Evidence map›Paper›PMID 19896097›Full record

ReviewClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2009

Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.

Craig D Logsdon, Baoan Ji

Open access · greenAbstract readReview
In one paragraph

Review in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
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  11. Review
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  15. Article
  16. Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2017
    Review
  17. Article
  18. Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Review
  19. Article
  20. Elevated miR-483-3p expression is an early event and indicates poor prognosis in pancreatic ductal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
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

2 authors at 1 institution in 1 country.

Craig D LogsdonDepartment of Cancer Biology and GI Medical Oncology, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. clogsdon@mdanderson.org
Baoan Ji
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
SPORE in Pancreatic CancerP20CA101936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABBRUZZESE, JAMES L. · 2003 to 2009
$5.4M
MOLECULAR MECHANISMS OF PANCREATITISR01DK052067 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGSDON, CRAIG D · 1998 to 2015
$4.4M
Alcohol Induced Chronic PancreatitisR01AA020822 · NIAAA · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGSDON, CRAIG D · 2012 to 2016
$1.7M
The Role of Trypsin in PancreatitisR21DK068414 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI JI, BAOAN · 2007 to 2008
$408k
NCI NIH HHS CA16672NCI NIH HHS P20 CA101936NCI NIH HHS P30 CA016672NIAAA NIH HHS R01 AA020822NIDDK NIH HHS 5R21DK068414NIDDK NIH HHS DK052067NIDDK NIH HHS R01 DK052067NIDDK NIH HHS R21 DK068414
6 · The paper itself

Abstract

The relationship between chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) is unclear. CP is a risk factor for PDAC, CP is found within the vicinity of PDAC, and both share many similar genetic alterations. However, it has been long thought that PDAC arises only from duct cells. However, we have recently found that excessive activity within the Ras signaling pathway can lead to acinar cell death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from acinar cells through the full complement of preneoplastic (pancreatic intraepithelial neoplasia) lesions. Therefore, it is time to reevaluate the relationship between CP and PDAC. We proposed a new model in which Ras activity is the direct link between these 2 diseases. Here we will briefly review the shared properties between CP and PDAC and describe the new model.

Indexed as

Genes, rasAdenocarcinomaCarcinoma, Pancreatic DuctalHumansModels, BiologicalPancreatitis, ChronicSignal Transduction

Identifiers

PMID19896097
PMCPMC3050544
OpenAlexW2054671198

What OpenQuestion holds

Textmetadata
LicenceTDM
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.