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Ruxolitinib in elderly patients with myelofibrosis: impact of age and genotype. A multicentre study on 291 elderly patients
Author(s) -
Palandri Francesca,
Catani Lucia,
Bonifacio Massimiliano,
Benevolo Giulia,
Heidel Florian,
Palumbo Giuseppe A.,
Crugnola Monica,
Abruzzese Elisabetta,
Bartoletti Daniela,
Polverelli Nicola,
Bergamaschi Micaela,
Tiribelli Mario,
Iurlo Alessandra,
Breccia Massimo,
Cavazzini Francesco,
Tieghi Alessia,
Binotto Gianni,
Isidori Alessandro,
Martino Bruno,
D'Adda Mariella,
Bosi Costanza,
Sabattini Elena,
Vitolo Umberto,
Aversa Franco,
Ibatici Adalberto,
Lemoli Roberto M.,
Sgherza Nicola,
Cuneo Antonio,
Martinelli Giovanni,
Semenzato Giampietro,
Cavo Michele,
Vianelli Nicola,
Sapienza Maria R.,
Latagliata Roberto
Publication year - 2018
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.15497
Subject(s) - ruxolitinib , medicine , myelofibrosis , discontinuation , hematology , genotype , survival analysis , anemia , oncology , bone marrow , gene , biology , biochemistry
Summary Ruxolitinib is a JAK 1/2 inhibitor that may control myelofibrosis ( MF )‐related splenomegaly and symptoms and can be prescribed regardless of age. While aging is known to correlate with worse prognosis, no specific analysis is available to confirm that ruxolitinib is suitable for use in older populations. A clinical database was created in 23 European Haematology Centres and retrospective data on 291 MF patients treated with ruxolitinib when aged ≥65 years were analysed in order to assess the impact of age and molecular genotype on responses, toxicities and survival. Additional mutations were evaluated by a next generation sequencing ( NGS ) approach in 69 patients with available peripheral blood samples at the start of ruxolitinib treatment. Compared to older (age 65–74 years) patients, elderly (≥75 years) showed comparable responses to ruxolitinib, but higher rates of drug‐induced anaemia and thrombocytopenia and worse survival. Nonetheless, the ruxolitinib discontinuation rate was comparable in the two age groups. Number and types of molecular abnormalities were comparable across age groups. However, the presence of high molecular risk ( HMR ) mutations significantly affected survival, counterbalancing the effect of aging. Indeed, elderly patients with <2 HMR mutated genes had a comparable survival to older patients with ≥2 HMR mutations. Given that responses were not influenced by age, older age per se should not be a limitation for ruxolitinib administration. NGS analysis of HMR mutations also confirmed a strong predictive value in elderly patients.