Evidence map›Paper›PMID 30771154›Full record

ArticleTheory in biosciences = Theorie in den Biowissenschaften2019

A mathematical solution to Peto's paradox using Polya's urn model: implications for the aetiology of cancer in general.

Anastasio Salazar-Bañuelos

Abstract read
In one paragraph

Article in Theory in biosciences = Theorie in den Biowissenschaften, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Anastasio Salazar-BañuelosFaculty of Medicine, Hotchkiss Brain Institute, University of Calgary, 1403 - 29 street NW, Calgary, AB, Canada. salazara@ucalgary.ca.ORCID http://orcid.org/0000-0001-7333-5862

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ageing is the leading risk factor for the emergence of cancer in humans. Accumulation of pro-carcinogenic events throughout life is believed to explain this observation; however, the lack of direct correlation between the number of cells in an organism and cancer incidence, known as Peto's Paradox, is at odds with this assumption. Finding the events responsible for this discrepancy can unveil mechanisms with potential uses in prevention and treatment of cancer in humans. On the other hand, the immune system is important in preventing the development of clinically relevant tumours by maintaining a fine equilibrium between reactive and suppressive lymphocyte clones. It is suggested here that the loss of this equilibrium is what ultimately leads to increased risk of cancer and to propose a mechanism for the changes in clonal proportions based on decreased proliferative capacity of lymphocyte clones as a natural phenomenon of ageing. This mechanism, being a function of the number of cells, provides an explanation for Peto's Paradox.

Indexed as

AgingAlgorithmsAnimalsBalaenopteraCarcinogenesisFanconi AnemiaHumansImmune SystemImmunosenescenceIncidenceLymphocytesMiceModels, TheoreticalMutationNeoplasmsProbabilityCancerImmunologyLongevityLymphocytesPólya’s urn

Identifiers

PMID30771154
PMCPMC6800849

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.