Evidence map›Paper›PMID 25956158›Full record

ReviewMolecular cancer research : MCR2015

Dissecting the Dual Role of AMPK in Cancer: From Experimental to Human Studies.

Giorgia Zadra, Julie L Batista, Massimo Loda

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
11.3field-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

117 citing papers in PubMed, 191 citations in OpenAlex.

  1. Article
  2. Review
  3. Metabolic convergence of diabetes and prostate cancer: from dysglycemia to tumor microenvironment reprogramming.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  19. Integrative Analysis of the AMPK subunits in Colorectal Adeno Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  20. Article

57 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.

Giorgia ZadraDepartment of Medical Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts. Department of Pathology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts.
Julie L BatistaDepartment of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Channing Division of Network Medicine, Brigham and Women's Hospital/Harvard Medical School Boston, Massachusetts.
Massimo LodaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts. Department of Pathology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Boston, Massachusetts. The Broad Institute, Cambridge, Massachusetts. Division of Cancer Studies, King's College London, United Kingdom. massimo_loda@dfci.harvard.edu.
Harvard University · US

Funding

Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI LODA, MASSIMO · 2002 to 2017
$36.2M
Molecular Link Between Metabolic Syndrome and Prostate CancerR01CA131945 · NCI · DANA-FARBER CANCER INST · PI LODA, MASSIMO · 2008 to 2018
$4.0M
Targeting the p110beta isoform of PI3 kinase in prostate cancerR01CA187918 · NCI · DANA-FARBER CANCER INST · PI LODA, MASSIMO, ROBERTS, THOMAS M · 2015 to 2019
$2.8M
NCI NIH HHS 2R01CA131945NCI NIH HHS P50 CA090381NCI NIH HHS P50 CA90381NCI NIH HHS R01 CA131945NCI NIH HHS R01 CA187918
6 · The paper itself

Abstract

The precise role of 5'AMP-activated kinase (AMPK) in cancer and its potential as a therapeutic target is controversial. Although it is well established that activation of this energy sensor inhibits the main anabolic processes that sustain cancer cell proliferation and growth, AMPK activation can confer on cancer cells the plasticity to survive under metabolic stress such as hypoxia and glucose deprivation, which are commonly observed in fast growing tumors. Thus, AMPK is referred to as both a "conditional" tumor suppressor and "contextual" oncogene. To add a further layer of complexity, AMPK activation in human cancer tissues and its correlation with tumor aggressiveness and progression appears to vary in different contexts. The current review discusses the different faces of this metabolic regulator, the therapeutic implications of its modulation, and provides an overview of the most relevant data available on AMPK activation and AMPK-activating drugs in human studies.

Indexed as

AMP-Activated Protein KinasesAnimalsAntineoplastic AgentsCell HypoxiaCell ProliferationGenes, Tumor SuppressorHumansNeoplasmsOncogenesStress, PhysiologicalAMP-Activated Protein KinasesAntineoplastic Agents

Identifiers

PMID25956158
PMCPMC4504770
OpenAlexW2132413659

What OpenQuestion holds

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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.