ArticleJournal of cancer research and clinical oncology2022
Hairy cell leukemia: a specific 17-gene expression signature points to new targets for therapy.
Article in Journal of cancer research and clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- DUSP1 is a key driver of disease persistence and potential therapeutic target in hairy cell leukemia.Blood advances · 2026Article
- Closing the gap between biology and classification in splenic B-cell lymphomas.Histopathology · 2025Review
- Developing a Predictive Model for Metastatic Potential in Pancreatic Neuroendocrine Tumor.The Journal of clinical endocrinology and metabolism · 2024Article
- Non-canonicalOncology research · 2024Review
- BRAF(V600E) mutation together with loss of Trp53 or pTEN drives the origination of hairy cell leukemia from B-lymphocytes.Molecular cancer · 2023Article
- Hairy Cell Leukemia: Where Are We in 2023?Current oncology reports · 2023Review
- Broadening the horizon: potential applications of CAR-T cells beyond current indications.Frontiers in immunology · 2023Review
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Authors and funding
10 authors.
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Abstract
backgroundHairy cell leukemia (HCL) is a rare chronic B cell malignancy, characterized by infiltration of bone marrow, blood and spleen by typical "hairy cells" that bear the BRAFV600E mutation. However, in addition to the intrinsic activation of the MAP kinase pathway as a consequence of the BRAFV600E mutation, the potential participation of other signaling pathways to the pathophysiology of the disease remains unclear as the precise origin of the malignant hairy B cells. MATERIALS AND
methodsUsing mRNA gene expression profiling based on the Nanostring technology and the analysis of 290 genes with crucial roles in B cell lymphomas, we defined a 17 gene expression signature specific for HCL.
resultsSeparate analysis of samples from classical and variant forms of hairy cell leukemia showed almost similar mRNA expression profiles apart from overexpression in vHCL of the immune checkpoints CD274 and PDCD1LG2 and underexpression of FAS. Our results point to a post-germinal memory B cell origin and in some samples to the activation of the non-canonical NF-κB pathway.
conclusionsThis study provides a better understanding of the pathogenesis of HCL and describes new and potential targets for treatment approaches and guidance for studies in the molecular mechanisms of HCL.
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