Evidence map›Paper›PMID 26702059›Full record

ArticleBlood2016

Diverse roles of cell-specific hypoxia-inducible factor 1 in cancer-associated hypercoagulation.

Colin E Evans, Pär-Ola Bendahl, Mattias Belting, Cristina Branco, Randall S Johnson

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  9. MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer.Frontiers in cell and developmental biology · 2021
    Article
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  20. Clinical Characteristics and Risk Factors of Patients with Lung Cancer Complicated with Pulmonary Embolism: A Case Control Study.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    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

5 authors at 3 institutions in 2 countries.

Colin E EvansDepartment of Physiology, Development and Neuroscience and British Heart Foundation Centre of Research Excellence, University of Cambridge, Cambridge, United Kingdom;
Pär-Ola BendahlDepartment of Clinical Sciences, Lund University, Lund, Sweden; and.
Mattias BeltingDepartment of Clinical Sciences, Lund University, Lund, Sweden; and.
Cristina BrancoDepartment of Physiology, Development and Neuroscience and.
Randall S JohnsonDepartment of Physiology, Development and Neuroscience and Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Lund University · SEBritish Heart Foundation · GBKarolinska Institutet · SE

Funding

TRANSCRIPTIONAL RESPONSE TO HYPOXIA IN TRANSFORMED CELLSR01CA082515 · NCI · UNIVERSITY OF CAMBRIDGE · PI JOHNSON, RANDALL SCOTT · 1999 to 2012
$3.8M
Breast Cancer Now 2014MAYSF275British Heart FoundationNCI NIH HHS R01 CA082515Wellcome Trust 092738Wellcome Trust 092738MA
6 · The paper itself

Abstract

Despite the increased risk of thrombosis in cancer patients compared with healthy individuals, mechanisms that regulate cancer-induced hypercoagulation are incompletely understood. The aim of this study was to investigate whether cell-specific hypoxia-inducible factor (HIF) 1α regulates cancer-associated hypercoagulation, using in vitro clotting assays and in vivo cancer models. In mouse lung and mammary tumor cells, hypoxia led to increases in cell adhesion, clotting, and fibrin deposition; these increases were eliminated in HIF1α null cells. Increased levels of HIF1α were also associated with increased tissue factor expression in human breast tumor samples. Conversely, deletion of endothelial (but not myeloid) cell-specific HIF1α doubled pulmonary fibrin deposition, and trebled thrombus formation compared with wildtype littermates in tumor-bearing mice. Our data suggest that tumor and endothelial cell-specific HIF1α may have opposing roles in cancer-associated coagulation and thrombosis. Off-target effects of manipulating the HIF1 axis in cancer patients should be carefully considered when managing thrombotic complications.

Indexed as

Blood CoagulationAnimalsBreast NeoplasmsCell AdhesionEndothelial CellsFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMammary Neoplasms, ExperimentalMiceMice, KnockoutThrombophiliaHIF1A protein, humanHif1a protein, mouseHypoxia-Inducible Factor 1, alpha Subunit

Identifiers

PMID26702059
PMCPMC6343824
OpenAlexW2228291152

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.