Evidence map›Paper›PMID 30791936›Full record

ReviewBreast cancer research : BCR2019

AMP-activated protein kinase: a potential therapeutic target for triple-negative breast cancer.

Wei Cao, Jieqing Li, Qiongyu Hao, Jaydutt V Vadgama, Yong Wu

Open access · goldAbstract readReview
In one paragraph

Review in Breast cancer research : BCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 83 citations in OpenAlex.

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  11. Adjuvant Properties of Caffeic Acid in Cancer Treatment.International journal of molecular sciences · 2024
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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

5 authors at 3 institutions in 2 countries.

Wei CaoDepartment of Nuclear Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Jieqing LiDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, David Geffen UCLA School of Medicine, and UCLA Jonsson Comprehensive Cancer Center, 1748 E. 118th Street, Los Angeles, CA, 90059, USA.
Qiongyu HaoDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, David Geffen UCLA School of Medicine, and UCLA Jonsson Comprehensive Cancer Center, 1748 E. 118th Street, Los Angeles, CA, 90059, USA.
Jaydutt V VadgamaDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, David Geffen UCLA School of Medicine, and UCLA Jonsson Comprehensive Cancer Center, 1748 E. 118th Street, Los Angeles, CA, 90059, USA. jayvadgama@cdrewu.edu.
Yong WuDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, David Geffen UCLA School of Medicine, and UCLA Jonsson Comprehensive Cancer Center, 1748 E. 118th Street, Los Angeles, CA, 90059, USA. yongwu@cdrewu.edu.ORCID 0000-0002-1698-0897
Charles R. Drew University of Medicine and Science · USTianjin Central Hospital of Gynecology Obstetrics · CNUnion Hospital · CN

Funding

Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Ali Andalibi, Jose A Torres-Ruiz · 2012 to 2026
$60.0M
UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Supporting African American Churches to Promote Cancer ScreeningU54CA143931 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI VADGAMA, JAYDUTT V. · 2009 to 2022
$19.7M
Training and Mentoring ProgramsU54CA143930 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PIETRAS, RICHARD JOSEPH · 2009 to 2020
$7.5M
Mechanisms behind hyperglycemia-associated breast cancer risk and progressionSC1CA200517 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI WU, YONG · 2015 to 2018
$1.4M
Drew/UCLA Cancer Partnership ProgramU56CA101599 · NCI · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI VADGAMA, JAYDUTT V. · 2003 to 2009
$1.3M
NCATS NIH HHS UL1 TR000124NCI NIH HHS SC1 CA200517NCI NIH HHS U54 CA143930NCI NIH HHS U54 CA143931NCI NIH HHS U56 CA101599NIH HHS SC1CA200517NIH HHS U54CA14393NIH HHS U56CA101599-01NIH HHS UL1TR000124NIMHD NIH HHS U54 MD007598NIMHD NIH HHS U54MD007598
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive subset of breast carcinomas that lack expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2). Unlike other breast cancer subtypes, targeted therapy is presently unavailable for patients with TNBC. In spite of initial responses to chemotherapy, drug resistance tends to develop rapidly and the prognosis of metastatic TNBC is poor. Hence, there is an urgent need for novel-targeted treatment methods or development of safe and effective alternatives with recognized mechanism(s) of action. AMP-activated protein kinase (AMPK), an energy sensor, can regulate protein and lipid metabolism responding to alterations in energy supply. In the past 10 years, interest in AMPK has increased widely since it appeared as an attractive targeting molecule for cancer therapy. There has been a deep understanding of the possible role of abnormal AMPK signaling pathways in the regulation of growth and survival and the development of drug resistance in TNBC. The increasing popularity of using AMPK regulators for TNBC-targeted therapy is supported by a considerable development in ascertaining the molecular pathways implicated. This review highlights the available evidence for AMPK-targeted anti-TNBC activity of various agents or treatment strategies, with special attention placed on recent preclinical and clinical advances in the manipulation of AMPK in TNBC. The elaborative analysis of these AMPK-related signaling pathways will have a noteworthy impact on the development of AMPK regulators, resulting in efficacious treatments for this lethal disease.

Indexed as

AMP-Activated Protein KinasesAntineoplastic AgentsCell Line, TumorEnzyme ActivatorsFemaleGenetic TherapyHumansMetabolic Networks and PathwaysMicroRNAsMolecular Targeted TherapyProtein Kinase InhibitorsSignal TransductionTriple Negative Breast NeoplasmsAMP-Activated Protein KinasesAntineoplastic AgentsEnzyme ActivatorsMicroRNAsMIRN200 microRNA, humanProtein Kinase InhibitorsAMP-activated protein kinaseChemotherapyTargeted treatmentTriple-negative breast cancer

Identifiers

PMID30791936
PMCPMC6385460
OpenAlexW2921066798

What OpenQuestion holds

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Registered trials

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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.