Evidence map›Paper›PMID 24874733›Full record

ReviewCell death & disease2014

Cell-to-cell variability in cell death: can systems biology help us make sense of it all?

X Xia, M S Owen, R E C Lee, S Gaudet

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 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
  2. A morphology and secretome map of pyroptosis.Molecular biology of the cell · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The impact of non-genetic heterogeneity on cancer cell death.Critical reviews in biochemistry and molecular biology · 2018
    Review
  15. Article
  16. IRES inhibition induces terminal differentiation and synchronized death in triple-negative breast cancer and glioblastoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Article
  18. Article
  19. Computer modeling of ischemic stroke.Drug discovery today. Disease models · 2016
    Article
  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

4 authors.

X Xia1] Department of Cancer Biology and Center for Cancer Systems Biology, Dana Farber Cancer Institute, Boston, MA 02215, USA [2] Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
M S Owen1] Department of Cancer Biology and Center for Cancer Systems Biology, Dana Farber Cancer Institute, Boston, MA 02215, USA [2] Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
R E C Lee1] Department of Cancer Biology and Center for Cancer Systems Biology, Dana Farber Cancer Institute, Boston, MA 02215, USA [2] Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
S Gaudet1] Department of Cancer Biology and Center for Cancer Systems Biology, Dana Farber Cancer Institute, Boston, MA 02215, USA [2] Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.

Funding

Quantitative Analysis of Cell Death Pathways in CancerP01CA139980 · NCI · HARVARD MEDICAL SCHOOL · PI WEISSLEDER, MD, PHD, RALPH · 2010 to 2014
$9.0M
Single-cell analysis of TNF-induced signaling, transcription and fate decisionsR01GM104247 · NIGMS · DANA-FARBER CANCER INST · PI GAUDET, SUZANNE · 2013 to 2017
$1.7M
CIHRNCI NIH HHS P01 CA139980NCI NIH HHS P01-CA139980NIGMS NIH HHS R01 GM104247NIGMS NIH HHS R01-GM104247
6 · The paper itself

Abstract

One of the most common observations in cell death assays is that not all cells die at the same time, or at the same treatment dose. Here, using the perspective of the systems biology of apoptosis and the context of cancer treatment, we discuss possible sources of this cell-to-cell variability as well as its implications for quantitative measurements and computational models of cell death. Many different factors, both within and outside of the apoptosis signaling networks, have been correlated with the variable responses to various death-inducing treatments. Systems biology models offer us the opportunity to take a more synoptic view of the cell death process to identify multifactorial determinants of the cell death decision. Finally, with an eye toward 'systems pharmacology', we discuss how leveraging this new understanding should help us develop combination treatment strategies to compel cancer cells toward apoptosis by manipulating either the biochemical state of cancer cells or the dynamics of signal transduction.

Indexed as

ApoptosisComputer SimulationModels, BiologicalSignal TransductionAnimalsHumansNeoplasmsSystems Biology

Identifiers

PMID24874733
PMCPMC4047886

What OpenQuestion holds

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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.