Impact of Targeted Therapy on Outcome of Chronic Lymphocytic Leukemia Patients with Relapsed Del(17p13.1) Karyotype at a Single Center

Letter to the Editor Chronic lymphocytic leukemia (CLL) patients with del(17p13.1) exhibit short survival once disease progression necessitates therapy and respond poorly to traditional treatments compared with other cytogenetic subgroups (1). Poor outcome associated with del(17p13.1) is at least partially linked to malfunction of the tumor suppressor gene TP53 [located on 17p (2)], which inhibits apoptosis induced by chemotherapy (3-5). Therefore, despite general advances in CLL therapy with chemoimmunotherapy, progress in this subgroup has been limited. Current guidelines suggest allogeneic stem cell transplant as part of initial therapy (6), as salvage treatment for del(17p13.1) portends an even graver prognosis. Recently, novel therapeutic agents have demonstrated promising clinical activity in del(17p13.1) patients, specifically, cyclin-dependent kinase inbibitors (CDKis; flavopiridol and dinaciclib) and a Bruton's tyrosine kinase inhibitor (BTKi; ibrutinib)(7-9). To elucidate potential impact of CDKi and BTKi in this population, we examined outcomes of consecutive relapsed/refractory del(17p13.1) patients seen at Ohio State University (OSU), who received salvage therapy with one of these agents or alternative therapy. Our dat