Evidence map›Paper›PMID 24511380›Full record

ArticleInterface focus2013

Evolution of intratumoral phenotypic heterogeneity: the role of trait inheritance.

Jill Gallaher, Alexander R A Anderson

Abstract read
In one paragraph

Article in Interface focus, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
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  6. Review
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  15. Learning-accelerated discovery of immune-tumour interactions.Molecular systems design & engineering · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. A population genetics perspective on the determinants of intra-tumor heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
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.

Jill GallaherDepartment of Mathematical Oncology, H. Lee Moffitt Cancer Center, Tampa, FL 33612 , USA.
Alexander R A AndersonDepartment of Mathematical Oncology, H. Lee Moffitt Cancer Center, Tampa, FL 33612 , USA.

Funding

TrainingU54CA113007 · NCI · VANDERBILT UNIVERSITY · PI QUARANTA, VITO · 2004 to 2014
$19.2M
Predicting Prostate Cancer AggressivenessU01CA151924 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, AYALA, GUSTAVO ENRIQUE · 2011 to 2015
$2.8M
NCI NIH HHS U01 CA151924NCI NIH HHS U54 CA113007
6 · The paper itself

Abstract

A tumour is a heterogeneous population of cells that competes for limited resources. In the clinic, we typically probe the tumour by biopsy, and then characterize it by the dominant genetic clone. But genotypes are only the first link in the chain of hierarchical events that leads to a specific cell phenotype. The relationship between genotype and phenotype is not simple, and the so-called genotype to phenotype map is poorly understood. Many genotypes can produce the same phenotype, so genetic heterogeneity may not translate directly to phenotypic heterogeneity. We therefore choose to focus on the functional endpoint, the phenotype as defined by a collection of cellular traits (e.g. proliferative and migratory ability). Here, we will examine how phenotypic heterogeneity evolves in space and time and how the way in which phenotypes are inherited will drive this evolution. A tumour can be thought of as an ecosystem, which critically means that we cannot just consider it as a collection of mutated cells but more as a complex system of many interacting cellular and microenvironmental elements. At its simplest, a growing tumour with increased proliferation capacity must compete for space as a limited resource. Hypercellularity leads to a contact-inhibited core with a competitive proliferating rim. Evolution and selection occurs, and an individual cell's capacity to survive and propagate is determined by its combination of traits and interaction with the environment. With heterogeneity in phenotypes, the clone that will dominate is not always obvious as there are both local interactions and global pressures. Several combinations of phenotypes can coexist, changing the fitness of the whole. To understand some aspects of heterogeneity in a growing tumour, we build an off-lattice agent-based model consisting of individual cells with assigned trait values for proliferation and migration rates. We represent heterogeneity in these traits with frequency distributions and combinations of traits with density maps. How the distributions change over time is dependent on how traits are passed on to progeny cells, which is our main enquiry. We bypass the translation of genetics to behaviour by focusing on the functional end result of inheritance of the phenotype combined with the environmental influence of limited space.

Indexed as

evolutionheterogeneityphenotypic inheritance

Identifiers

PMID24511380
PMCPMC3915835

What OpenQuestion holds

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Registered trials

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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.