ArticleLeukemia2016
Highly recurrent mutations of SGK1, DUSP2 and JUNB in nodular lymphocyte predominant Hodgkin lymphoma.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 98 citations in OpenAlex.
- The dual specificity phosphatase 2 act as distal regulatory node in T cell signaling.iScience · 2026Article
- Distinct cell state ecosystems for nodular lymphocyte-predominant Hodgkin lymphoma.Nature communications · 2025Article
- Article
- SGK1 repression by WT1 may confer a survival advantage to leukemic cells under stress conditions.Annals of hematology · 2025Article
- Nodular Lymphocyte-Predominant Hodgkin Lymphoma: Update on Biology and Treatment.Hematological oncology · 2025Review
- Aberrant Expression and Oncogenic Activity of SPP1 in Hodgkin Lymphoma.Biomedicines · 2025Article
- Circulating tumor DNA in lymphoma: technologies and applications.Journal of hematology & oncology · 2025Review
- B Cell Differentiation and the Origin and Pathogenesis of Human B Cell Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Histopathologic Features and Differential Diagnosis in Challenging Cases of Nodular Lymphocyte Predominant B-cell Lymphoma/Nodular Lymphocyte Predominant Hodgkin Lymphoma.Journal of clinical and translational pathology · 2024Article
- Spatial phenotyping of nodular lymphocyte predominant Hodgkin lymphoma and T-cell/histiocyte-rich large B-cell lymphoma.Blood cancer journal · 2024Article
- B-cell receptor reactivity againstHaematologica · 2023Article
- Expanding the bacterial origins of nodular lymphocyte-predominant Hodgkin lymphoma.Haematologica · 2023Article
- Review
- The spectrum of nodular lymphocyte predominant Hodgkin lymphoma: a report of the lymphoma workshop of the 20th meeting of the European Association for Haematopathology.Virchows Archiv : an international journal of pathology · 2023Review
- [Classification of Hodgkin lymphoma and related entities : News and open questions].Pathologie (Heidelberg, Germany) · 2023Review
- Review
- SWI/SNF complexes in hematological malignancies: biological implications and therapeutic opportunities.Molecular cancer · 2023Review
- The Immunology of DLBCL.Cancers · 2023Review
- Genetic Profiling in Diffuse Large B-Cell Lymphoma: The Promise and the Challenge.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2023Review
- Role of RNA Splicing Mutations in Diffuse Large B Cell Lymphoma.International journal of general medicine · 2023Review
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 at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL)-a subtype of Hodgkin lymphoma (HL)-is characterized by a low content of tumor cells, the lymphocyte predominant (LP) cells. Transformation into diffuse large B-cell lymphoma (DLBCL) occurs in about 10% of patients. We performed whole-genome mutation analysis of the DLBCL components from two composite lymphomas consisting of clonally related NLPHL and DLBCL as a means to identify candidate tumor suppressor genes and oncogenes in NLPHL. The analysis of LP cells for selected mutations of the DLBCL revealed that most mutations are also present in the LP cells, indicating a close relationship between the two components. The analysis of 62 selected genes in NLPHL by targeted ultra-deep sequencing revealed three novel highly recurrently mutated genes (each mutated in ~50% of cases), that is, DUSP2, SGK1 and JUNB. SGK1 was expressed in the LP cells of primary NLPHL cases and in the NLPHL cell line DEV. Administration of an SGK1 inhibitor induced apoptosis in the NLPHL cell line DEV and the DLBCL cell line Farage, suggesting a pathogenetic role of SGK1 in the LP and DLBCL cells. In summary, the present study identifies SGK1, DUSP2 and JUNB as novel key players in the pathogenesis of NLPHL.
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.