancer: age structure.
Article in Proceedings. Biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed.
- Prediction of Solitary Plasmacytoma of Bone in Elderly Patients: A Nomogram and a Risk Classification System for Overall Survival.BioMed research international · 2022Article
- Convergent evolution of a genomic rearrangement may explain cancer resistance in hystrico- and sciuromorpha rodents.NPJ aging and mechanisms of disease · 2021Article
- Positive selection and gene duplications in tumour suppressor genes reveal clues about how cetaceans resist cancer.Proceedings. Biological sciences · 2021Article
- Lifespan Extension in Long-Lived Vertebrates Rooted in Ecological Adaptation.Frontiers in cell and developmental biology · 2021Review
- The Danaid Theory of Aging.Frontiers in cell and developmental biology · 2021Review
- Variability Matters.International journal of environmental research and public health · 2020Article
- Nomograms Predict Overall Survival and Cancer-Specific Survival in Patients with Fibrosarcoma: A SEER-Based Study.Journal of oncology · 2020Article
- Article
- DNA helix: the importance of being AT-rich.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is significant recent interest in Peto's paradox and the related problem of the evolution of large, long-lived organisms in terms of cancer robustness. Peto's paradox refers to the expectation that large, long-lived organisms have a higher lifetime cancer risk, which is not the case: a paradox. This paradox, however, is circular: large, long-lived organisms are large and long-lived because they are cancer robust. Lifetime risk, meanwhile, depends on the age distributions of both cancer and competing risks: if cancer strikes before competing risks, then lifetime risk is high; if not, not. Because no set of competing risks is generally prevalent, it is instructive to temporarily dispose of competing risks and investigate the pure age dynamics of cancer under the multistage model of carcinogenesis. In addition to augmenting earlier results, I show that in terms of cancer-free lifespan large organisms reap greater benefits from an increase in cellular cancer robustness than smaller organisms. Conversely, a higher cellular cancer robustness renders cancer-free lifespan more resilient to an increase in size. This interaction may be an important driver of the evolution of large, cancer-robust organisms.
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What OpenQuestion holds
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.