ArticleNAR cancer2025
Co-expression of CD30 and SLFN11 serves as a dual biomarker for the treatment of cutaneous T-cell lymphoma.
Article in NAR cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Topoisomerase I inhibitor antibody-drug conjugates in breast cancer: the relevance of the DNA damage response to resistance, response, and combination treatment strategies.Breast cancer research and treatment · 2026Review
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Authors and funding
7 authors.
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Abstract
Advanced-stage cutaneous T-cell lymphoma (CTCL) is treated with diverse modalities, including DNA-damaging agents, anti-CD30 antibody-drug conjugates, and histone deacetylase (HDAC) inhibitors. Schlafen 11 (SLFN11) has emerged as a key determinant of sensitivity to DNA-damaging agents, yet its role in CTCL remains unclear. Here, we examined SLFN11 expression in two major CTCL subtypes-mycosis fungoides (MF) and Sézary syndrome (SS). Immunohistochemistry revealed SLFN11 positivity in 52% of MF (13/25) and 80% of SS (4/5) cases, with multivariate analysis showing a significant correlation between SLFN11 and CD30 expression. In normal human peripheral blood mononuclear cells, CD3/CD28/IL-2 stimulation induced co-expression of SLFN11 and CD30 in T cells, which was accompanied by heightened sensitivity to DNA-damaging agents. The JAK inhibitor cerdulatinib suppressed both markers. Among five CTCL cell lines, HUT78-expressing the highest SLFN11 levels-was the most sensitive to DNA-damaging agents, whereas SLFN11 knockout conferred resistance. Attempts to restore SLFN11 expression in SLFN11-low CTCL cells using six (pre)clinical HDAC inhibitors produced inconsistent results across cell lines and drugs. Together, these findings identify SLFN11 and CD30 as co-expressed therapeutic targets in CTCL and support the rationale for CD30-directed antibody-DNA-damaging agent conjugates as a precision treatment strategy.
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