Evidence map›Paper›PMID 31471681›Full record

ReviewCellular and molecular life sciences : CMLS2020

Mechanisms of resistance to estrogen receptor modulators in ER+/HER2- advanced breast cancer.

Jin Zhang, Qianying Wang, Qing Wang, Jiangran Cao, Jiafu Sun, Zhengmao Zhu

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

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  9. High expression of autophagy-related geneWorld journal of clinical cases · 2023
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  20. Design, synthesis and biological evaluation of a new thieno[2,3-Journal of enzyme inhibition and medicinal chemistry · 2020
    Article
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

6 authors at 1 institution in 1 country.

Jin ZhangTianjin Key Laboratory of Protein Science, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Qianying WangTianjin Key Laboratory of Protein Science, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Qing WangTianjin Key Laboratory of Protein Science, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jiangran CaoTianjin Key Laboratory of Protein Science, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jiafu SunTianjin Key Laboratory of Protein Science, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Zhengmao ZhuTianjin Key Laboratory of Protein Science, Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China. zhuzhengmao@nankai.edu.cn.ORCID http://orcid.org/0000-0002-8734-8020
Nankai University · CN

Funding

National Natural Science Foundation of China 91649107the Natural Science Foundation of Tianjin City of China 17JCYBJC24100
6 · The paper itself

Abstract

Endocrine therapy represents a mainstay adjuvant treatment of estrogen receptor-positive (ER+) breast cancer in clinical practice with an overall survival (OS) benefit. However, the emergence of resistance is inevitable over time and is present in one-third of the ER+ breast tumors. Several mechanisms of endocrine resistance in ER+/HER2- advanced breast cancers, through ERα itself, receptor tyrosine signaling, or cell cycle pathway, have been identified to be pivotal in endocrine therapy. The epigenetic alterations also contribute to ensuring tumor cells' escape from endocrine therapies. The strategy of combined hormone therapy with targeted pharmaceutical compounds has shown an improvement of progression-free survival or OS in clinical practice, including three different classes of drugs: CDK4/6 inhibitors, selective inhibitor of PI3Kα and mTOR inhibitors. Many therapeutic targets of cell cycle pathway and cell signaling and their combination strategies have recently entered clinical trials. This review focuses on Cyclin D-CDK4/6-RB axis, PI3K pathway and HDACs. Additionally, genomic evolution is complex in tumors exposed to hormonal therapy. We highlight the genomic alterations present in ESR1 and PIK3CA genes to elucidate adaptive mechanisms of endocrine resistance, and discuss how these mutations may inform novel combinations to improve clinical outcomes in the future.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsBreast NeoplasmsCyclin DCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Erb-b2 Receptor Tyrosine KinasesEstrogen Receptor alphaEstrogen Receptor ModulatorsFemaleHumansMutationPhosphatidylinositol 3-KinasesSignal TransductionAntineoplastic AgentsCyclin DCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6ERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesESR1 protein, humanEstrogen Receptor alphaEstrogen Receptor ModulatorsPhosphatidylinositol 3-KinasesCDK4/6 inhibitorEndocrine resistanceESR1mutationHDAC inhibitorPI3K

Identifiers

PMID31471681
PMCPMC11105043
OpenAlexW2970776976

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.