Evidence map›Paper›PMID 35995341›Full record

ReviewSeminars in cancer biology2022

STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.

Grace L Wong, Sara G Manore, Daniel L Doheny, Hui-Wen Lo

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
10.9field-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

63 citing papers in PubMed, 103 citations in OpenAlex.

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3 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 1 institution in 1 country.

Grace L WongDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Sara G ManoreDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Daniel L DohenyDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Hui-Wen LoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Breast Cancer Center of Excellence, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Wake Forest Baptist Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC, USA. Electronic address: hlo@wakehealth.edu.
Wake Forest University · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Roles of tGLI1 and microRNA Network in Breast Cancer Brain MetastasisR01CA228137 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LO, HUI-WEN, WATABE, KOUNOSUKE · 2020 to 2025
$2.1M
Developing Pharmacological tGLI1 InhibitorsF31CA261027 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DOHENY, DANIEL · 2022 to 2022
$29k
NCI NIH HHS F31 CA261027NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA228137
6 · The paper itself

Abstract

Breast cancer is the most commonly diagnosed cancer and second-leading cause of cancer deaths in women. Breast cancer stem cells (BCSCs) promote metastasis and therapeutic resistance contributing to tumor relapse. Through activating genes important for BCSCs, transcription factors contribute to breast cancer metastasis and therapeutic resistance, including the signal transducer and activator of transcription (STAT) family of transcription factors. The STAT family consists of six major isoforms, STAT1, STAT2, STAT3, STAT4, STAT5, and STAT6. Canonical STAT signaling is activated by the binding of an extracellular ligand to a cell-surface receptor followed by STAT phosphorylation, leading to STAT nuclear translocation and transactivation of target genes. It is important to note that STAT transcription factors exhibit diverse effects in breast cancer; some are either pro- or anti-tumorigenic while others maintain dual, context-dependent roles. Among the STAT transcription factors, STAT3 is the most widely studied STAT protein in breast cancer for its critical roles in promoting BCSCs, breast cancer cell proliferation, invasion, angiogenesis, metastasis, and immune evasion. Consequently, there have been substantial efforts in developing cancer therapeutics to target breast cancer with dysregulated STAT3 signaling. In this comprehensive review, we will summarize the diverse roles that each STAT family member plays in breast cancer pathobiology, as well as, the opportunities and challenges in pharmacologically targeting STAT proteins and their upstream activators in the context of breast cancer treatment.

Indexed as

Breast NeoplasmsNeoplasms, Second PrimaryCarcinogenesisFemaleHumansNeoplasm Recurrence, LocalNeoplastic Stem CellsBreast cancerBreast cancer stem cells (BCSCs)Breast cancer therapeuticsSignal transducer and activator of transcription (STAT)STAT inhibitors

Identifiers

PMID35995341
PMCPMC9714692
OpenAlexW4293275146

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.