Evidence map›Paper›PMID 28056859›Full record

ReviewBMC cancer2017

Molecular chess? Hallmarks of anti-cancer drug resistance.

Ian A Cree, Peter Charlton

Open access · goldAbstract readReview
In one paragraph

Review in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 1 pooled it
22.1field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 1 synthesis or guideline pooled it, 327 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Review
  12. Inhibition of ABCG2 by SCO-101 Enhances Chemotherapy Efficacy in Cancer.International journal of molecular sciences · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Current Trends in Clinical Trials of Prodrugs.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  18. Article
  19. Review
  20. Review

83 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 at 2 institutions in 1 country.

Ian A CreeDepartment of Pathology, University Hospitals Coventry and Warwickshire, Coventry, CV2 2DX, UK. iancreebmc@gmail.com.
Peter CharltonImperial Innovations, 52 Princes Gate, Exhibition Road, London, SW7 2PG, UK.
Imperial Innovations (United Kingdom) · GBUniversity Hospitals Coventry and Warwickshire NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe development of resistance is a problem shared by both classical chemotherapy and targeted therapy. Patients may respond well at first, but relapse is inevitable for many cancer patients, despite many improvements in drugs and their use over the last 40 years. REVIEW: Resistance to anti-cancer drugs can be acquired by several mechanisms within neoplastic cells, defined as (1) alteration of drug targets, (2) expression of drug pumps, (3) expression of detoxification mechanisms, (4) reduced susceptibility to apoptosis, (5) increased ability to repair DNA damage, and (6) altered proliferation. It is clear, however, that changes in stroma and tumour microenvironment, and local immunity can also contribute to the development of resistance. Cancer cells can and do use several of these mechanisms at one time, and there is considerable heterogeneity between tumours, necessitating an individualised approach to cancer treatment. As tumours are heterogeneous, positive selection of a drug-resistant population could help drive resistance, although acquired resistance cannot simply be viewed as overgrowth of a resistant cancer cell population. The development of such resistance mechanisms can be predicted from pre-existing genomic and proteomic profiles, and there are increasingly sophisticated methods to measure and then tackle these mechanisms in patients.

conclusionThe oncologist is now required to be at least one step ahead of the cancer, a process that can be likened to 'molecular chess'. Thus, as well as an increasing role for predictive biomarkers to clinically stratify patients, it is becoming clear that personalised strategies are required to obtain best results.

Indexed as

Drug Resistance, NeoplasmHumansMedical OncologyNeoplasmsPrecision MedicineApoptosisCancerChemotherapyDetoxificationDNA damageHeterogeneityMicroenvironmentProliferationResistanceTyrosine kinase inhibitor

Identifiers

PMID28056859
PMCPMC5214767
OpenAlexW2568368705

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.