ArticleBlood advances2024
Genomic profiling of mycosis fungoides identifies patients at high risk of disease progression.
Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Review
- Mycosis Fungoides Is a Proliferation of Multiple Mutational Subclones.The Journal of dermatology · 2026Review
- When Cellulitis Is Not Cellulitis: A Case of Suspected Mycosis Fungoides With Nondiagnostic Biopsies.Cureus · 2026Article
- Persistent racial and socioeconomic inequities in mycosis fungoides survival: a population-based study.Frontiers in public health · 2026Article
- Established and emerging prognostic factors in mycosis fungoides and Sézary syndrome.Frontiers in oncology · 2026Review
- Epigenetic dysregulation in mycosis fungoides and sézary syndrome.Frontiers in cell and developmental biology · 2026Review
- Early nail involvement in mycosis fungoides with rapid systemic progression: rethinking the role of Ki-67: a case report.Journal of medical case reports · 2025Article
- Integrative Mutational Landscape of Mycosis Fungoides Using a National Genomics Repository.Cancers · 2025Article
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Authors and funding
35 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractMycosis fungoides (MF) is the most prevalent primary cutaneous T-cell lymphoma, with an indolent or aggressive course and poor survival. The pathogenesis of MF remains unclear, and prognostic factors in the early stages are not well established. Here, we characterized the most recurrent genomic alterations using whole-exome sequencing of 67 samples from 48 patients from Lille University Hospital (France), including 18 sequential samples drawn across stages of the malignancy. Genomic data were analyzed on the Broad Institute's Terra bioinformatics platform. We found that gain7q, gain10p15.1 (IL2RA and IL15RA), del10p11.22 (ZEB1), or mutations in JUNB and TET2 are associated with high-risk disease stages. Furthermore, gain7q, gain10p15.1 (IL2RA and IL15RA), del10p11.22 (ZEB1), and del6q16.3 (TNFAIP3) are coupled with shorter survival. Del6q16.3 (TNFAIP3) was a risk factor for progression in patients at low risk. By analyzing the clonal heterogeneity and the clonal evolution of the cohort, we defined different phylogenetic pathways of the disease with acquisition of JUNB, gain10p15.1 (IL2RA and IL15RA), or del12p13.1 (CDKN1B) at progression. These results establish the genomics and clonality of MF and identify potential patients at risk of progression, independent of their clinical stage.
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