Evidence map›Paper›PMID 31088482›Full record

SynthesisJournal of experimental & clinical cancer research : CR2019

STAT3 as a potential therapeutic target in triple negative breast cancer: a systematic review.

Jiang-Jiang Qin, Li Yan, Jia Zhang, Wei-Dong Zhang

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 1 pooled it
21.4field-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

226 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. AXL is associated with STAT3 activation in breast cancer.Molecular and clinical oncology · 2026
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166 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

4 authors at 4 institutions in 1 country.

Jiang-Jiang QinCollege of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, Binjiang District, Hangzhou, 310053, Zhejiang, China. jqin@zcmu.edu.cn.ORCID http://orcid.org/0000-0002-8559-616X
Li YanSchool of Pharmacy, Naval Medical University, 325 Guohe Road, Yangpu District, Shanghai, 200433, China.
Jia ZhangShanxi Institute of Traditional Chinese Medicine, Taiyuan, 030012, China.
Wei-Dong ZhangSchool of Pharmacy, Naval Medical University, 325 Guohe Road, Yangpu District, Shanghai, 200433, China. wdzhangy@hotmail.com.
Guiyang Medical University · CNSecond Military Medical University · CNShanxi Province Hospital of Traditional Chinese Medicine · CNZhejiang Chinese Medical University · CN

Funding

National Key Research and Development Program of China 2017YFC1700200NSFC 81520108030, 21472238Scientific Foundation of Shanghai China 13401900103, 13401900101Shanghai Engineering Research Center for the Preparation of Bioactive Natural Products 16DZ2280200Zhejiang Chinese Medical University Startup Funding 111100E014
6 · The paper itself

Abstract

Triple negative breast cancer (TNBC), which is typically lack of expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), represents the most aggressive and mortal subtype of breast cancer. Currently, only a few treatment options are available for TNBC due to the absence of molecular targets, which underscores the need for developing novel therapeutic and preventive approaches for this disease. Recent evidence from clinical trials and preclinical studies has demonstrated a pivotal role of signal transducer and activator of transcription 3 (STAT3) in the initiation, progression, metastasis, and immune evasion of TNBC. STAT3 is overexpressed and constitutively activated in TNBC cells and contributes to cell survival, proliferation, cell cycle progression, anti-apoptosis, migration, invasion, angiogenesis, chemoresistance, immunosuppression, and stem cells self-renewal and differentiation by regulating the expression of its downstream target genes. STAT3 small molecule inhibitors have been developed and shown excellent anticancer activities in in vitro and in vivo models of TNBC. This review discusses the recent advances in the understanding of STAT3, with a focus on STAT3's oncogenic role in TNBC. The current targeting strategies and representative small molecule inhibitors of STAT3 are highlighted. We also propose potential strategies that can be further examined for developing more specific and effective inhibitors for TNBC prevention and therapy.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmHumansNeoplastic Stem CellsNeovascularization, PathologicOncogenesSignal TransductionSTAT3 Transcription FactorTriple Negative Breast NeoplasmsTumor EscapeAntineoplastic AgentsBiomarkers, TumorSTAT3 protein, humanSTAT3 Transcription FactorImmune escapeOncogeneSmall molecule inhibitorsSTAT3Triple negative breast cancer

Identifiers

PMID31088482
PMCPMC6518732
OpenAlexW2946899637

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.