ArticleLeukemia2025
Genetic lesions in nodular lymphocyte-predominant Hodgkin lymphoma and T cell/histiocyte-rich large B-cell lymphoma identified by whole genome sequencing.
Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) is a rare malignant lymphoma characterised by a few large tumour cells expressing B-cell antigens in an inflammatory background. T-cell/histiocyte-rich large B-cell lymphoma (THRLBCL) is now considered to be closely related to NLPHL. Little is known about the mutational spectrum of the lymphoma cells in primary NLPHL and THRLBCL due to the rarity of the diseases and the technical challenges of analysing these tumours. Therefore, the aim of the present study was to elucidate mechanisms contributing to the pathogenesis of NLPHL and THRLBCL by whole genome sequencing of laser microdissected tumour cells from seven cases. We observed a heterogeneity of transforming events, with cases showing abundant somatic mutations, others with a predominance of structural variations, and cases with few aberrations. The genes that were most frequently affected by aberrations encode factors influencing JAK-STAT, NF-κB, and/or WNT signaling, and apoptosis regulators. However, the mutated genes, such as SOCS3, JUNB, IRF1 and ITPKB, were not the typical targets known from classical Hodgkin lymphoma (cHL). Two cases showed recurrent rearrangements of BCL6 and CD74. In conclusion, our data enrich our understanding of NLPHL and THRLBCL and highlight common and distinct features with respect to cHL.
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.