Evidence map›Paper›PMID 24564919›Full record

ArticleBMC systems biology2013

A 3D multiscale model of cancer stem cell in tumor development.

Fuhai Li, Hua Tan, Jaykrishna Singh, Jian Yang, Xiaofeng Xia, Jiguang Bao, Jinwen Ma, Ming Zhan, Stephen T C Wong

Open access · diamondAbstract read
In one paragraph

Article in BMC systems biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Computational systems biology in cancer brain metastasis.Frontiers in bioscience (Scholar edition) · 2016
    Review
  13. Review
  14. 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

9 authors at 3 institutions in 2 countries.

Fuhai Li
Hua Tan
Jaykrishna Singh
Jian Yang
Xiaofeng Xia
Jiguang Bao
Jinwen Ma
Ming Zhan
Stephen T C Wong
Cornell University · USMethodist Hospital · USBeijing Normal University · CN

Funding

Defining lineage-specific determinants of K-Ras "addiction" in human cancersR00CA149169 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SINGH, ANURAG · 2012 to 2014
$710k
Defining lineage-specific determinants of K-Ras "addiction" in human cancersK99CA149169 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SINGH, ANURAG · 2010 to 2011
$268k
NCI NIH HHS NIH U54CA149169
6 · The paper itself

Abstract

backgroundRecent reports indicate that a subgroup of tumor cells named cancer stem cells (CSCs) or tumor initiating cells (TICs) are responsible for tumor initiation, growth and drug resistance. This subgroup of tumor cells has self-renewal capacity and could differentiate into heterogeneous tumor cell populations through asymmetric proliferation. The idea of CSC provides informative insights into tumor initiation, metastasis and treatment. However, the underlying mechanisms of CSCs regulating tumor behaviors are unclear due to the complex cancer system. To study the functions of CSCs in the complex tumor system, a few mathematical modeling studies have been proposed. Whereas, the effect of microenvironment (mE) factors, the behaviors of CSCs, progenitor tumor cells (PCs) and differentiated tumor cells (TCs), and the impact of CSC fraction and signaling heterogeneity, are not adequately explored yet.

methodsIn this study, a novel 3D multi-scale mathematical modeling is proposed to investigate the behaviors of CSCsin tumor progressions. The model integrates CSCs, PCs, and TCs together with a few essential mE factors. With this model, we simulated and investigated the tumor development and drug response under different CSC content and heterogeneity.

resultsThe simulation results shown that the fraction of CSCs plays a critical role in driving the tumor progression and drug resistance. It is also showed that the pure chemo-drug treatment was not a successful treatment, as it resulted in a significant increase of the CSC fraction. It further shown that the self-renew heterogeneity of the initial CSC population is a cause of the heterogeneity of the derived tumors in terms of the CSC fraction and response to drug treatments.

conclusionsThe proposed 3D multi-scale model provides a new tool for investigating the behaviors of CSC in CSC-initiated tumors, which enables scientists to investigate and generate testable hypotheses about CSCs in tumor development and drug response under different microenvironments and drug perturbations.

Indexed as

CarcinogenesisModels, BiologicalAntineoplastic AgentsCell DifferentiationNeoplastic Stem CellsTreatment OutcomeAntineoplastic Agents

Identifiers

PMID24564919
PMCPMC3866259
OpenAlexW2141590267

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.