Evidence map›Paper›PMID 26586478›Full record

ArticleOncotarget2016

Angiogenic gene signature in human pancreatic cancer correlates with TGF-beta and inflammatory transcriptomes.

Kelly E Craven, Jesse Gore, Julie L Wilson, Murray Korc

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  3. TGFβ in Pancreas and Colorectal Cancer: Opportunities to Overcome Therapeutic Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
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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

4 authors at 2 institutions in 1 country.

Kelly E CravenDepartments of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Jesse GoreDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Julie L WilsonDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Murray KorcDepartments of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Indiana University – Purdue University Indianapolis · USIndiana University Health · US

Funding

Indiana Medical Scientist/Engineer Training ProgramT32GM077229 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI GASTON, BENJAMIN, HERBERT, BRITTNEY-SHEA · 2008 to 2022
$6.0M
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
Mechanistic and Informatics Based Analysis of STAT1 Actions in Pancreatic CancerF30CA200301 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI CRAVEN, KELLY EILEEN · 2015 to 2017
$121k
NCI NIH HHS CA-75059NCI NIH HHS F30 CA200301NCI NIH HHS F30CA200301NCI NIH HHS R01 CA075059NCI NIH HHS R37 CA075059NIGMS NIH HHS T32 GM077229
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinomas (PDACs) are hypovascular, but overexpress pro-angiogenic factors and exhibit regions of microvasculature. Using RNA-seq data from The Cancer Genome Atlas (TCGA), we previously reported that ~12% of PDACs have an angiogenesis gene signature with increased expression of multiple pro-angiogenic genes. By analyzing the recently expanded TCGA dataset, we now report that this signature is present in ~35% of PDACs but that it is mostly distinct from an angiogenesis signature present in pancreatic neuroendocrine tumors (PNETs). These PDACs exhibit a transcriptome that reflects active TGF-β signaling, and up-regulation of several pro-inflammatory genes, and many members of JAK signaling pathways. Moreover, expression of SMAD4 and HDAC9 correlates with endothelial cell abundance in PDAC tissues. Concomitantly targeting the TGF-β type I receptor (TβRI) kinase with SB505124 and JAK1-2 with ruxolitinib suppresses JAK1 phosphorylation and blocks proliferative cross-talk between human pancreatic cancer cells (PCCs) and human endothelial cells (ECs), and these anti-proliferative effects were mimicked by JAK1 silencing in ECs. By contrast, either inhibitor alone does not suppress their enhanced proliferation in 3D co-cultures. These findings suggest that targeting both TGF-β and JAK1 signaling could be explored therapeutically in the 35% of PDAC patients whose cancers exhibit an angiogenesis gene signature.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Pancreatic DuctalCell Line, TumorCells, CulturedCluster AnalysisCoculture TechniquesEndothelial CellsGene Expression ProfilingHistone DeacetylasesHumansImmunoblottingInflammation MediatorsJanus Kinase 1Neovascularization, PathologicPancreatic NeoplasmsProtein Serine-Threonine KinasesHDAC9 protein, humanHistone DeacetylasesInflammation MediatorsJAK1 protein, humanJanus Kinase 1Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IRepressor ProteinsSmad4 ProteinTransforming Growth Factor betaangiogenesisinflammationpancreatic cancerTCGATGF-β

Identifiers

PMID26586478
PMCPMC4808001
OpenAlexW2177948512

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.