Evidence map›Paper›PMID 25220419›Full record

ReviewOncogene2015

Cancer systems biology: embracing complexity to develop better anticancer therapeutic strategies.

W Du, O Elemento

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing 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

84 citing papers in PubMed.

  1. Molecular origin, discovery, validation and application of neoantigens.Asian journal of pharmaceutical sciences · 2026
    Review
  2. Article
  3. Article
  4. EGFR-targeted tyrosine kinase inhibitors: advancements in cancer therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. A Review on Medicinal Approaches of Novel Imatinib Derivatives.Current topics in medicinal chemistry · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

24 more citing papers are in PubMed but not listed here.

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

2 authors.

W DuLaboratory of Cancer Systems Biology, Sandra and Edward Meyer Cancer Center, Department of Physiology and Biophysics, Institute for Computational Biomedicine and Institute for Precision Medicine, Weill Cornell Medical College, New York, NY, USA.
O ElementoLaboratory of Cancer Systems Biology, Sandra and Edward Meyer Cancer Center, Department of Physiology and Biophysics, Institute for Computational Biomedicine and Institute for Precision Medicine, Weill Cornell Medical College, New York, NY, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transformation of normal cells into cancer cells and maintenance of the malignant state and phenotypes are associated with genetic and epigenetic deregulations, altered cellular signaling responses and aberrant interactions with the microenvironment. These alterations are constantly evolving as tumor cells face changing selective pressures induced by the cells themselves, the microenvironment and drug treatments. Tumors are also complex ecosystems where different, sometime heterogeneous, subclonal tumor populations and a variety of nontumor cells coexist in a constantly evolving manner. The interactions between molecules and between cells that arise as a result of these alterations and ecosystems are even more complex. The cancer research community is increasingly embracing this complexity and adopting a combination of systems biology methods and integrated analyses to understand and predictively model the activity of cancer cells. Systems biology approaches are helping to understand the mechanisms of tumor progression and design more effective cancer therapies. These approaches work in tandem with rapid technological advancements that enable data acquisition on a broader scale, with finer accuracy, higher dimensionality and higher throughput than ever. Using such data, computational and mathematical models help identify key deregulated functions and processes, establish predictive biomarkers and optimize therapeutic strategies. Moving forward, implementing patient-specific computational and mathematical models of cancer will significantly improve the specificity and efficacy of targeted therapy, and will accelerate the adoption of personalized and precision cancer medicine.

Indexed as

AnimalsAntineoplastic AgentsDrug DiscoveryGenomicsHumansNeoplasmsPrecision MedicineSystems BiologyAntineoplastic Agents

Identifiers

PMID25220419

What OpenQuestion holds

Textmetadata
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.