Evidence map›Paper›PMID 27548161›Full record

ReviewInternational journal of molecular sciences2016

Tamoxifen Resistance: Emerging Molecular Targets.

Milena Rondón-Lagos, Victoria E Villegas, Nelson Rangel, Magda Carolina Sánchez, Peter G Zaphiropoulos

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
13.2field-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

75 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
  2. Review
  3. Genetic Variation inJournal of personalized medicine · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. miRNAs as emerging predictors of tamoxifen resistance in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

15 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

5 authors at 3 institutions in 3 countries.

Milena Rondón-LagosDepartment of Medical Sciences, University of Turin, Turin 10126, Italy. srondonl@unito.it.
Victoria E VillegasFaculty of Natural Sciences and Mathematics, Universidad del Rosario, Bogotá 11001000, Colombia. victoria.villegas@urosario.edu.co.
Nelson RangelDepartment of Medical Sciences, University of Turin, Turin 10126, Italy. nrangel@unito.it.
Magda Carolina SánchezFaculty of Natural Sciences and Mathematics, Universidad del Rosario, Bogotá 11001000, Colombia. magda.sanchez@urosario.edu.com.
Peter G ZaphiropoulosDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge 14183, Sweden. peter.zaphiropoulos@ki.se.
Universidad del Rosario · COUniversity of Turin · ITKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

17β-Estradiol (E2) plays a pivotal role in the development and progression of breast cancer. As a result, blockade of the E2 signal through either tamoxifen (TAM) or aromatase inhibitors is an important therapeutic strategy to treat or prevent estrogen receptor (ER) positive breast cancer. However, resistance to TAM is the major obstacle in endocrine therapy. This resistance occurs either de novo or is acquired after an initial beneficial response. The underlying mechanisms for TAM resistance are probably multifactorial and remain largely unknown. Considering that breast cancer is a very heterogeneous disease and patients respond differently to treatment, the molecular analysis of TAM's biological activity could provide the necessary framework to understand the complex effects of this drug in target cells. Moreover, this could explain, at least in part, the development of resistance and indicate an optimal therapeutic option. This review highlights the implications of TAM in breast cancer as well as the role of receptors/signal pathways recently suggested to be involved in the development of TAM resistance. G protein-coupled estrogen receptor, Androgen Receptor and Hedgehog signaling pathways are emerging as novel therapeutic targets and prognostic indicators for breast cancer, based on their ability to mediate estrogenic signaling in ERα-positive or -negative breast cancer.

Indexed as

Antineoplastic Agents, HormonalBreast NeoplasmsDrug Resistance, NeoplasmFemaleHumansReceptors, AndrogenReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenAntineoplastic Agents, HormonalReceptors, AndrogenReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenandrogen receptor (AR)breast cancerendocrine resistanceestrogen receptors (ERs)G protein-coupled estrogen receptor (GPER)Hedgehog (HH) signaling pathwaytamoxifen

Identifiers

PMID27548161
PMCPMC5000752
OpenAlexW2514511766

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.