Evidence map›Paper›PMID 10070856›Full record

ArticleBritish journal of cancer1999

Altered expression of the IGF-1 receptor in a tamoxifen-resistant human breast cancer cell line.

J P Parisot, X F Hu, M DeLuise, J R Zalcberg

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Obesity and endocrine therapy resistance in breast cancer: Mechanistic insights and perspectives.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Resistance and Overcoming Resistance in Breast Cancer.Breast cancer (Dove Medical Press) · 2020
    Review
  10. Article
  11. Article
  12. Tamoxifen Resistance: Emerging Molecular Targets.International journal of molecular sciences · 2016
    Review
  13. Article
  14. Sensitive Detection of Mono- and Polyclonal ESR1 Mutations in Primary Tumors, Metastatic Lesions, and Cell-Free DNA of Breast Cancer Patients.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  15. Article
  16. Review
  17. Article
  18. Phase I dose-escalation study of MEDI-573, a bispecific, antiligand monoclonal antibody against IGFI and IGFII, in patients with advanced solid tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  19. 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 at 2 institutions in 1 country.

J P ParisotDivision of Haematology and Medical Oncology, Peter MacCallum Cancer Institute, Melbourne, Australia.
X F Hu
M DeLuise
J R Zalcberg
Peter MacCallum Cancer Centre · AUHeidelberg Repatriation Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The relationship between oestrogen (E2) and insulin-like growth factor-one (IGF-1) was examined in both tamoxifen-sensitive (MCF 7/5-21) and tamoxifen-resistant (MCF 7/5-23) subclones of the MCF 7 cell line. Both subclones were grown in defined, serum-free (SF) medium over a period of 7 days with the addition of E2 or IGF-1 or a combination of both agents. Growth of both MCF 7/5-21 and 7/5-23 cells was stimulated (245% and 350%, respectively) by E2. However, only the growth of MCF 7/5-23 cells was stimulated (266%) by IGF-1. A combination of E2 and IGF-1 significantly enhanced MCF 7/5-21 and 7/5-23 cell growth (581% and 695%, respectively). E2-induced IGF-1 receptor (IGF-1R) levels (as measured by 125I-IGF-1 binding and Northern analyses) in only MCF 7/5-23 cells. This effect was partially inhibited by tamoxifen. In medium containing serum, the growth of only the MCF 7/5-23 cells was significantly inhibited by the IGF-1R monoclonal antibody, alphaIR-3. The detection of E2-induced expression of IGF-2 using RT-PCR was demonstrated in the MCF 7/5-23 cells. These experiments indicate that E2 may sensitize tamoxifen-resistant MCF 7/5-23 cells to the growth stimulatory actions of IGF-2 via up-regulation of the IGF-1R and describes a cell-survival mechanism that may manifest itself as tamoxifen resistance.

Indexed as

Drug Resistance, NeoplasmBreast NeoplasmsCell DivisionClone CellsCulture Media, Serum-FreeEstradiolFemaleGene Expression Regulation, NeoplasticHistonesHumansInsulin-Like Growth Factor IInsulin-Like Growth Factor IIKineticsReceptor, IGF Type 1Reverse Transcriptase Polymerase Chain ReactionTamoxifenCulture Media, Serum-FreeEstradiolHistonesInsulin-Like Growth Factor IInsulin-Like Growth Factor IIReceptor, IGF Type 1Tamoxifen

Identifiers

PMID10070856
PMCPMC2362670
OpenAlexW2053252897

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY
measurements read5
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.