Evidence map›Paper›PMID 29187407›Full record

ArticleCancer research2018

Modeling the Subclonal Evolution of Cancer Cell Populations.

Diego Chowell, James Napier, Rohan Gupta, Karen S Anderson, Carlo C Maley, Melissa A Wilson Sayres

Abstract read
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. Measuring collective behavior: an ecological approach.Theory in biosciences = Theorie in den Biowissenschaften · 2021
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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

6 authors.

Diego ChowellSimon A. Levin Mathematical, Computational and Modeling Sciences Center, Arizona State University, Tempe, Arizona.
James NapierResearch Computing Center, Tempe, Arizona.
Rohan GuptaResearch Computing Center, Tempe, Arizona.
Karen S AndersonBiodesign Institute, Tempe, Arizona.
Carlo C MaleyBiodesign Institute, Tempe, Arizona. melissa.wilsonsayres@asu.edu maley@asu.edu.
Melissa A Wilson SayresBiodesign Institute, Tempe, Arizona. melissa.wilsonsayres@asu.edu maley@asu.edu.

Funding

PHYLOGENIES of Barrett's Esophagus LineagesP01CA091955 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2002 to 2019
$35.9M
Modeling Neoplastic Progression in Barrett's Esophagus - Renewal -2R01CA140657 · NCI · WISTAR INSTITUTE · PI Carlo Maley · 2009 to 2026
$5.0M
Stem Cells, Differentiation and Therapeutic Resistance in AMLR01CA149566 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CARROLL, MARTIN · 2011 to 2015
$3.0M
Application of Evolutionary Principles to Maintain Cancer Control (PQ21)R01CA170595 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI GATENBY, ROBERT A · 2012 to 2015
$2.1M
(PQC3) Genomic Diversity and Microenvironment as Drivers of Metastasis in DCISR01CA185138 · NCI · DUKE UNIVERSITY · PI HWANG, E.SHELLEY, MALEY, CARLO · 2014 to 2017
$2.0M
Single Cell Technologies for Rapid Detection of Tumor HeterogeneityR21CA196460 · NCI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI ANDERSON, KAREN SUE, BLATTMAN, JOSEPH N · 2015 to 2017
$694k
NCI NIH HHS P01 CA091955NCI NIH HHS R01 CA140657NCI NIH HHS R01 CA149566NCI NIH HHS R01 CA170595NCI NIH HHS R01 CA185138NCI NIH HHS R21 CA196460
6 · The paper itself

Abstract

Increasing evidence shows that tumor clonal architectures are often the consequence of a complex branching process, yet little is known about the expected dynamics and extent to which these divergent subclonal expansions occur. Here, we develop and implement more than 88,000 instances of a stochastic evolutionary model simulating genetic drift and neoplastic progression. Under different combinations of population genetic parameter values, including those estimated for colorectal cancer and glioblastoma multiforme, the distribution of sizes of subclones carrying driver mutations had a heavy right tail at the time of tumor detection, with only 1 to 4 dominant clones present at ≥10% frequency. In contrast, the vast majority of subclones were present at <10% frequency, many of which had higher fitness than currently dominant clones. The number of dominant clones (≥10% frequency) in a tumor correlated strongly with the number of subclones (<10% of the tumor). Overall, these subclones were frequently below current standard detection thresholds, frequently harbored treatment-resistant mutations, and were more common in slow-growing tumors.

Indexed as

Clonal EvolutionModels, TheoreticalMutationSoftwareColorectal NeoplasmsGlioblastomaHumans

Identifiers

PMID29187407
PMCPMC5811390

What OpenQuestion holds

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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.