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Table 2 The most promising novel therapeutic options in ENKTL are summarized. The biological basis for targeting these pathways along with available clinical data are shown

From: Molecular pathogenic pathways in extranodal NK/T cell lymphoma

Signaling pathway or therapeutic target Biological basis for selection as a therapeutic target Clinical data References
JAK3 JAK3 mutations are frequent in ENKTL. JAK3 inhibition is shown to have potent anti-tumor activity in pre-clinical models Clinical trials evaluating JAK inhibitors in ENKTL are in progress. (NCT02974647) Sim et al. [19]
Narisimagi et al. [24]
STAT-3 STAT3-mutant ENKTLs are sensitive to STAT3 inhibition in vitro. Not available. Sim et al. [19]
NF-κB NF-κB upregulation is an important event in ENKTL pathogenesis. Bortezomib is being evaluated in early phase clinical trials for ENKTL Chen et al. [35]
Tang et al. [36]
CD38 CD38 is upregulated in ENKTL. Daratumumab has good in vitro efficacy. One case report documenting complete response in a relapsed refractory patient. Mustafa et al. [153]
Hari et al. [154]
PD-1 PD-L1 is upregulated in ENKTL. Early clinical trials show potent single-agent activity of anti-PD-1 therapy in relapsed, refractory ENKTL. Kwong et al. [11]