Evidence map›Paper›PMID 19446912›Full record

ArticleJournal of hepatology2009

Establishment of cancer cell lines from rat hepatocholangiocarcinoma and assessment of the role of granulocyte-colony stimulating factor and hepatocyte growth factor in their growth, motility and survival.

Anna C Piscaglia, Thomas D Shupe, Giovanbattista Pani, Valentina Tesori, Antonio Gasbarrini, Bryon E Petersen

Abstract read
In one paragraph

Article in Journal of hepatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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  8. Tumor microenvironment: a main actor in the metastasis process.Clinical & experimental metastasis · 2012
    Review
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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 4 institutions in 2 countries.

Anna C PiscagliaDepartment of Internal Medicine, GI & Liver Stem Cell Research Group, Catholic University of Rome - Gemelli Hospital, Largo A. Gemelli 8, 00168 Rome, Italy. annachiarapiscaglia@hotmail.com
Thomas D Shupe
Giovanbattista Pani
Valentina Tesori
Antonio Gasbarrini
Bryon E Petersen
Università Cattolica del Sacro Cuore · ITUniversity of Florida · USSapienza University of Rome · ITUF Health Cancer Center

Funding

Mechanisms of Oval Cell Activation and DifferentiationR01DK058614 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PETERSEN, BRYON E · 2001 to 2014
$3.6M
Stem Cells in Liver Regeneration: Fusion or PlasticityR01DK065096 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PETERSEN, BRYON E · 2005 to 2013
$2.7M
NIDDK NIH HHS 2R01DK058614-05NIDDK NIH HHS R01 DK058614NIDDK NIH HHS R01 DK065096NIDDK NIH HHS R01DK065096
6 · The paper itself

Abstract

BACKGROUND/

aimsOval cells (OCs), putative hepatic stem cells, may give rise to liver cancers. We developed a carcinogenesis regimen, based upon induction of OC proliferation prior to carcinogen exposure. In our model, rats subjected to 2-acetylaminofluorene/ partial-hepatectomy followed by aflatoxin injection (APA regimen) developed well-differentiated hepatocholangiocarcinomas. The aim of this study was to establish and characterize cancer cell lines from this animal model.

methodsCancer cells were cultured from animals sacrificed eight months after treatment, and single clones were selected. The established cell lines, named LCSCs, were characterized, and their tumorigenicity was assessed in vivo. The roles of granulocyte-colony stimulating factor (G-CSF) and hepatocyte growth factor (HGF) in LCSC growth, survival and motility were also investigated.

resultsFrom primary tumors, six cell lines were developed. LCSCs shared with the primary tumors the expression of various OC-associated markers, including cMet and G-CSF receptor. In vitro, HGF conferred protection from death by serum withdrawal. Stimulation with G-CSF increased LCSC growth and motility, while the blockage of its receptor inhibited LCSC proliferation and migration.

conclusionsSix cancer cell lines were established from our model of hepatocholangiocarcinoma. HGF modulated LCSC resistance to apoptosis, while G-CSF acted on LCSCs as a proliferative and chemotactic agent.

Indexed as

2-AcetylaminofluoreneAflatoxin B1AnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationCell SurvivalCholangiocarcinomaGranulocyte Colony-Stimulating FactorHepatectomyHepatocyte Growth FactorLiver NeoplasmsMaleNeoplasm MetastasisProto-Oncogene Proteins c-met2-AcetylaminofluoreneAflatoxin B1Granulocyte Colony-Stimulating FactorHepatocyte Growth FactorProto-Oncogene Proteins c-metReceptors, Granulocyte Colony-Stimulating Factor

Identifiers

PMID19446912
PMCPMC2694236
OpenAlexW1965619669

What OpenQuestion holds

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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.