Evidence map›Paper›PMID 17456761›Full record

ArticleThe American journal of pathology2007

Direct involvement of breast tumor fibroblasts in the modulation of tamoxifen sensitivity.

Malathy P V Shekhar, Steven Santner, Kathryn A Carolin, Larry Tait

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  5. Article
  6. Head-to-Head Comparison between [Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  7. Article
  8. Review
  9. Review
  10. Breast Cancer CAFs: Spectrum of Phenotypes and Promising Targeting Avenues.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. The Microenvironment of Tongue Cancer.Advances in experimental medicine and biology · 2020
    Review
  15. Review
  16. Review
  17. Review
  18. Review
  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.

Malathy P V ShekharBreast Cancer Program, Karmanos Cancer Institute, Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA. shekharm@karmanos.org
Steven Santner
Kathryn A Carolin
Larry Tait
The Barbara Ann Karmanos Cancer Institute · USWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using contact-dependent three-dimensional coculture systems and serum-free conditions, we compared the ability of estrogen receptor (ER)-alpha(+) tamoxifen-sensitive premalignant (EIII8) or tumorigenic (MCF-7), ER-alpha(+) tamoxifen-resistant (EIII8-TAM(R)) or ER-alpha(-) MDA-MB-231 breast cancer cells to interact and undergo epithelial morphogenesis on association with breast tumor-derived fibroblasts. Although all breast cancer cell lines interacted with tumor fibroblasts, EIII8 and its intrinsically tamoxifen-resistant counterpart EIII8-TAM(R) cells were most receptive and responded with dramatic, albeit, aberrant epithelial morphogenesis. EIII8 cells underwent epithelial morphogenesis when cocultured with fibroblasts from ER-alpha(-)/PgR(-) or ER-alpha(+)/PgR(+) breast tumors; however, EIII8 cells cocultured with ER-alpha(-)/PgR(-) tumor-derived fibroblasts exhibited decreased tamoxifen sensitivity compared with cells cocultured with ER-alpha(+)/PgR(+) tumor fibroblasts. Fibroblast-induced tamoxifen resistance was accompanied by mitogen-activated protein kinase and Akt hyperactivation, reduced sensitivity to U0126 or LY294002, and ER-alpha hyperphosphorylation in the activation function-1 domain. The intrinsic tamoxifen resistance of EIII8-Tam(R) cells correlated with constitutive ER-alpha hyperphosphorylation that was unaffected by the tumor fibroblasts. Our results suggest that tumor fibroblast-induced tamoxifen resistance of EIII8 cells is not mediated by epidermal growth factor receptor or insulin-like growth factor (IGF)-1R axes because no correlation was found between expression levels of IGF-1, IGF-2, phosphorylated IGF-1R, or epidermal growth factor receptor, and tamoxifen sensitivity of EIII8 fibroblast cultures.

Indexed as

AnimalsBlotting, WesternBreast NeoplasmsCell Line, TumorCoculture TechniquesDrug Resistance, NeoplasmEstrogen Receptor alphaFemaleFibroblastsHumansMiceMitogen-Activated Protein KinasesPhosphorylationProto-Oncogene Proteins c-aktReceptors, ProgesteroneSelective Estrogen Receptor ModulatorsEstrogen Receptor alphaMitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktReceptors, ProgesteroneSelective Estrogen Receptor ModulatorsTamoxifen

Identifiers

PMID17456761
PMCPMC1854950
OpenAlexW2078469315

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.