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 Blood, 1 May 2005, Vol. 105, No. 9, pp. 3743-3745.
Prepublished online as a Blood First Edition Paper on January 4, 2005; DOI 10.1182/blood-2004-07-2949.

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NEOPLASIA
Brief report

Farnesyltransferase inhibitor tipifarnib (R115777) preferentially inhibits in vitro autonomous erythropoiesis of polycythemia vera patient cells

Jérôme Larghero, Nathalie Gervais, Bruno Cassinat, Jean-Didier Rain, Marie-Hélène Schlageter, Rose Ann Padua, Christine Chomienne, and Philippe Rousselot

From the Laboratoire de Biologie Cellulaire Hématopoïétique, Institut d'Hématologie and Service de Médecine Nucléaire, Hôpital Saint-Louis, Paris, France; Service Clinique des Maladies du Sang, Hôpital Saint-Louis, Paris, France; and Unité de Thérapie Cellulaire, Hôpital Saint-Louis, Paris, France.

Polycythemia vera (PV) is an acquired myeloproliferative disorder with primary expansion of the red cell mass leading to an increased risk of thrombosis and less frequently to myelofibrosis and secondary acute leukemia. Standard therapies include cytoreduction with either phlebotomy or chemotherapeutic agents and antithrombotic drugs. Because long-term exposure to cytotoxic chemotherapy may increase the risk of acute transformation, new therapeutic options are needed. Tipifarnib is a nonpeptidomimetic inhibitor of farnesyl transferase that was developed as a potential inhibitor of RAS signaling. In the present study we report that tipifarnib used at pharmacologically achievable concentrations strongly inhibits the erythroid burst-forming unit (BFU-E) autonomous growth that characterizes patients with PV. Moreover, at low tipifarnib concentrations (0.15 µM), the inhibitory effect was preferentially observed in PV BFU-E progenitors and not in normal BFU-E progenitors and was not rescued by erythropoietin (EPO). Thus tipifarnib may specifically target PV stem cells and may be of clinical interest in the treatment of patients with PV.


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