Evidence map›Paper›PMID 30134550›Full record

SynthesisInternational journal of molecular sciences2018

New Hope for Pancreatic Ductal Adenocarcinoma Treatment Targeting Endoplasmic Reticulum Stress Response: A Systematic Review.

Nuria Garcia-Carbonero, Weiyao Li, Marticela Cabeza-Morales, Javier Martinez-Useros, Jesus Garcia-Foncillas

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 33 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

5 authors at 1 institution in 1 country.

Nuria Garcia-CarboneroTranslational Oncology Division, OncoHealth Institute, Health Research Institute-University Hospital Fundación Jiménez Díaz-UAM, Avda Reyes Catolicos 2, 28040 Madrid, Spain. nuria.garciac@quironsalud.es.
Weiyao LiTranslational Oncology Division, OncoHealth Institute, Health Research Institute-University Hospital Fundación Jiménez Díaz-UAM, Avda Reyes Catolicos 2, 28040 Madrid, Spain. weiyao.li@quironsalud.es.
Marticela Cabeza-MoralesTranslational Oncology Division, OncoHealth Institute, Health Research Institute-University Hospital Fundación Jiménez Díaz-UAM, Avda Reyes Catolicos 2, 28040 Madrid, Spain. marticelacabezamorales@gmail.com.
Javier Martinez-UserosTranslational Oncology Division, OncoHealth Institute, Health Research Institute-University Hospital Fundación Jiménez Díaz-UAM, Avda Reyes Catolicos 2, 28040 Madrid, Spain. javier.museros@oncohealth.eu.ORCID 0000-0001-9007-828X
Jesus Garcia-FoncillasTranslational Oncology Division, OncoHealth Institute, Health Research Institute-University Hospital Fundación Jiménez Díaz-UAM, Avda Reyes Catolicos 2, 28040 Madrid, Spain. jesus.garciafoncillas@oncohealth.eu.
Hospital Universitario Fundación Jiménez Díaz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of tumours, and its incidence is rising worldwide. Although survival can be improved by surgical resection when these tumours are detected at an early stage, this cancer is usually asymptomatic, and disease only becomes apparent after metastasis. Several risk factors are associated with this disease, the most relevant being chronic pancreatitis, diabetes, tobacco and alcohol intake, cadmium, arsenic and lead exposure, certain infectious diseases, and the mutational status of some genes associated to a familial component. PDAC incidence has increased in recent decades, and there are few alternatives for chemotherapeutic treatment. Endoplasmic reticulum (ER) stress factors such as GRP78/BiP (78 kDa glucose-regulated protein), ATF6α (activating transcription factor 6 isoform α), IRE1α (inositol-requiring enzyme 1 isoform α), and PERK (protein kinase RNA-like endoplasmic reticulum kinase) activate the transcription of several genes involved in both survival and apoptosis. Some of these factors aid in inducing a non-proliferative state in cancer called dormancy. Modulation of endoplasmic reticulum stress could induce dormancy of tumour cells, thus prolonging patient survival. In this systematic review, we have compiled relevant results concerning those endoplasmic reticulum stress factors involved in PDAC, and we have analysed the mechanism of dormancy associated to endoplasmic reticulum stress and its potential use as a chemotherapeutic target against PDAC.

Indexed as

Activating Transcription Factor 6AnimalsAntibodiesCarcinoma, Pancreatic DuctalCommunicable DiseasesDeoxycytidineDiabetes ComplicationsDisease Models, AnimaleIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesGemcitabineGene Expression RegulationHeat-Shock ProteinsHumans4-(2-aminoethyl)benzenesulfonylfluorideActivating Transcription Factor 6AntibodiesATF6 protein, humanDeoxycytidineEIF2AK3 protein, humaneIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN1 protein, humanGemcitabineHeat-Shock ProteinsHSPA5 protein, humanMLN8866Protein Serine-Threonine KinasesRNA, Small InterferingSulfonesATF4ATF6αdormancyER stressGRP78IRE1αP38pancreatic ductal adenocarcinomaPERKUPR

Identifiers

PMID30134550
PMCPMC6165247
OpenAlexW2888330783

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.