Figure 5
Figure 5. Activating JAK3 mutation identified in MF tumor and CTCL cell line. (A) JAK3 schematic with functional domains denoted. Activating JAK3 mutations previously reported and identified in this study marked with asterisks. (B) Chromatographs of Sanger sequencing of normal and tumor DNA from patient 1. The C1718T transition is detected in the tumor sample only. (C) Sequencing of CTCL cell lines showing the C1718T transition in Hut-78 cells. (D) western blots of JAK3 and proteins in its downstream pathway in CTCL cell lines; phosphorylated JAK3 (pJAK3) phosphorylated STAT5 (pSTAT5). (E) Viable cell numbers of CTCL cell lines at intervals following addition of 200 nM tofacitinib. (F-G) CTCL cell lines subjected to MTS assay (tofacitinib 1, 10, 100, 250, and 500 nM) (F) and western blot (tofacitinib 10, 100, 200 nM) (G) after 48 hours of treatment.

Activating JAK3 mutation identified in MF tumor and CTCL cell line. (A) JAK3 schematic with functional domains denoted. Activating JAK3 mutations previously reported and identified in this study marked with asterisks. (B) Chromatographs of Sanger sequencing of normal and tumor DNA from patient 1. The C1718T transition is detected in the tumor sample only. (C) Sequencing of CTCL cell lines showing the C1718T transition in Hut-78 cells. (D) western blots of JAK3 and proteins in its downstream pathway in CTCL cell lines; phosphorylated JAK3 (pJAK3) phosphorylated STAT5 (pSTAT5). (E) Viable cell numbers of CTCL cell lines at intervals following addition of 200 nM tofacitinib. (F-G) CTCL cell lines subjected to MTS assay (tofacitinib 1, 10, 100, 250, and 500 nM) (F) and western blot (tofacitinib 10, 100, 200 nM) (G) after 48 hours of treatment.

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