Evidence map›Paper›PMID 25136070›Full record

ReviewCancer research2014

ACVR1 mutations in DIPG: lessons learned from FOP.

Kathryn R Taylor, Maria Vinci, Alex N Bullock, Chris Jones

Open access · greenAbstract readReview
In one paragraph

Review in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Discovery of highly potent and ALK2/ALK1 selective kinase inhibitors using DNA-encoded chemistry technology.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. BMP signaling in cancer stemness and differentiation.Cell regeneration (London, England) · 2023
    Review
  8. Article
  9. Article
  10. Upfront Biology-Guided Therapy in Diffuse Intrinsic Pontine Glioma: Therapeutic, Molecular, and Biomarker Outcomes from PNOC003.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Pathogenic ACVR1The EMBO journal · 2021
    Article
  20. 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

4 authors at 2 institutions in 1 country.

Kathryn R TaylorDivision of Molecular Pathology, The Institute of Cancer Research, London, United Kingdom. Division of Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom.
Maria VinciDivision of Molecular Pathology, The Institute of Cancer Research, London, United Kingdom. Division of Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom.
Alex N BullockStructural Genomics Consortium, University of Oxford, Oxford, United Kingdom.
Chris JonesDivision of Molecular Pathology, The Institute of Cancer Research, London, United Kingdom. Division of Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom. chris.jones@icr.ac.uk.
Institute of Cancer Research · GBGenomics (United Kingdom) · GB

Funding

Cancer Research UK A14078Wellcome Trust 092809Wellcome Trust 092809/Z/10/Z
6 · The paper itself

Abstract

Whole-genome sequencing studies have recently identified a quarter of cases of the rare childhood brainstem tumor diffuse intrinsic pontine glioma to harbor somatic mutations in ACVR1. This gene encodes the type I bone morphogenic protein receptor ALK2, with the residues affected identical to those that, when mutated in the germline, give rise to the congenital malformation syndrome fibrodysplasia ossificans progressiva (FOP), resulting in the transformation of soft tissue into bone. This unexpected link points toward the importance of developmental biology processes in tumorigenesis and provides an extensive experience in mechanistic understanding and drug development hard-won by FOP researchers to pediatric neurooncology. Here, we review the literature in both fields and identify potential areas for collaboration and rapid advancement for patients of both diseases.

Indexed as

Activin Receptors, Type IAnimalsBrain Stem NeoplasmsCell Transformation, NeoplasticGliomaHumansMutationMyositis OssificansActivin Receptors, Type I

Identifiers

PMID25136070
PMCPMC4154859
OpenAlexW2098463208

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.