ReviewLeukemia2014
MYD88 and beyond: novel opportunities for diagnosis, prognosis and treatment in Waldenström's Macroglobulinemia.
Review in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 21 citations in OpenAlex.
- Transformation and survival in patients with Waldenström macroglobulinemia: a population-based study.Discover oncology · 2025Article
- Clinical, biological, electrophysiological and therapeutic profile of patients with anti-MAG neuropathy according to MYD88Journal of neurology · 2024Article
- Bleeding Propensity in Waldenström Macroglobulinemia: Potential Causes and Evaluation.Thrombosis and haemostasis · 2022Review
- Loss of TNFAIP3 enhances MYD88Blood cancer journal · 2018Article
- New developments in the management of Waldenström macroglobulinemia.Cancer management and research · 2017Review
- [The clinical features of patients with lymphoplasmacytic diseases harboring MyD88 L265P mutation].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Waldenström's Macroglobulinemia (WM) is a rare disease of the elderly with a median age of 63-68 years at diagnosis. Despite recent progress in biological insights and therapeutics, WM remains clinically challenging to diagnose and is difficult to manage with significant morbidity and lack of established curative therapies. Recently, the use of whole-genome sequencing has helped to identify a highly recurrent somatic mutation, myeloid differentiation factor 88 [MYD88] L265P in WM. This has fueled major interest in the field and as newer evidence accumulates, it is clear that that discovery of MYD88 L265P mutation may represent an important breakthrough in understanding the pathogenesis of WM and lymphoproliferative disorders. Recent scientific work in this field has also guided the identification of new targets such as CXCR4 and PI3K-delta that may have major implications in the future treatment of WM. This review discusses the role of MYD88 L265P mutations as well as targets beyond MYD88 in the setting of pathogenesis and development of future rational therapeutic trials focusing on patients diagnosed with WM.
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.