Evidence map›Paper›PMID 27386488›Full record

ReviewAnnals of translational medicine2016

PDX1 associated therapy in translational medicine.

Juehua Yu, Shi-He Liu, Robbi Sanchez, John Nemunaitis, Enrique Rozengurt, F Charles Brunicardi

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Annals of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. A Phase II Study of the Efficacy and Safety of Oral Selinexor in Recurrent Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Trial
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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

6 authors at 2 institutions in 1 country.

Juehua Yu1 Division of General Surgery, Department of Surgery, David Geffen School of Medicine at University of California Los Angeles, CA, USA ; 2 Mary Crowley Cancer Research Center, Dallas, TX, USA ; 3 Division of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA, USA.
Shi-He Liu1 Division of General Surgery, Department of Surgery, David Geffen School of Medicine at University of California Los Angeles, CA, USA ; 2 Mary Crowley Cancer Research Center, Dallas, TX, USA ; 3 Division of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA, USA.
Robbi Sanchez1 Division of General Surgery, Department of Surgery, David Geffen School of Medicine at University of California Los Angeles, CA, USA ; 2 Mary Crowley Cancer Research Center, Dallas, TX, USA ; 3 Division of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA, USA.
John Nemunaitis1 Division of General Surgery, Department of Surgery, David Geffen School of Medicine at University of California Los Angeles, CA, USA ; 2 Mary Crowley Cancer Research Center, Dallas, TX, USA ; 3 Division of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA, USA.
Enrique Rozengurt1 Division of General Surgery, Department of Surgery, David Geffen School of Medicine at University of California Los Angeles, CA, USA ; 2 Mary Crowley Cancer Research Center, Dallas, TX, USA ; 3 Division of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA, USA.
F Charles Brunicardi1 Division of General Surgery, Department of Surgery, David Geffen School of Medicine at University of California Los Angeles, CA, USA ; 2 Mary Crowley Cancer Research Center, Dallas, TX, USA ; 3 Division of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA, USA.
University of California, Los Angeles · USMary Crowley Cancer Research Center · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Targeting diet-induced promotion of Kras-initiated pancreatic adenocarcinomaP01CA163200 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2012 to 2016
$6.2M
PDX-1 is a Therapeutic Target for Pancreatic CancerR01CA095731 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRUNICARDI, FRANCIS CHARLES · 2002 to 2012
$2.6M
Intraislet Communication in Surgically-Altered PancreasR01DK046441 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BRUNICARDI, FRANCIS CHARLES · 1998 to 2007
$1.9M
NCI NIH HHS P01 CA163200NCI NIH HHS R01 CA095731NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R01 DK046441
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extremely poor prognosis and a low median survival due to lack of the early and reliable detection and effective therapeutic options, despite improvements observed for many other cancers in last decade. Pancreatic and duodenal homeobox 1 (PDX1), which is a homeodomain-containing transcription factor and a key regulator for insulin gene expression, β cell maturation and proper β cell function maintenance in the pancreas. Our previous studies revealed that PDX1 promotes tumorigenesis and it is a promising therapeutic target for PDAC. For translational purposes, we developed three therapeutic platforms utilizing RNA interference (RNAi), gene therapy and small inhibitory drug targeting PDX1, and further validated them in PDAC preclinical models both in vitro and in vivo. These PDX1 targeted therapies significantly inhibited PDX1 expression in PDAC cells, ablated PDX1-expressing human PDAC xenograft tumor growth, and prolonged survival in the PDAC mouse models. The data from these preclinical studies proved the translational potentials of PDX1 targeted therapies in PDAC and suggest that the strategy of developing PDX1 targeted therapies would permit a rapid bench-to-bedside translation of other relevant gene therapies, which would eventually benefit the patients suffering from this deadly disease.

Indexed as

metforminPancreatic and duodenal homeobox 1 (PDX1)pancreatic cancerRIP-TKRNA interference (RNAi)

Identifiers

PMID27386488
PMCPMC4916355
OpenAlexW2346680660

What OpenQuestion holds

Textmetadata
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.