Evidence map›Paper›PMID 30132150›Full record

Trial reportAngiogenesis2019

Activin receptor-like kinase 1 is associated with immune cell infiltration and regulates CLEC14A transcription in cancer.

Matteo Bocci, Jonas Sjölund, Ewa Kurzejamska, David Lindgren, Nour-Al-Dain Marzouka, Michael Bartoschek, Mattias Höglund, Kristian Pietras

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Angiogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Matteo BocciDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Building 404:A3, 223 81, Lund, Sweden.ORCID 0000-0002-8774-0006
Jonas SjölundDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Building 404:A3, 223 81, Lund, Sweden.ORCID 0000-0002-6992-3415
Ewa KurzejamskaDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Building 404:A3, 223 81, Lund, Sweden.ORCID 0000-0002-8050-6516
David LindgrenDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Building 404:A3, 223 81, Lund, Sweden.
Nour-Al-Dain MarzoukaUnit of Urothelial Cancer Genomics, Department of Oncology and Pathology, Lund University, Scheelevägen 8, 22363, Lund, Sweden.ORCID 0000-0002-9029-3702
Michael BartoschekDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Building 404:A3, 223 81, Lund, Sweden.ORCID 0000-0002-1567-795X
Mattias HöglundUnit of Urothelial Cancer Genomics, Department of Oncology and Pathology, Lund University, Scheelevägen 8, 22363, Lund, Sweden.ORCID 0000-0001-9283-4421
Kristian PietrasDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Building 404:A3, 223 81, Lund, Sweden. kristian.pietras@med.lu.se.ORCID 0000-0001-6738-4705
Lund University · SE

Funding

European Research Council 309322 TUMORGAN
6 · The paper itself

Abstract

Cancer cells sustain their metabolic needs through nutrients and oxygen supplied by the bloodstream. The requirement for tumor angiogenesis has been therapeutically exploited in the clinical setting mainly by means of inhibition of the vascular endothelial growth factor family of ligands and receptors. Despite promising results in preclinical models, the benefits for patients proved to be limited. Inadequate efficacy similarly halted the development of agents impinging on the activity of the activin receptor-like kinase (ALK)1, a member of the transforming growth factor-β superfamily. Notwithstanding its characterization as an endothelial cell marker, the full spectrum of biological processes associated with ALK1 is essentially unexplored. Here, we present data revealing the genetic network associated with ACVRL1 (the gene encoding for ALK1) expression in human cancer tissues. Computational analysis unveiled a hitherto unknown role for ACVRL1 in relation to genes modulating the functionality of the immune cell compartment. Moreover, we generated a signature of 8 genes co-expressed with ACVRL1 across different tumor types and characterized the c-type lectin domain containing protein (CLEC)14A as a potential downstream target of ACVRL1. Considering the lack of reagents for ALK1 detection that has hampered the field to date, our work provides the opportunity to validate the 8-gene signature and CLEC14A as biomarkers for ALK1 activity. Ultimately, this may help revisit the clinical development of already existing ALK1-blocking compounds as precision medicines for cancer.

Indexed as

Activin Receptors, Type IIAnimalsBiomarkers, TumorCell Adhesion MoleculesFemaleGene Expression Regulation, NeoplasticHumansLectins, C-TypeMaleMiceNeoplasmsTranscription, GeneticActivin Receptors, Type IIACVRL1 protein, humanBiomarkers, TumorCell Adhesion MoleculesCLEC14A protein, humanLectins, C-TypeALK1AngiogenesisCell signalingEndothelial cellPathophysiologyTumor biology

Identifiers

PMID30132150
PMCPMC6510886
OpenAlexW2888704375

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.