Evidence map›Paper›PMID 26378019›Full record

ArticleOncotarget2015

Cranberry proanthocyanidins inhibit esophageal adenocarcinoma in vitro and in vivo through pleiotropic cell death induction and PI3K/AKT/mTOR inactivation.

Laura A Kresty, Katherine M Weh, Bree Zeyzus-Johns, Laura N Perez, Amy B Howell

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 66 citations in OpenAlex.

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  6. Unlocking the mechanistic potential ofJournal of traditional and complementary medicine · 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 2 institutions in 1 country.

Laura A KrestyDivision of Hematology and Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Katherine M WehDivision of Hematology and Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Bree Zeyzus-JohnsDivision of Hematology and Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Laura N PerezDivision of Hematology and Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Amy B HowellMarucci Center for Blueberry and Cranberry Research, Rutgers University, Chatsworth, New Jersey, USA.
Medical College of Wisconsin · USCranberry Institute · 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 CA158319NCI NIH HHS R01CA158319
6 · The paper itself

Abstract

Cranberries are rich in bioactive constituents known to improve urinary tract health and more recent evidence supports cranberries possess cancer inhibitory properties. However, mechanisms of cancer inhibition by cranberries remain to be elucidated, particularly in vivo. Properties of a purified cranberry-derived proanthocyanidin extract (C-PAC) were investigated utilizing acid-sensitive and acid-resistant human esophageal adenocarcinoma (EAC) cell lines and esophageal tumor xenografts in athymic NU/NU mice. C-PAC induced caspase-independent cell death mainly via autophagy and low levels of apoptosis in acid-sensitive JHAD1 and OE33 cells, but resulted in cellular necrosis in acid-resistant OE19 cells. Similarly, C-PAC induced necrosis in JHAD1 cells pushed to acid-resistance via repeated exposures to an acidified bile cocktail. C-PAC associated cell death involved PI3K/AKT/mTOR inactivation, pro-apoptotic protein induction (BAX, BAK1, deamidated BCL-xL, Cytochrome C, PARP), modulation of MAPKs (P-P38/P-JNK) and G2-M cell cycle arrest in vitro. Importantly, oral delivery of C-PAC significantly inhibited OE19 tumor xenograft growth via modulation of AKT/mTOR/MAPK signaling and induction of the autophagic form of LC3B supporting in vivo efficacy against EAC for the first time. C-PAC is a potent inducer of EAC cell death and is efficacious in vivo at non-toxic behaviorally achievable concentrations, holding promise for preventive or therapeutic interventions in cohorts at increased risk for EAC, a rapidly rising and extremely deadly malignancy.

Indexed as

AdenocarcinomaAnimalsApoptosisCell DeathCell Line, TumorEnzyme InhibitorsEsophageal NeoplasmsHumansMaleMiceMice, NudeOncogene Protein v-aktPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPlant ExtractsProanthocyanidinsEnzyme InhibitorsOncogene Protein v-aktPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPlant ExtractsProanthocyanidinsTOR Serine-Threonine Kinasesautophagybile acidcranberry proanthocyanidinsesophageal adenocarcinomaPI3K/AKT/mTOR

Identifiers

PMID26378019
PMCPMC4741777
OpenAlexW2186679996

What OpenQuestion holds

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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.