Evidence map›Paper›PMID 27696537›Full record

ArticleMolecular carcinogenesis2016

Expression, modulation, and clinical correlates of the autophagy protein Beclin-1 in esophageal adenocarcinoma.

Katherine M Weh, Amy B Howell, Laura A Kresty

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 52 citations in OpenAlex.

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  12. Construction and Evaluation of a Risk Score Model for Autophagy-Related Genes in Esophageal Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2021
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  14. Associations ofPathology oncology research : POR · 2021
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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

3 authors at 2 institutions in 1 country.

Katherine M WehDivision of Hematology & Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Amy B HowellBlueberry and Cranberry Research Center, Rutgers University, Chatsworth, New Jersey.
Laura A KrestyDivision of Hematology & Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin. LKresty@mcw.edu.
Medical College of Wisconsin · USRutgers, The State University of New Jersey · US

Funding

Inhibition of Reflux-Induced Esophageal Adenocarcinoma by ProanthocyanidinsR01CA158319 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KRESTY, LAURA A · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA158319
6 · The paper itself

Abstract

Esophageal adenocarcinoma (EAC) is characterized by rapidly increasing incidence and mortality rates and poor survival. Efficacious preventive and treatment options are urgently needed. An increasing number of pharmacologic agents targeting cancer cell death via autophagy mechanisms are being evaluated in hopes of circumventing apoptotic and therapeutic resistance. We report for the first time, loss of Beclin-1, a key mediator of autophagy, was significantly linked to prognostic factors in EAC. Specifically, Beclin-1 expression loss occurred in 49.0% of EAC patients versus 4.8% of controls. There was a significant inverse correlation between loss of Beclin-1 with histologic grade and tumor stage supporting a tumor suppressive role for Beclin-1. Autophagy modulation linked to cell death was examined in EAC cell lines following treatment with a proanthocyanidin-rich cranberry extract, C-PAC, and the commonly used autophagy inducer, rapamycin. C-PAC induced Beclin-1-independent autophagy in EAC cells characterized by reduced phosphorylation at serine 15 and 93, and significant cell death induction. In contrast, rapamycin-induced autophagy resulted in concomitant, increases in total Beclin-1 levels as well as Beclin-1-phosphorylation in a cell line specific manner, leading to long-term cell survival. Furthermore, autophagic LC3-II was induced by C-PAC following siRNA suppression of Beclin-1 in EAC cells. Together these data support a prognostic role of Beclin-1 in EAC with evidence that Beclin-dependent autophagy induction is agent specific. Future studies are necessary to fully interrogate the role autophagy plays in the progression of normal tissue to EAC and how specific agents targeting autophagic mechanisms can be efficaciously applied for cancer prevention or treatment. © 2015 Wiley Periodicals, Inc.

Indexed as

AdenocarcinomaAnthocyaninsAutophagyBeclin-1Cell Line, TumorEsophageal NeoplasmsGene Expression Regulation, NeoplasticHumansNeoplasm GradingNeoplasm StagingPhosphorylationPlant ExtractsPrognosisSirolimusSurvival AnalysisVaccinium macrocarponAnthocyaninsBeclin-1BECN1 protein, humanPlant ExtractsSirolimusautophagyesophagusnatural productrapamycin

Identifiers

PMID27696537
PMCPMC5987534
OpenAlexW2241111255

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.