Evidence map›Paper›PMID 21179426›Full record

ArticlePloS one2010

The therapeutic implications of plasticity of the cancer stem cell phenotype.

Kevin Leder, Eric C Holland, Franziska Michor

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. 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
3.2field-weighted citation impact, top 8% of its field
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, 62 citations in OpenAlex.

  1. MicroRNA-222 Regulates Melanoma Plasticity.Journal of clinical medicine · 2020
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Breast cancer stem cell: the roles and therapeutic implications.Cellular and molecular life sciences : CMLS · 2017
    Review
  7. Stem Cell Plasticity and Niche Dynamics in Cancer Progression.IEEE transactions on bio-medical engineering · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Episensitization: Defying Time's Arrow.Frontiers in oncology · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Kevin LederDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Eric C Holland
Franziska Michor
Dana-Farber Cancer Institute · USMemorial Sloan Kettering Cancer Center · US

Funding

The Cell-Of-Origin of Human CancersU54CA143798 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MICHOR, FRANZISKA · 2009 to 2014
$11.2M
The Role of Signaling Pathways in Brain Tumors in MiceR01CA100688 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI HOLLAND, ERIC C. · 2003 to 2013
$3.8M
NCI NIH HHS R01 CA100688NCI NIH HHS U54 CA143798NCI NIH HHS U54CA143798
6 · The paper itself

Abstract

The cancer stem cell hypothesis suggests that tumors contain a small population of cancer cells that have the ability to undergo symmetric self-renewing cell division. In tumors that follow this model, cancer stem cells produce various kinds of specified precursors that divide a limited number of times before terminally differentiating or undergoing apoptosis. As cells within the tumor mature, they become progressively more restricted in the cell types to which they can give rise. However, in some tumor types, the presence of certain extra- or intracellular signals can induce committed cancer progenitors to revert to a multipotential cancer stem cell state. In this paper, we design a novel mathematical model to investigate the dynamics of tumor progression in such situations, and study the implications of a reversible cancer stem cell phenotype for therapeutic interventions. We find that higher levels of dedifferentiation substantially reduce the effectiveness of therapy directed at cancer stem cells by leading to higher rates of resistance. We conclude that plasticity of the cancer stem cell phenotype is an important determinant of the prognosis of tumors. This model represents the first mathematical investigation of this tumor trait and contributes to a quantitative understanding of cancer.

Indexed as

AlgorithmsApoptosisCell DifferentiationDisease ProgressionDrug Resistance, NeoplasmHumansModels, StatisticalModels, TheoreticalMutationNeoplasmsNeoplastic Stem CellsPhenotypePrognosisSignal TransductionStem Cells

Identifiers

PMID21179426
PMCPMC3003707
OpenAlexW2129118821

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.