Evidence map›Paper›PMID 25869286›Full record

ReviewBlood2015

α-Globin as a molecular target in the treatment of β-thalassemia.

Sachith Mettananda, Richard J Gibbons, Douglas R Higgs

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Thalassaemia.Nature reviews. Disease primers · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Cardiac Dysfunction in β-Thalassemia: A Narrative Review.Research in heart yield and translational medicine · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Sachith MettanandaMedical Research Council Molecular Hematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom; Department of Pediatrics, Faculty of Medicine, University of Kelaniya, Sri Lanka; and.ORCID http://orcid.org/0000-0002-0760-0418
Richard J GibbonsMedical Research Council Molecular Hematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
Douglas R HiggsMedical Research Council Molecular Hematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom; Oxford National Institute for Health Research Biomedical Research Centre, Blood Theme, Oxford University Hospital, Oxford, United Kingdom.
National Institute for Health Research · GBUniversity of Kelaniya · LKUniversity of Oxford · GB

Funding

Medical Research Council G1000801Medical Research Council MC_U137961144Medical Research Council MC_U137961145Medical Research Council MC_UU_12009/3
6 · The paper itself

Abstract

The thalassemias, together with sickle cell anemia and its variants, are the world's most common form of inherited anemia, and in economically undeveloped countries, they still account for tens of thousands of premature deaths every year. In developed countries, treatment of thalassemia is also still far from ideal, requiring lifelong transfusion or allogeneic bone marrow transplantation. Clinical and molecular genetic studies over the course of the last 50 years have demonstrated how coinheritance of modifier genes, which alter the balance of α-like and β-like globin gene expression, may transform severe, transfusion-dependent thalassemia into relatively mild forms of anemia. Most attention has been paid to pathways that increase γ-globin expression, and hence the production of fetal hemoglobin. Here we review the evidence that reduction of α-globin expression may provide an equally plausible approach to ameliorating clinically severe forms of β-thalassemia, and in particular, the very common subgroup of patients with hemoglobin E β-thalassemia that makes up approximately half of all patients born each year with severe β-thalassemia.

Indexed as

alpha-GlobinsAnimalsbeta-ThalassemiaDown-RegulationGenetic TherapyHumansMolecular Targeted TherapyRNA InterferenceRNA, Small Interferingalpha-GlobinsRNA, Small Interfering

Identifiers

PMID25869286
PMCPMC4497969
OpenAlexW1785988192

What OpenQuestion holds

Textmetadata
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.