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Background: Recent studies demonstrated that classical Hodgkin lymphoma (cHL) is characterized by chromosome 9p24.1 amplification with associated overexpression of PD-1 ligands and JAK2 tyrosine kinase activation. JAK2 signaling augments tumor cell proliferation. Given this biology, we tested the combined inhibition of PDL1 pathway and JAK2 signaling in cHL patients who had progressed after prior PD-1 blocking therapy.
Introduction: Approximately 20% of patients (pts) with classic Hodgkin lymphoma (cHL) relapse after frontline therapy. Salvage chemotherapy and autologous stem cell transplant (ASCT) have cure rates of 60%–70%. Prior to brentuximab vedotin (BV) and checkpoint inhibitors (CPI), the median overall survival (OS) of pts with cHL relapse after ASCT was 2–3 years.
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