TREATMENT WITH RUXOLITINIB IN PATIENTS WITH PRIMARY OR SECONDARY MYELOFIBROSIS: SINGLE CENTER EXPERIENCE
(Abstract release date: 05/21/15)
EHA Library. Sotiropoulos D. 06/12/15; 102977; PB1932
Dr. Damianos Sotiropoulos
Contributions
Contributions
Abstract
Abstract: PB1932
Type: Publication Only
Background
Myelofibrosis is one of the classical Philadelphia negative myeloproliferative neoplasms (MPNs), either appearing de novo (primary MF[PMF]) or following a previous ET or PV (post-ET or post-PV MF). The disease is essentially the same. The therapeutic landscape of MF has changed with the introduction of JAK inhibitors.
Aims
To evaluate the efficacy and safety of ruxolitinib treatment in patients with MF.
Methods
Eighteen patients with MF (12 male and 6 female), median age 62.5 (33-75) years old were evaluated: 7 with PMF, 5 post PV, 3 post ET, 3 post MPN-U. Median follow up since ruxolitinib initiation was 4 (1-33) months, whereas total follow up since diagnosis was 5 (2-19) years. JAK2 mutational status was available in 14/18 patients, 12/14 being positive for the V617F mutation. Cytogenetic study was available in 12/18 patients, 8 of them having normal karyotype, 2 with deletion of long arm of chromosome 20 [del(20)(q13.1)], one with trisomy 8 and one with complex karyotype [48,XX,+8,+9,t(12:14)(q24.1:q24)]. According to dynamic international prognostic scoring system (DIPSS) upon ruxolitinib initiation, risk group was low in 2, intermediate-1 (int-1) in 4, intermediate-2 (int-2) in 7 and high in 5 patients.
Results
Spleen volume (SV) reduction was observed in 11/18 (61%) patients with a mean SV reduction of 33.7%. Constitutional symptoms subsided in all patients within 2 weeks of ruxolitinib initiation. Fifteen out eighteen patients had weight gain and quality of life improvement. Hematologic toxicity involving anemia and thrombocytopenia was observed in 6/18 (33%) and 2/18 (11%) patients respectively. Red cell transfusion was required in one patient. Dose adjustment with dosage de-escalation was required in 2 patients due to platelet count decrease or preexisting thrombocytopenia, while upgrading and dosage escalation in 3 patients was performed due to platelet count increase (6th, 8th and 12th week). Low dose hydroxyurea administration was continued as concomitant medication in post-PV and post-MPN-U MF patients.
Summary
JAK inhibitors, such as ruxolitinib, have significantly improved the treatment of MF. The clinical experience of the drug has shown that it is generally well tolerated. Long term effects and impact on disease natural history remain to be further studied through diligent monitoring.
Keyword(s): Myelofibrosis
Session topic: Publication Only
Type: Publication Only
Background
Myelofibrosis is one of the classical Philadelphia negative myeloproliferative neoplasms (MPNs), either appearing de novo (primary MF[PMF]) or following a previous ET or PV (post-ET or post-PV MF). The disease is essentially the same. The therapeutic landscape of MF has changed with the introduction of JAK inhibitors.
Aims
To evaluate the efficacy and safety of ruxolitinib treatment in patients with MF.
Methods
Eighteen patients with MF (12 male and 6 female), median age 62.5 (33-75) years old were evaluated: 7 with PMF, 5 post PV, 3 post ET, 3 post MPN-U. Median follow up since ruxolitinib initiation was 4 (1-33) months, whereas total follow up since diagnosis was 5 (2-19) years. JAK2 mutational status was available in 14/18 patients, 12/14 being positive for the V617F mutation. Cytogenetic study was available in 12/18 patients, 8 of them having normal karyotype, 2 with deletion of long arm of chromosome 20 [del(20)(q13.1)], one with trisomy 8 and one with complex karyotype [48,XX,+8,+9,t(12:14)(q24.1:q24)]. According to dynamic international prognostic scoring system (DIPSS) upon ruxolitinib initiation, risk group was low in 2, intermediate-1 (int-1) in 4, intermediate-2 (int-2) in 7 and high in 5 patients.
Results
Spleen volume (SV) reduction was observed in 11/18 (61%) patients with a mean SV reduction of 33.7%. Constitutional symptoms subsided in all patients within 2 weeks of ruxolitinib initiation. Fifteen out eighteen patients had weight gain and quality of life improvement. Hematologic toxicity involving anemia and thrombocytopenia was observed in 6/18 (33%) and 2/18 (11%) patients respectively. Red cell transfusion was required in one patient. Dose adjustment with dosage de-escalation was required in 2 patients due to platelet count decrease or preexisting thrombocytopenia, while upgrading and dosage escalation in 3 patients was performed due to platelet count increase (6th, 8th and 12th week). Low dose hydroxyurea administration was continued as concomitant medication in post-PV and post-MPN-U MF patients.
Summary
JAK inhibitors, such as ruxolitinib, have significantly improved the treatment of MF. The clinical experience of the drug has shown that it is generally well tolerated. Long term effects and impact on disease natural history remain to be further studied through diligent monitoring.
Keyword(s): Myelofibrosis
Session topic: Publication Only
Abstract: PB1932
Type: Publication Only
Background
Myelofibrosis is one of the classical Philadelphia negative myeloproliferative neoplasms (MPNs), either appearing de novo (primary MF[PMF]) or following a previous ET or PV (post-ET or post-PV MF). The disease is essentially the same. The therapeutic landscape of MF has changed with the introduction of JAK inhibitors.
Aims
To evaluate the efficacy and safety of ruxolitinib treatment in patients with MF.
Methods
Eighteen patients with MF (12 male and 6 female), median age 62.5 (33-75) years old were evaluated: 7 with PMF, 5 post PV, 3 post ET, 3 post MPN-U. Median follow up since ruxolitinib initiation was 4 (1-33) months, whereas total follow up since diagnosis was 5 (2-19) years. JAK2 mutational status was available in 14/18 patients, 12/14 being positive for the V617F mutation. Cytogenetic study was available in 12/18 patients, 8 of them having normal karyotype, 2 with deletion of long arm of chromosome 20 [del(20)(q13.1)], one with trisomy 8 and one with complex karyotype [48,XX,+8,+9,t(12:14)(q24.1:q24)]. According to dynamic international prognostic scoring system (DIPSS) upon ruxolitinib initiation, risk group was low in 2, intermediate-1 (int-1) in 4, intermediate-2 (int-2) in 7 and high in 5 patients.
Results
Spleen volume (SV) reduction was observed in 11/18 (61%) patients with a mean SV reduction of 33.7%. Constitutional symptoms subsided in all patients within 2 weeks of ruxolitinib initiation. Fifteen out eighteen patients had weight gain and quality of life improvement. Hematologic toxicity involving anemia and thrombocytopenia was observed in 6/18 (33%) and 2/18 (11%) patients respectively. Red cell transfusion was required in one patient. Dose adjustment with dosage de-escalation was required in 2 patients due to platelet count decrease or preexisting thrombocytopenia, while upgrading and dosage escalation in 3 patients was performed due to platelet count increase (6th, 8th and 12th week). Low dose hydroxyurea administration was continued as concomitant medication in post-PV and post-MPN-U MF patients.
Summary
JAK inhibitors, such as ruxolitinib, have significantly improved the treatment of MF. The clinical experience of the drug has shown that it is generally well tolerated. Long term effects and impact on disease natural history remain to be further studied through diligent monitoring.
Keyword(s): Myelofibrosis
Session topic: Publication Only
Type: Publication Only
Background
Myelofibrosis is one of the classical Philadelphia negative myeloproliferative neoplasms (MPNs), either appearing de novo (primary MF[PMF]) or following a previous ET or PV (post-ET or post-PV MF). The disease is essentially the same. The therapeutic landscape of MF has changed with the introduction of JAK inhibitors.
Aims
To evaluate the efficacy and safety of ruxolitinib treatment in patients with MF.
Methods
Eighteen patients with MF (12 male and 6 female), median age 62.5 (33-75) years old were evaluated: 7 with PMF, 5 post PV, 3 post ET, 3 post MPN-U. Median follow up since ruxolitinib initiation was 4 (1-33) months, whereas total follow up since diagnosis was 5 (2-19) years. JAK2 mutational status was available in 14/18 patients, 12/14 being positive for the V617F mutation. Cytogenetic study was available in 12/18 patients, 8 of them having normal karyotype, 2 with deletion of long arm of chromosome 20 [del(20)(q13.1)], one with trisomy 8 and one with complex karyotype [48,XX,+8,+9,t(12:14)(q24.1:q24)]. According to dynamic international prognostic scoring system (DIPSS) upon ruxolitinib initiation, risk group was low in 2, intermediate-1 (int-1) in 4, intermediate-2 (int-2) in 7 and high in 5 patients.
Results
Spleen volume (SV) reduction was observed in 11/18 (61%) patients with a mean SV reduction of 33.7%. Constitutional symptoms subsided in all patients within 2 weeks of ruxolitinib initiation. Fifteen out eighteen patients had weight gain and quality of life improvement. Hematologic toxicity involving anemia and thrombocytopenia was observed in 6/18 (33%) and 2/18 (11%) patients respectively. Red cell transfusion was required in one patient. Dose adjustment with dosage de-escalation was required in 2 patients due to platelet count decrease or preexisting thrombocytopenia, while upgrading and dosage escalation in 3 patients was performed due to platelet count increase (6th, 8th and 12th week). Low dose hydroxyurea administration was continued as concomitant medication in post-PV and post-MPN-U MF patients.
Summary
JAK inhibitors, such as ruxolitinib, have significantly improved the treatment of MF. The clinical experience of the drug has shown that it is generally well tolerated. Long term effects and impact on disease natural history remain to be further studied through diligent monitoring.
Keyword(s): Myelofibrosis
Session topic: Publication Only
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