ArticleGenes and immunity2014
Absence of somatic MYD88 L265P mutations in patients with primary Sjogren's syndrome.
Article in Genes and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Pathogenetic Mechanisms Implicated in Sjögren's Syndrome Lymphomagenesis: A Review of the Literature.Journal of clinical medicine · 2020Review
- Contribution of Genetic Factors to Sjögren's Syndrome and Sjögren's Syndrome Related Lymphomagenesis.Journal of immunology research · 2015Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjogren's syndrome (SS) is a chronic autoimmune disorder with the highest risk for lymphoma development among all autoimmune diseases. In order to evaluate whether the presence of the recently described MYD88 L265P mutation in patients with Waldenström's macroglobulinemia (WM) is contributory to SS-associated lymphomagenesis, a quantitative allele-specific PCR method was performed in peripheral blood derived from 90 SS patients as well as in minor salivary gland tissues derived from 12 primary SS patients with or without lymphoma. MYD88 L265P was not detected in either of the samples tested. Although the absence of the MyD88 L265P somatic mutation in our SS cohort does not exclude a common germline susceptibility gene in SS, it might suggest a distinct operating pathogenetic mechanism in SS-related lymphoma compared with WM and other hematological malignancies.
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