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. 2025 Apr 15;135(8):e180417.
doi: 10.1172/JCI180417.

Addiction of primary cutaneous γδ T cell lymphomas to JAK/STAT signaling

Affiliations

Addiction of primary cutaneous γδ T cell lymphomas to JAK/STAT signaling

Yue Zhang et al. J Clin Invest. .
No abstract available

Keywords: Bioinformatics; Cancer; Dermatology; Oncology; Skin cancer.

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Figures

Figure 1
Figure 1. PCGDTL regression with JAK inhibitor monotherapy and mechanisms of acquired resistance.
(A) Clinical response of patient 1 to ruxolitinib. (B) WGS of PCGDTL in patient 1 revealed a deletion in p13.13, containing the SOCS1 locus. CN, copy number; LRR, log R ratio. (C) GSEA of Hallmark IL-2/STAT5 signaling of 2 tumor samples against 3 normal mature Vδ1 T cells revealed increased activity. (D) The post-relapse PCGDTL contained an acquired STAT5B p.N642H mutation. (E) STAT5B p.N642H increased the IC50 of ruxolitinib in SOCS1-deficient Ba/F3 cells. (F) Clinical response of patient 2 to cerdulatinib. (G) NGS of PCGDTL in patient 2 revealed a JAK3 p.A573V mutation and a post-relapse JAK3 p.M511I mutation. (H) GSEA of Hallmark IL-2/STAT5 signaling of 3 tumor samples against 3 normal mature Vδ1 T cells revealed increased activity. (I) Post-relapse leukemic PCGDTL contained an additional JAK1 p.L783F and subclonal JAK1 p.T901A mutations. (J) JAK3 p.M511I and JAK1 p.L783F increased the IC50 of cerdulatinib in Ba/F3 cells containing JAK3 p.A573V in the absence of IL-3. ****P < 0.0001, by multiple-comparison 2-way ANOVA (E and J). Created with BioRender.com.

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