Evidence map›Paper›PMID 39472320›Full record

ArticleBulletin of mathematical biology2024

Accumulation of Oncogenic Mutations During Progression from Healthy Tissue to Cancer.

Ruibo Zhang, Ivana Bozic

Abstract read
In one paragraph

Article in Bulletin of mathematical biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

2 authors.

Ruibo ZhangDepartment of Applied Mathematics, University of Washington, Lewis Hall 201, Box 353925, Seattle, WA, 98195, USA.
Ivana BozicDepartment of Applied Mathematics, University of Washington, Lewis Hall 201, Box 353925, Seattle, WA, 98195, USA. ibozic@uw.edu.ORCID 0000-0003-2761-825X

Funding

National Science Foundation DMS-2045166
6 · The paper itself

Abstract

Cancers are typically fueled by sequential accumulation of driver mutations in a previously healthy cell. Some of these mutations, such as inactivation of the first copy of a tumor suppressor gene, can be neutral, and some, like those resulting in activation of oncogenes, may provide cells with a selective growth advantage. We study a multi-type branching process that starts with healthy tissue in homeostasis and models accumulation of neutral and advantageous mutations on the way to cancer. We provide results regarding the sizes of premalignant populations and the waiting times to the first cell with a particular combination of mutations, including the waiting time to malignancy. Finally, we apply our results to two specific biological settings: initiation of colorectal cancer and age incidence of chronic myeloid leukemia. Our model allows for any order of neutral and advantageous mutations and can be applied to other evolutionary settings.

Indexed as

Colorectal NeoplasmsDisease ProgressionLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMathematical ConceptsModels, GeneticMutationOncogenesCarcinogenesisComputer SimulationHumansMutation AccumulationNeoplasmsPrecancerous ConditionsBranching processCancer incidenceCancer initiationDriver mutations

Identifiers

PMID39472320
PMCPMC11522190

What Socratic 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 Socratic graph.