ReviewJournal of blood medicine2021
Profiling the Genetic and Molecular Characteristics of Glanzmann Thrombasthenia: Can It Guide Current and Future Therapies?
Review in Journal of blood medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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.
Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Platelet-derived integrin- and tetraspanin-enriched tethers exacerbate severe inflammation.Science (New York, N.Y.) · 2026Article
- The Molecular Pathology of Non-Malignant Haematological Disease.British journal of biomedical science · 2026Review
- Functional classification of platelet gene variants using CRISPR HDR in CD34American journal of human genetics · 2025Article
- Molecular diagnosis of inherited platelet disorders: a tale of two realities - advanced vs. resource-limited setting.Thrombosis journal · 2025Review
- Molecular Pathogenesis of Inherited Platelet Dysfunction.Biomolecules · 2025Review
- Role of channels in the ObioRxiv : the preprint server for biology · 2025Article
- Epidemiological and clinical characteristics of children and young adults with Glanzmann's thrombasthenia in upper Egypt: a multicenter cross-sectional study.Annals of hematology · 2025Observational
- A single F153Sβ3 mutation causes constitutive integrin αIIbβ3 activation in a variant form of Glanzmann thrombasthenia.Blood advances · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glanzmann thrombasthenia (GT) is the most widely studied inherited disease of platelet function. Platelets fail to aggregate due to a defect in platelet-to-platelet attachment. The hemostatic plug fails to form and a moderate to severe bleeding diathesis results. Classically of autosomal recessive inheritance, GT is caused by defects within the
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.