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EHA 2026 | The rationale for exploring XPO1 inhibition in myelofibrosis
In this video, Alessandro Lucchesi, MD, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy, shares insights into the biological rationale for exploring XPO1 inhibition with agents such as selinexor in myelofibrosis, highlighting that this drug acts on four different pathways. This interview took place at the 31st Congress of the European Hematology Association (EHA) in Stockholm, Sweden.
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Transcript
Well, selinexor is a very interesting drug because it can fix the increased exportation of nuclear factors such as oncosuppressors and mRNA and it inhibits the growth of malignant cells by acting on four different axes. One of the axes is the cell cycle. The other one is the apoptosis. So it retains P53 within the nucleus and activates P53-mediated apoptosis. Then inflammation is dampened. It’s demonstrated by the reduction of very important pathophysiological cytokines in MF and it also helps the backbone of MF to increase the inhibition of the JAK-STAT axis...
Well, selinexor is a very interesting drug because it can fix the increased exportation of nuclear factors such as oncosuppressors and mRNA and it inhibits the growth of malignant cells by acting on four different axes. One of the axes is the cell cycle. The other one is the apoptosis. So it retains P53 within the nucleus and activates P53-mediated apoptosis. Then inflammation is dampened. It’s demonstrated by the reduction of very important pathophysiological cytokines in MF and it also helps the backbone of MF to increase the inhibition of the JAK-STAT axis. So it’s four axis rather than one. This is the biological rationale for using that in myelofibrosis. Well, Selinexor is a very interesting drug because it can fix the increased exportation of nuclear factors such as oncosuppressors and mRNA and it inhibits the growth of malignant cells by acting on four different axes. One of the axes is the cell cycle. The other one is the apoptosis. So it retains P53 within the nucleus and activates P53-mediated apoptosis. Then inflammation is dampened. It’s demonstrated by the reduction of very important pathophysiological cytokines in MF and it also helps the backbone of MF to increase the inhibition of the JAK-STAT axis. So it’s four axis rather than one. This is the biological rationale for using that in myelofibrosis.
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