Evidence map›Paper›PMID 22440254›Full record

ArticleThe American journal of pathology2012

Enhanced expression of fibroblast growth factor receptor 2 IIIc promotes human pancreatic cancer cell proliferation.

Toshiyuki Ishiwata, Yoko Matsuda, Tetsushi Yamamoto, Eiji Uchida, Murray Korc, Zenya Naito

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 67 citations in OpenAlex.

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  17. An FGFR/AKT/SOX2 Signaling Axis Controls Pancreatic Cancer Stemness.Frontiers in cell and developmental biology · 2020
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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 3 institutions in 2 countries.

Toshiyuki IshiwataDepartment of Pathology and Integrative Oncological Pathology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan. ishiwata@nms.ac.jp
Yoko Matsuda
Tetsushi Yamamoto
Eiji Uchida
Murray Korc
Zenya Naito
Nippon Medical School · JPIndiana University – Purdue University Indianapolis · USNippon Medical School Hospital · JP

Funding

Novel aspects of Epithelial-Mesenchymal Transition(EMT)in pancreatic cancerR01CA075059 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KORC, MURRAY · 1997 to 2018
$4.3M
Dysregulation of TGF Beta Action Pancreatic CancerR37CA075059 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KORC, MURRAY · 2008 to 2012
$2.2M
NCI NIH HHS R01 CA075059NCI NIH HHS R37 CA075059NCI NIH HHS R37-CA-075059
6 · The paper itself

Abstract

In pancreatic ductal adenocarcinoma (PDAC), the fibroblast growth factor receptor 1 (FGFR-1) IIIb isoform correlates with the inhibition of cancer cell proliferation, migration, and invasion, whereas FGFR-1 IIIc enhances cancer cell proliferation. The FGFR-2 IIIb isoform is expressed in PDAC, and its expression correlates with increased venous invasion. We examined the role of FGFR-2 IIIc in PDAC. FGFR-2 IIIc was expressed in all six pancreatic cancer cell lines examined and was highest in PANC-1 cells. FGFR-2 IIIc was abundant in the cancer cells from 83 of 117 PDAC cases, which correlated with decreased duration to development of liver metastasis after surgery. FGFR-2 IIIc-transfected cells exhibited increased proliferation in vitro and formed larger subcutaneous and orthotopic tumors, the latter producing more liver metastases. Moreover, FGF-2 exerted a more rapid stimulatory effect on the levels of phosphorylated extracellular signal-regulated kinase (p-ERK) in FGFR-2 IIIc stably transfected PANC-1 cells, compared with control cells. FGFR-2 IIIc-transfected cells also formed more spheres and contained more side population cells. Suppression of FGFR-2 IIIc expression inhibited the proliferation of PANC-1 cells, whereas an anti-FGFR-2 IIIc antibody inhibited the proliferation and migration of PANC-1 cells. Thus, high FGFR-2 IIIc levels in PDAC contribute to disease aggressiveness and confer to pancreatic cancer cells features suggestive of cancer stem cells, indicating that FGFR-2 IIIc may be a novel and important therapeutic target in PDAC.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overAnimalsCell Line, TumorCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiceMice, NudeMiddle AgedFGFR2 protein, humanNeoplasm ProteinsProtein IsoformsReceptor, Fibroblast Growth Factor, Type 2RNA, MessengerRNA, Neoplasm

Identifiers

PMID22440254
PMCPMC3349828
OpenAlexW2053694975

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.