ArticleGenes, chromosomes & cancer2018
Genomic analysis reveals recurrent deletion of JAK-STAT signaling inhibitors HNRNPK and SOCS1 in mycosis fungoides.
Article in Genes, chromosomes & cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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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
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- Development of Cutaneous T-Cell Lymphoma Following Biologic Treatment: A Systematic Review.American journal of clinical dermatology · 2023Pooled it
- Pooled it
- LyP vs advanced-stage CTCLs: single-cell profiling reveals markers of self-limited vs aggressive disease behavior.Blood advances · 2026Article
- Review
- Cutaneous Lymphoma Associated with JAK Inhibitors: A Pharmacovigilance Analysis of the FAERS Database and Literature Review.Acta dermato-venereologica · 2026Review
- Established and emerging prognostic factors in mycosis fungoides and Sézary syndrome.Frontiers in oncology · 2026Review
- Cellular and molecular aberrations generating new immunotherapeutic approaches in mycosis fungoides and Sézary syndrome: a comprehensive review of literature.Frontiers in immunology · 2026Review
- Common origins of autoimmune diseases and lymphoid malignancies.Trends in immunology · 2025Review
- Integrative Mutational Landscape of Mycosis Fungoides Using a National Genomics Repository.Cancers · 2025Article
- A novel knockout mouse model to assess the impact of one-copy loss of Hnrnpk in CD4 + T cells in chronically inflamed skin as a prelude to CTCL.Scientific reports · 2025Article
- Butyrate-producingGut · 2025Article
- Review
- Janus kinase inhibitors - a role for the treatment of cutaneous T-cell lymphomas?Oncology reviews · 2025Review
- Genomic profiling of mycosis fungoides identifies patients at high risk of disease progression.Blood advances · 2024Article
- Article
- Unravelling the druggability and immunological roles of the SOCS-family proteins.Frontiers in immunology · 2024Review
- Atypical presentation of γ/δ mycosis fungoides with an unusual phenotype andOpen life sciences · 2024Article
- "Next top" mouse models advancing CTCL research.Frontiers in cell and developmental biology · 2024Review
- Socs1-knockout in skin-resident CD4Biochemistry and biophysics reports · 2023Article
- Deciphering the spectrum of cutaneous lymphomas expressing TFH markers.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycosis fungoides (MF) is the most common cutaneous T-cell lymphoma (CTCL). Causative genetic alterations in MF are unknown. The low recurrence of pathogenic small-scale mutations (ie, nucleotide substitutions, indels) in the disease, calls for the study of additional aspects of MF genetics. Here, we investigated structural genomic alterations in tumor-stage MF by integrating whole-genome sequencing and RNA-sequencing. Multiple genes with roles in cell physiology (n = 113) and metabolism (n = 92) were found to be impacted by genomic rearrangements, including 47 genes currently implicated in cancer. Fusion transcripts involving genes of interest such as DOT1L, KDM6A, LIFR, TP53, and TP63 were also observed. Additionally, we identified recurrent deletions of genes involved in cell cycle control, chromatin regulation, the JAK-STAT pathway, and the PI-3-K pathway. Remarkably, many of these deletions result from genomic rearrangements. Deletion of tumor suppressors HNRNPK and SOCS1 were the most frequent genetic alterations in MF after deletion of CDKN2A. Notably, SOCS1 deletion could be detected in early-stage MF. In agreement with the observed genomic alterations, transcriptome analysis revealed up-regulation of the cell cycle, JAK-STAT, PI-3-K and developmental pathways. Our results position inactivation of HNRNPK and SOCS1 as potential driver events in MF development.
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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.