Evidence map›Paper›PMID 23008097›Full record

ReviewAnnals of biomedical engineering2012

Multiscale models of breast cancer progression.

Anirikh Chakrabarti, Scott Verbridge, Abraham D Stroock, Claudia Fischbach, Jeffrey D Varner

Abstract readReview
In one paragraph

Review in Annals of biomedical engineering, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. A HYBRID THREE-SCALE MODEL OF TUMOR GROWTH.Mathematical models & methods in applied sciences : M3AS · 2018
    Article
  9. Review
  10. Modeling of the metabolic energy dissipation for restricted tumor growth.Journal of bioenergetics and biomembranes · 2017
    Article
  11. Article
  12. Article
  13. Editorial: Special Section on Multiscale Cancer Modeling.IEEE transactions on bio-medical engineering · 2017
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

5 authors.

Anirikh ChakrabartiSchool of Chemical and Biomolecular Engineering, 244 Olin Hall, Cornell University, Ithaca, NY 14853, USA.
Scott Verbridge
Abraham D Stroock
Claudia Fischbach
Jeffrey D Varner

Funding

TRANS-NETWORK PROJECTSU54CA143876 · NCI · CORNELL UNIVERSITY · PI SHULER, MICHAEL L · 2009 to 2014
$12.6M
NCI NIH HHS U54 CA143876NCI NIH HHS U54CA143876
6 · The paper itself

Abstract

Breast cancer initiation, invasion and metastasis span multiple length and time scales. Molecular events at short length scales lead to an initial tumorigenic population, which left unchecked by immune action, acts at increasingly longer length scales until eventually the cancer cells escape from the primary tumor site. This series of events is highly complex, involving multiple cell types interacting with (and shaping) the microenvironment. Multiscale mathematical models have emerged as a powerful tool to quantitatively integrate the convective-diffusion-reaction processes occurring on the systemic scale, with the molecular signaling processes occurring on the cellular and subcellular scales. In this study, we reviewed the current state of the art in cancer modeling across multiple length scales, with an emphasis on the integration of intracellular signal transduction models with pro-tumorigenic chemical and mechanical microenvironmental cues. First, we reviewed the underlying biomolecular origin of breast cancer, with a special emphasis on angiogenesis. Then, we summarized the development of tissue engineering platforms which could provide high-fidelity ex vivo experimental models to identify and validate multiscale simulations. Lastly, we reviewed top-down and bottom-up multiscale strategies that integrate subcellular networks with the microenvironment. We present models of a variety of cancers, in addition to breast cancer specific models. Taken together, we expect as the sophistication of the simulations increase, that multiscale modeling and bottom-up agent-based models in particular will become an increasingly important platform technology for basic scientific discovery, as well as the identification and validation of potentially novel therapeutic targets.

Indexed as

Models, BiologicalBreast NeoplasmsDisease ProgressionFemaleHumansNeovascularization, Pathologic

Identifiers

PMID23008097
PMCPMC3868441

What OpenQuestion holds

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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.