Evidence map›Paper›PMID 34623477›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2021

Endocrine resistance in breast cancer: from molecular mechanisms to therapeutic strategies.

Ozge Saatci, Kim-Tuyen Huynh-Dam, Ozgur Sahin

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
11.9field-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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

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35 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

3 authors at 1 institution in 1 country.

Ozge SaatciDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, 715, Sumter Street, CLS609D, Columbia, SC, 29208, USA.
Kim-Tuyen Huynh-DamDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, 715, Sumter Street, CLS609D, Columbia, SC, 29208, USA.
Ozgur SahinDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, 715, Sumter Street, CLS609D, Columbia, SC, 29208, USA. sahin@cop.sc.edu.ORCID 0000-0002-8033-7089
University of South Carolina Sumter · US

Funding

Targeting NMDA Receptors and Brain Estradiol to Rescue Memory in Aging FemalesP20GM109091 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RONINSON, IGOR B · 2014 to 2024
$25.2M
NIGMS NIH HHS P20 GM109091
6 · The paper itself

Abstract

Estrogen receptor-positive (ER +) breast cancer accounts for approximately 75% of all breast cancers. Endocrine therapies, including selective ER modulators (SERMs), aromatase inhibitors (AIs), and selective ER down-regulators (SERDs) provide substantial clinical benefit by reducing the risk of disease recurrence and mortality. However, resistance to endocrine therapies represents a major challenge, limiting the success of ER + breast cancer treatment. Mechanisms of endocrine resistance involve alterations in ER signaling via modulation of ER (e.g., ER downregulation, ESR1 mutations or fusions); alterations in ER coactivators/corepressors, transcription factors (TFs), nuclear receptors and epigenetic modulators; regulation of signaling pathways; modulation of cell cycle regulators; stress signaling; and alterations in tumor microenvironment, nutrient stress, and metabolic regulation. Current therapeutic strategies to improve outcome of endocrine-resistant patients in clinics include inhibitors against mechanistic target of rapamycin (mTOR), cyclin-dependent kinase (CDK) 4/6, and the phosphoinositide 3-kinase (PI3K) subunit, p110α. Preclinical studies reveal novel therapeutic targets, some of which are currently tested in clinical trials as single agents or in combination with endocrine therapies, such as ER partial agonists, ER proteolysis targeting chimeras (PROTACs), next-generation SERDs, AKT inhibitors, epidermal growth factor receptor 1 and 2 (EGFR/HER2) dual inhibitors, HER2 targeting antibody-drug conjugates (ADCs) and histone deacetylase (HDAC) inhibitors. In this review, we summarize the established and emerging mechanisms of endocrine resistance, alterations during metastatic recurrence, and discuss the approved therapies and ongoing clinical trials testing the combination of novel targeted therapies with endocrine therapy in endocrine-resistant ER + breast cancer patients.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsAromatase InhibitorsBreast NeoplasmsEstrogen Receptor ModulatorsFemaleHumansNeoplasm Recurrence, LocalReceptors, EstrogenAntineoplastic AgentsAromatase InhibitorsEstrogen Receptor ModulatorsReceptors, EstrogenBreast cancerEndocrine resistanceMechanisms of resistanceTherapy

Identifiers

PMID34623477
PMCPMC8611518
OpenAlexW3202828068

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.