Evidence map›Paper›PMID 34907918›Full record

ArticleThe Journal of clinical investigation2021

The role of estrogen receptor signaling in suppressing the immune response to cancer.

James M Rae, Marc E Lippman

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Differentiation and mitochondrial metabolic characteristics of CD8Cancer immunology, immunotherapy : CII · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

James M RaeDivision of Hematology and Oncology, Department of Internal Medicine, and.
Marc E LippmanGeorgetown Lombardi Comprehensive Cancer Center, Georgetown University, Washington DC, USA.
Georgetown University · USUniversity of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint blockade (ICB) therapies are standard of care for the treatment of many solid tumors. While some patients with cancer experience exceptional and long-term responses, intrinsic and acquired mechanisms of resistance limit the clinical efficacy of ICBs. In addition, ICBs can elicit life-threatening side effects. Alternative options that can increase ICB responses without added toxicities are needed. In this issue of the JCI, Chakraborty et al. explored the role of estrogen receptor α (ERα) in modulating ICB activity. Using transcriptomics and preclinical melanoma models, the authors show that ERα signaling in tumor-associated macrophages contributed to an immune-suppressive state within the tumor microenvironment (TME) by promoting CD8+ T cell dysfunction and exhaustion. Further, in murine melanoma models, the addition of fulvestrant, a selective estrogen receptor downregulator (SERD) approved for the treatment of breast cancer, enhanced the antitumor effects of ICB. These results provide a rationale for human trials to test the combination of antiestrogens with ICBs.

Indexed as

Breast NeoplasmsReceptors, EstrogenAnimalsEstrogen Receptor alphaFemaleFulvestrantHumansImmunityMiceTumor MicroenvironmentEstrogen Receptor alphaFulvestrantReceptors, Estrogen

Identifiers

PMID34907918
PMCPMC8670827
OpenAlexW4200081636

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.