Evidence map›Paper›PMID 24885890›Full record

ArticleBMC cancer2014

Antagonism of sorafenib and regorafenib actions by platelet factors in hepatocellular carcinoma cell lines.

Rosalba D'Alessandro, Maria G Refolo, Catia Lippolis, Grazia Giannuzzi, Nicola Carella, Caterina Messa, Aldo Cavallini, Brian I Carr

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
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  8. Pancreatic Cancer and Platelets Crosstalk: A Potential Biomarker and Target.Frontiers in cell and developmental biology · 2021
    Review
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  19. Resistance to multikinase inhibitor actions mediated by insulin like growth factor-1.Journal of experimental & clinical cancer research : CR · 2015
    Article
  20. 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

8 authors at 2 institutions in 1 country.

Rosalba D'Alessandro
Maria G Refolo
Catia Lippolis
Grazia Giannuzzi
Nicola Carella
Caterina Messa
Aldo Cavallini
Brian I CarrLaboratory of Biochemistry, National Institute for Digestive Diseases, IRCCS "Saverio de Bellis", Via Turi 27, 70013, Castellana Grotte, BA, Italy. brianicarr@hotmail.com.
Gastroenterology Hospital "Saverio de Bellis" · ITAzienda Ospedaliera Santa Maria Degli Angeli · IT

Funding

K VITAMINS--A NEW CLASS OF LIVER CELL GROWTH INHIBITORSR01CA082723 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CARR, BRIAN I · 2000 to 2008
$2.3M
NCI NIH HHS CA82723
6 · The paper itself

Abstract

backgroundPlatelets are frequently altered in hepatocellular carcinoma (HCC) patients. Platelet lysates (hPL) can enhance HCC cell growth and decrease apoptosis. The aims were to evaluate whether hPL can modulate the actions of sorafenib or regorafenib, two clinical HCC multikinase antagonists.

methodsSeveral human HCC cell lines were grown in the presence and absence of sorafenib or regorafenib, with or without hPL. Growth was measured by MTT assay, apoptosis was assessed by Annexin V and by western blot, and autophagy and MAPK growth signaling were also measured by western blot, and migration and invasion were measured by standard in vitro assays.

resultsBoth sorafenib and regorafenib-mediated inhibition of cell growth, migration and invasion were all antagonized by hPL. Drug-mediated apoptosis and decrease in phospho-ERK levels were both blocked by hPL, which also increased anti-apoptotic phospho-STAT, Bax and Bcl-xL levels. Preliminary data, obtained with epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I), included in hPL, revealed that these factors were able to antagonized sorafenib in a proliferation assay, in particular when used in combination.

conclusionsPlatelet factors can antagonize sorafenib or regorafenib-mediated growth inhibition and apoptosis in HCC cells. The modulation of platelet activity or numbers has the potential to enhance multikinase drug actions.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBlood PlateletsCarcinoma, HepatocellularCell MovementCell ProliferationEnzyme ActivationEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesHep G2 CellsHumansInsulin-Like Growth Factor ILiver NeoplasmsNeoplasm InvasivenessNiacinamideAntineoplastic AgentsApoptosis Regulatory ProteinsEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesIGF1 protein, humanInsulin-Like Growth Factor INiacinamidePhenylurea CompoundsProtein Kinase InhibitorsPyridinesregorafenibSorafenib

Identifiers

PMID24885890
PMCPMC4038078
OpenAlexW1990881151

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.