Evidence map›Paper›PMID 31428571›Full record

ArticleFrontiers in oncology2019

Digitoxin Inhibits Epithelial-to-Mesenchymal-Transition in Hereditary Castration Resistant Prostate Cancer.

Bette S Pollard, Mark A Suckow, William R Wolter, Joshua M Starr, Ofer Eidelman, Clifton L Dalgard, Parameet Kumar, Sharmistha Battacharyya, Meera Srivastava, Roopa Biswas and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

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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

14 authors at 3 institutions in 1 country.

Bette S PollardSilver Pharmaceuticals, Rockville, MD, United States.
Mark A SuckowLobund Institute, University of Notre Dame, Notre Dame, IN, United States.
William R WolterLobund Institute, University of Notre Dame, Notre Dame, IN, United States.
Joshua M StarrDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Ofer EidelmanDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Clifton L DalgardDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Parameet KumarDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Sharmistha BattacharyyaDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Meera SrivastavaDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Roopa BiswasDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Matthew D WilkersonDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Xijun ZhangDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Qingfeng YangDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Harvey B PollardDepartment of Anatomy, Physiology and Genetics, Uniformed Services University School of Medicine-America's Medical School, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
Uniformed Services University of the Health Sciences · USWomen's Health Initiative · USUniversity of Notre Dame · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Castration Resistant Prostate Cancer (CRPC) is thought to be driven by a collaborative mechanism between TNFα/NFκB and TGFβ signaling, leading to inflammation, Epithelial-to-Mesenchymal-Transition (EMT), and metastasis. Initially, TGFβ is a tumor suppressor, but in advanced metastatic disease it switches to being a tumor promoter. TGFBR2 may play a critical role in this collaboration, as its expression is driven by NFκB and it is the primary receptor for TGFβ. We have previously reported that the cardenolide drug digitoxin blocks TNFα/NFκB-driven proinflammatory signaling. We therefore hypothesized that digitoxin might break the collaborative process between NFκB and TGFβ by also inhibiting expression of TGFBR2. We therefore tested whether TGFβ-driven EMT and resulting metastases would be suppressed. Here we show,

Indexed as

digitoxinhereditaryHSPB1NFκBprostate cancerTGFBR2TGFβ

Identifiers

PMID31428571
PMCPMC6687970
OpenAlexW2964456733

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.