Evidence map›Paper›PMID 17088909›Full record

Trial reportBritish journal of cancer2006

Molecular subtypes of breast cancer and amplification of topoisomerase II alpha: predictive role in dose intensive adjuvant chemotherapy.

J Hannemann, P Kristel, H van Tinteren, M Bontenbal, Q G C M van Hoesel, W M Smit, M A Nooij, E E Voest, E van der Wall, P Hupperets and 3 more

Abstract readClinical Trial, Phase IIIMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in British journal of cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Guideline
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Assessment ofAging · 2019
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Free circulating tumor DNA as a diagnostic marker for breast cancer.Journal of clinical laboratory analysis · 2012
    Article
  14. Topoisomerase 2 alpha: a real predictor of anthracycline efficacy?Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2012
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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

13 authors.

J HannemannDivision of Experimental Therapy, The Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam, The Netherlands.
P Kristel
H van Tinteren
M Bontenbal
Q G C M van Hoesel
W M Smit
M A Nooij
E E Voest
E van der Wall
P Hupperets
E G E de Vries
S Rodenhuis
M J van de Vijver

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benefit from chemotherapy treatment in breast cancer patients is determined by the molecular make-up of the tumour. In a retrospective analysis, we determined the molecular subtypes of breast cancer originally defined by expression microarrays by immunohistochemistry in tumours of patients who took part in a randomised study of adjuvant high-dose chemotherapy in breast cancer. In addition, the topoisomerase II alpha (TOP2A) amplification status was determined by fluorescence in situ hybridisation and chromogenic in situ hybridisation. 411 of the 753 tumours (55%) were classified as luminal-like, 137 (18%) as basal-like and 205 (27%) as human epithelial receptor type 2 (HER2) amplified. The basal-like tumours were defined as having no expression of ER and HER2; 98 of them did express epidermal growth factor receptor and/or cytokeratin 5/6. The luminal-like tumours had a significantly better recurrence free and overall survival than the other two groups. From the 194 HER2-positive tumours, 47 (24%) were shown to harbour an amplification of TOP2A. Patients with an HER2-amplified tumour randomised to the high-dose therapy arm did worse than those in the conventional treatment arm, possibly caused by the lower cumulative anthracycline dose in the high-dose arm. The tumours with a TOP2A amplification contributed hardly to this difference, suggesting that TOP2A amplification is not the cause of the steep dose-response curve for anthracyclines in breast cancer. Possibly, the difference of the cumulative dose of only 25% between the treatment arms was insufficient to yield a survival difference.

Indexed as

Gene AmplificationAdultAnthracyclinesAntigens, NeoplasmAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBreast NeoplasmsCarboplatinChemotherapy, AdjuvantCyclophosphamideDNA-Binding ProteinsDNA Topoisomerases, Type IIErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHumansAnthracyclinesAntigens, NeoplasmBiomarkers, TumorCarboplatinCyclophosphamideDNA-Binding ProteinsDNA Topoisomerases, Type IIErb-b2 Receptor Tyrosine KinasesPoly-ADP-Ribose Binding ProteinsThiotepaTOP2A protein, human

Identifiers

PMID17088909
PMCPMC2360599

What OpenQuestion holds

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Registered trials

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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.