ArticleDiagnostic molecular pathology : the American journal of surgical pathology, part B2009
No evidence for the JAK2 (V617F) or JAK2 exon 12 mutations in primary mediastinal large B-cell lymphoma.
Article in Diagnostic molecular pathology : the American journal of surgical pathology, part B, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Genetic alterations of 9p24 in lymphomas and their impact for cancer (immuno-)therapy.Virchows Archiv : an international journal of pathology · 2019Article
- Selective JAK2 inhibition specifically decreases Hodgkin lymphoma and mediastinal large B-cell lymphoma growth in vitro and in vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Beyond chemotherapy: new agents for targeted treatment of lymphoma.Nature reviews. Clinical oncology · 2011Review
- Cooperative epigenetic modulation by cancer amplicon genes.Cancer cell · 2010Article
- New developments in the pathology of malignant lymphoma: a review of the literature published from August to November 2009.Journal of hematopathology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Dysregulated JAK2 signaling has been shown to play a significant role in the pathogenesis of myeloproliferative disorders. Recently, our work comparing gene expression signatures of primary mediastinal large B-cell lymphomas (PMLBCL) versus nodal diffuse large B-cell lymphomas revealed a relative increase in JAK2 transcripts in the former, suggesting a role for increased JAK2 signaling in a subset of these tumors. Given the likelihood of increased JAK2 signaling in PMLBCL, we sought to determine whether JAK2 activating mutations were an alternative mechanism for increased JAK2 signaling in untreated PMLBCLs. We performed amplification refractory mutation analysis for the JAK2 (V617F) mutation and bidirectional sequencing for the recently described JAK2 exon 12 mutations on genomic DNA isolated from a well-characterized cohort of PMLBCLs. No evidence of the mutant JAK2 (V617F) allele or JAK2 exon 12 mutations was detected in 31 PMLBCL cases tested. Analysis using cell lines derived from PMLBCLs (n = 1) and from the molecularly similar classic Hodgkin lymphoma (n = 4) also failed to reveal involvement of a mutant JAK2 allele. Taken together, these results suggest that JAK2 signaling in PMLBCLs occurs by mechanisms distinct from JAK2 (V617F) or JAK2 exon 12 activating mutations.
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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.