Evidence map›Paper›PMID 18797454›Full record

ArticleBritish journal of cancer2008

A new role for tamoxifen in oestrogen receptor-negative breast cancer when it is combined with epigallocatechin gallate.

M J Scandlyn, E C Stuart, T J Somers-Edgar, A R Menzies, R J Rosengren

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Mycoscience · 2021
    Article
  7. Review
  8. Article
  9. Review
  10. Bioavailability of Tea Catechins and Its Improvement.Molecules (Basel, Switzerland) · 2018
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Tamoxifen Action in ER-Negative Breast Cancer.Signal transduction insights · 2016
    Article
  17. Review
  18. Review
  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

5 authors at 1 institution in 1 country.

M J ScandlynDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
E C Stuart
T J Somers-Edgar
A R Menzies
R J Rosengren
University of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that tamoxifen+epigallocatechin gallate (EGCG) is synergistically cytotoxic towards oestrogen receptor (ER)-negative breast cancer cells. To determine if this response would correlate with significant tumour suppression in vivo, athymic nude female mice were implanted with MDA-MB-231 cells and treated with tamoxifen, EGCG, EGCG+tamoxifen, or vehicle control for 10 weeks. Tumour volume in EGCG- (25 mg kg(-1))+tamoxifen (75 microg kg(-1))-treated mice decreased by 71% as compared with vehicle control (P<0.05), whereas tumour weight was decreased by 80% compared with control (P<0.01). Epigallocatechin gallate treatment did not alter ER protein expression in MDA-MB-231 cells and thus was not a mechanism for the observed tumour suppression. However, western blotting of tumour extracts demonstrated that epidermal growth factor receptor (EGFR; 85% lower than control), pEGFR (78% lower than control), mammalian target of rapamycin (mTOR; 78% lower than control), and CYP1B1 (75% lower than control) were significantly lower after the combination treatment as compared with all other treatments. Nuclear factor-kappaB (NF-kappaB), b-Raf, p-MEK, S6K, 4EBP1, Akt, vascular EGFR-1 (VEGFR-1) and VEGF expressions were decreased in control but not in the individual treatments, whereas MEK, phospholipase D 1/2, TGF alpha, and ERK expressions were not changed after any treatment. The results demonstrate that tamoxifen at realistic doses (75 mug kg(-1)) can suppress the growth of ER-negative breast cancer when combined with EGCG. In addition, the dominant mechanism for tumour suppression is the concomitant decrease in tumour protein expressions of mTOR and the EGFR.

Indexed as

AnimalsAntineoplastic Agents, HormonalAryl Hydrocarbon HydroxylasesBlotting, WesternBreast NeoplasmsCatechinCell Line, TumorCytochrome P-450 CYP1B1Down-RegulationDrug Therapy, CombinationErbB ReceptorsFemaleHumansMiceMice, NudeProtein KinasesAntineoplastic Agents, HormonalAryl Hydrocarbon HydroxylasesCatechinCYP1B1 protein, humanCyp1b1 protein, mouseCytochrome P-450 CYP1B1epigallocatechin gallateErbB ReceptorsMTOR protein, humanmTOR protein, mouseProtein KinasesReceptors, EstrogenTamoxifenTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID18797454
PMCPMC2567064
OpenAlexW2028433832

What OpenQuestion holds

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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.