Evidence map›Paper›PMID 36336145›Full record

ReviewBiochimica et biophysica acta. Reviews on cancer2023

ESR1 activating mutations: From structure to clinical application.

Albert Grinshpun, Vincent Chen, Zachary M Sandusky, Sean W Fanning, Rinath Jeselsohn

Open access · hybridAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Reviews on cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Article
  7. Article
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  11. Review
  12. Article
  13. Article
  14. ESR1 fusions in breast cancer: functions, mechanisms and therapeutic opportunities.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026
    Review
  15. Review
  16. Article
  17. Exploration of targeted anti-tumor therapy · 2026
    Review
  18. Article
  19. Article
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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 1 country.

Albert GrinshpunDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States of America; Breast Oncology Center, Dana-Farber Cancer Center, Boston, MA, United States of America.
Vincent ChenDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States of America; Breast Oncology Center, Dana-Farber Cancer Center, Boston, MA, United States of America.
Zachary M SanduskyDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States of America; Center for Functional Cancer Epigenetics, Dana Farber-Cancer Institute, Boston, MA, United States of America.
Sean W FanningDepartment of Cancer Biology, Loyola University, Chicago, IL, United States of America.
Rinath JeselsohnDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States of America; Breast Oncology Center, Dana-Farber Cancer Center, Boston, MA, United States of America; Center for Functional Cancer Epigenetics, Dana Farber-Cancer Institute, Boston, MA, United States of America. Electronic address: rinath_jeselsohn@dfci.harvard.edu.
Dana-Farber Brigham Cancer Center · USDana-Farber Cancer Institute · USLoyola University Chicago · US

Funding

Cancer Chemical Biology and Metabolism Training ProgramT32CA236754 · NCI · DANA-FARBER CANCER INST · PI Nika N Danial, THOMAS M ROBERTS · 2019 to 2026
$2.6M
Optimizing CDK7 Inhibitor Therapeutic Strategies for ER+ Breast CancerR01CA237414 · NCI · DANA-FARBER CANCER INST · PI Rinath M. Jeselsohn · 2019 to 2026
$2.3M
NCI NIH HHS R01 CA237414NCI NIH HHS T32 CA236754
6 · The paper itself

Abstract

Estrogen receptor-positive breast cancer is the most common type of both early and advanced breast cancer. Estrogen receptor alpha (ER) is a nuclear hormone receptor and a key driver of tumorigenesis and tumor progression in these breast cancers. As such, it is a key treatment target and a biomarker predictive of response to endocrine therapy. Activating ESR1 ligand binding domain mutations engender constitutive/ligand independent transcriptional activities and emerge following prolonged first-line hormone therapy regimens, mainly from aromatase inhibitors. The full scale of the biological and clinical significance of these mutations continue to evolve and additional studies are required to further discern the multimodal effects of these mutations on ER transcription, metastatic propensity, and the tumor microenvironment. Furthermore, recent and ongoing studies highlight the potential clinical utility of these mutations as therapeutic targets and dynamic biomarkers. Herein, we review the structure, functional consequences, and clinical implications of the activating ESR1 mutations in advanced estrogen receptor-positive breast cancer.

Indexed as

Breast NeoplasmsReceptors, EstrogenAromatase InhibitorsFemaleHumansLigandsMutationTumor MicroenvironmentAromatase InhibitorsLigandsReceptors, EstrogenBreast cancerEndocrine resistanceEndocrine treatmentESR1 mutationEstrogen receptorStructure

Identifiers

PMID36336145
PMCPMC13423459
OpenAlexW4308073365

What OpenQuestion holds

Textmetadata
LicenceTDM
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.