Evidence map›Paper›PMID 19723334›Full record

ArticleBMC cancer2009

Histological evaluation of AMPK signalling in primary breast cancer.

Sirwan M Hadad, Lee Baker, Philip R Quinlan, Katherine E Robertson, Susan E Bray, George Thomson, David Kellock, Lee B Jordan, Colin A Purdie, David G Hardie and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
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  10. Journal of traditional and complementary medicine · 2023
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  11. The role of the SNF1 signaling pathway in the growth of Saccharomyces cerevisiae in different carbon and nitrogen sources.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
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39 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

12 authors at 2 institutions in 1 country.

Sirwan M HadadDepartment of Surgery and Molecular Oncology, Ninewells Hospital and Medical School, Dundee, UK. s.hadad@dundee.ac.uk
Lee Baker
Philip R Quinlan
Katherine E Robertson
Susan E Bray
George Thomson
David Kellock
Lee B Jordan
Colin A Purdie
David G Hardie
Stewart Fleming
Alastair M Thompson
Ninewells Hospital · GBUniversity of Dundee · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

backgroundAMP-activated protein kinase (AMPK) acts as a cellular fuel gauge that responds to energy stress by suppressing cell growth and biosynthetic processes, thus ensuring that energy-consuming processes proceed only if there are sufficient metabolic resources. Malfunction of the AMPK pathway may allow cancer cells to undergo uncontrolled proliferation irrespective of their molecular energy levels. The aim of this study was to examine the state of AMPK phosphorylation histologically in primary breast cancer in relation to clinical and pathological parameters.

methodsImmunohistochemistry was performed using antibodies to phospho-AMPK (pAMPK), phospho-Acetyl Co-A Carboxylase (pACC) an established target for AMPK, HER2, ERalpha, and Ki67 on Tissue Micro-Array (TMA) slides of two cohorts of 117 and 237 primary breast cancers. The quick score method was used for scoring and patterns of protein expression were compared with clinical and pathological data, including a minimum 5 years follow up.

resultsReduced signal, compared with the strong expression in normal breast epithelium, using a pAMPK antibody was demonstrated in 101/113 (89.4%) and 217/236 (91.9%) of two cohorts of patients. pACC was significantly associated with pAMPK expression (p = 0.007 & p = 0.014 respectively). For both cohorts, reduced pAMPK signal was significantly associated with higher histological grade (p = 0.010 & p = 0.021 respectively) and axillary node metastasis (p = 0.061 & p = 0.039 respectively). No significant association was found between pAMPK and any of HER2, ERalpha, or Ki67 expression, disease-free survival or overall survival.

conclusionThis study extends in vitro evidence through immunohistochemistry to confirm that AMPK is dysfunctional in primary breast cancer. Reduced signalling via the AMPK pathway, and the inverse relationship with histological grade and axillary node metastasis, suggests that AMPK re-activation could have therapeutic potential in breast cancer.

Indexed as

Signal TransductionAdultAgedAged, 80 and overAMP-Activated Protein KinasesBreast NeoplasmsCohort StudiesFemaleFollow-Up StudiesHumansImmunohistochemistryMiddle AgedPhosphorylationAMP-Activated Protein Kinases

Identifiers

PMID19723334
PMCPMC2744705
OpenAlexW2136887307

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.