Evidence map›Paper›PMID 30472780›Full record

ArticleJournal of thrombosis and haemostasis : JTH2019

mTOR kinase inhibition reduces tissue factor expression and growth of pancreatic neuroendocrine tumors.

C S Lewis, H Elnakat Thomas, M A Orr-Asman, L C Green, R E Boody, K Matiash, A Karve, Y M Hisada, H W Davis, X Qi and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Tissue Factor and Cancer: Regulation, Tumor Growth, and Metastasis.Seminars in thrombosis and hemostasis · 2019
    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

16 authors at 4 institutions in 1 country.

C S LewisDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
H Elnakat ThomasDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
M A Orr-AsmanDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
L C GreenDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
R E BoodyDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
K MatiashDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
A KarveDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Y M HisadaDivision of Hematology/Oncology, Department of Medicine, University of North Carolina at Chapel Hill, Cincinnati, OH, USA.
H W DavisDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
X QiDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
C A MercerDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
F V LucasDepartment of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
B J AronowComputational Medicine and Division of Biomedical Informatics, Cincinnati Children's Hospital and Medical Center, Cincinnati, OH, USA.
N MackmanDivision of Hematology/Oncology, Department of Medicine, University of North Carolina at Chapel Hill, Cincinnati, OH, USA.
H H VersteegEinthoven Laboratory for Experimental Vascular Medicine, Department of Internal Medicine, Leiden University Medical Center, Cincinnati, OH, USA.
V Y BogdanovDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0003-4968-1129
University of Cincinnati Medical Center · USUniversity of North Carolina at Chapel Hill · USCincinnati Children's Hospital Medical Center · USUniversity Medical Center · US

Funding

Research Training in Hematology at UNC Chapel HillT32HL007149 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Nigel S. Key · 1985 to 2026
$8.6M
Alternatively Spliced Tissue Factor and Pathobiology of Pancreatic CancerR01CA190717 · NCI · UNIVERSITY OF CINCINNATI · PI BOGDANOV, VLADIMIR · 2015 to 2019
$1.4M
NCI NIH HHS R01 CA190717NHLBI NIH HHS T32 HL007149
6 · The paper itself

Abstract

Essentials Tissue factor (TF) isoforms are expressed in pancreatic neuroendocrine tumors (pNET). TF knockdown inhibits proliferation of human pNET cells in vitro. mTOR kinase inhibitor sapanisertib/MLN0128 suppresses TF expression in human pNET cells. Sapanisertib suppresses TF expression and activity and reduces the growth of pNET tumors in vivo. SUMMARY: Background Full-length tissue factor (flTF) and alternatively spliced TF (asTF) contribute to growth and spread of pancreatic ductal adenocarcinoma. It is unknown, however, if flTF and/or asTF contribute to the pathobiology of pancreatic neuroendocrine tumors (pNETs). Objective To assess TF expression in pNETs and the effects of mTOR complex 1/2 (mTORC1/2) inhibition on pNET growth. Methods Human pNET specimens were immunostained for TF. Human pNET cell lines QGP1 and BON were evaluated for TF expression and responsiveness to mTOR inhibition. shRNA were used to knock down TF in BON. TF cofactor activity was assessed using a two-step FXa generation assay. TF promoter activity was assessed using transient transfection of human TF promoter-driven reporter constructs into cells. Mice bearing orthotopic BON tumors were treated with the mTORC1/2 ATP site competitive inhibitor sapanisertib/MLN0128 (3 mg kg

Indexed as

AdenineAnimalsAntineoplastic AgentsBenzoxazolesCell Line, TumorCell ProliferationHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Mice, NudeNeuroendocrine TumorsPancreatic NeoplasmsPromoter Regions, GeneticProtein Kinase InhibitorsPyrazolesPyrimidinesAdenineAntineoplastic AgentsBenzoxazolesMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MTOR protein, humanProtein Kinase InhibitorsPyrazolesPyrimidinessapanisertibThromboplastinTOR Serine-Threonine Kinasescarcinoma, neuroendocrineMLN0128mTOR protein, humanpancreatic neoplasmstissue factor

Identifiers

PMID30472780
PMCPMC6345540
OpenAlexW2901568177

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.