Evidence map›Paper›PMID 24874730›Full record

ReviewCell death & disease2014

From computational modelling of the intrinsic apoptosis pathway to a systems-based analysis of chemotherapy resistance: achievements, perspectives and challenges in systems medicine.

M L Würstle, E Zink, J H M Prehn, M Rehm

Abstract readReview
In one paragraph

Review in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Mathematical Descriptions of Damage to Cells and Tissues Following Heating.Advances in experimental medicine and biology · 2026
    Article
  2. Review
  3. Materials today. Bio · 2024
    Article
  4. Review
  5. Computational modeling of DLBCL predicts response to BH3-mimetics.NPJ systems biology and applications · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Defining rules for cancer cell proliferation in TRAIL stimulation.NPJ systems biology and applications · 2019
    Article
  13. Bax retrotranslocation potentiates Bcl-xCell death & disease · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

4 authors.

M L Würstle1] Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland [2] Centre for Systems Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland.
E Zink1] Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland [2] Centre for Systems Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland.
J H M Prehn1] Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland [2] Centre for Systems Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland.
M Rehm1] Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland [2] Centre for Systems Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our understanding of the mitochondrial or intrinsic apoptosis pathway and its role in chemotherapy resistance has increased significantly in recent years by a combination of experimental studies and mathematical modelling. This combined approach enhanced the quantitative and kinetic understanding of apoptosis signal transduction, but also provided new insights that systems-emanating functions (i.e., functions that cannot be attributed to individual network components but that are instead established by multi-component interplay) are crucial determinants of cell fate decisions. Among these features are molecular thresholds, cooperative protein functions, feedback loops and functional redundancies that provide systems robustness, and signalling topologies that allow ultrasensitivity or switch-like responses. The successful development of kinetic systems models that recapitulate biological signal transduction observed in living cells have now led to the first translational studies, which have exploited and validated such models in a clinical context. Bottom-up strategies that use pathway models in combination with higher-level modelling at the tissue, organ and whole body-level therefore carry great potential to eventually deliver a new generation of systems-based diagnostic tools that may contribute to the development of personalised and predictive medicine approaches. Here we review major achievements in the systems biology of intrinsic apoptosis signalling, discuss challenges for further model development, perspectives for higher-level integration of apoptosis models and finally discuss requirements for the development of systems medical solutions in the coming years.

Indexed as

ApoptosisComputer SimulationDrug ResistanceModels, BiologicalSystems BiologyAnimalsHumans

Identifiers

PMID24874730
PMCPMC4047923

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.