Evidence map›Paper›PMID 26053098›Full record

ArticleOncotarget2015

Identification and characterization of the gene expression profiles for protein coding and non-coding RNAs of pancreatic ductal adenocarcinomas.

María Laura Gutiérrez, Luis Corchete, Cristina Teodosio, María Eugenia Sarasquete, María del Mar Abad, Manuel Iglesias, Carmen Esteban, José María Sayagues, Alberto Orfao, Luis Muñoz-Bellvis

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 28% 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, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. A Cancer Cell Cluster Marked by LincRNAFrontiers in oncology · 2021
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Pancreatic Cancer, A Mis-interpreter of the Epigenetic Language.The Yale journal of biology and medicine · 2016
    Review
  9. Article
  10. Review
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

10 authors at 3 institutions in 1 country.

María Laura GutiérrezCytometry Service-NUCLEUS, Department of Medicine, Cancer Research Center (IBMCC-CSIC/USAL) and IBSAL (University of Salamanca), Salamanca, Spain.
Luis CorcheteCancer Research Center and Service of Hematology (University Hospital of Salamanca), Salamanca, Spain.
Cristina TeodosioCytometry Service-NUCLEUS, Department of Medicine, Cancer Research Center (IBMCC-CSIC/USAL) and IBSAL (University of Salamanca), Salamanca, Spain.
María Eugenia SarasqueteCancer Research Center and Service of Hematology (University Hospital of Salamanca), Salamanca, Spain.
María del Mar AbadDepartment of Pathology (University Hospital of Salamanca), Salamanca, Spain.
Manuel IglesiasService of General and Gastrointestinal Surgery and IBSAL (University Hospital of Salamanca), Salamanca, Spain.
Carmen EstebanService of General and Gastrointestinal Surgery and IBSAL (University Hospital of Salamanca), Salamanca, Spain.
José María SayaguesCytometry Service-NUCLEUS, Department of Medicine, Cancer Research Center (IBMCC-CSIC/USAL) and IBSAL (University of Salamanca), Salamanca, Spain.
Alberto OrfaoCytometry Service-NUCLEUS, Department of Medicine, Cancer Research Center (IBMCC-CSIC/USAL) and IBSAL (University of Salamanca), Salamanca, Spain.
Luis Muñoz-BellvisService of General and Gastrointestinal Surgery and IBSAL (University Hospital of Salamanca), Salamanca, Spain.
Centro de Investigación del Cáncer · ESUniversidad de Salamanca · ESInstituto de Investigación Biomédica de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Significant advances have been achieved in recent years in the identification of the genetic and the molecular alterations of pancreatic ductal adenocarcinoma (PDAC). Despite this, at present the understanding of the precise mechanisms involved in the development and malignant transformation of PDAC remain relatively limited. Here, we evaluated for the first time, the molecular heterogeneity of PDAC tumors, through simultaneous assessment of the gene expression profile (GEP) for both coding and non-coding genes of tumor samples from 27 consecutive PDAC patients. Overall, we identified a common GEP for all PDAC tumors, characterized by an increased expression of genes involved in PDAC cell proliferation, local invasion and metastatic capacity, together with a significant alteration of the early steps of the cellular immune response. At the same time, we confirm and extend on previous observations about the genetic complexity of PDAC tumors as revealed by the demonstration of two clearly distinct and unique GEPs (e.g. epithelial-like vs. mesenchymal-like) reflecting the alteration of different signaling pathways involved in the oncogenesis and progression of these tumors. Our results also highlight the potential role of the immune system microenvironment in these tumors, with potential diagnostic and therapeutic implications.

Indexed as

Open Reading FramesAdultAgedCarcinoma, Pancreatic DuctalFemaleGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMiddle AgedPancreatic NeoplasmsRNA, MessengerRNA, UntranslatedTranscriptomeMicroRNAsRNA, MessengerRNA, UntranslatedEMT-like tumorsgene expression profilemRNAnon-coding RNApancreatic ductal adenocarcinoma

Identifiers

PMID26053098
PMCPMC4662476
OpenAlexW1601935183

What OpenQuestion holds

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LicenceCC BY
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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.