Giuliana Farina

Assessment of cellular origin and EBV status in a PTLD after double cord blood transplantation.

Assessment of cellular origin and EBV status in a PTLD after double cord blood transplantation

Caspofungin for the treatment of candidaemia in patients with haematological malignancies

This study was prospectively conducted in 11 haematology divisions over a 2-year period to evaluate the efficacy of caspofungin in 24 neutropenic patients with haematological malignancies (HM) and candidaemia. These patients had received chemotherapy for HM and were neutropenic (PNN < 0.5 x 10(9)/L) for a median of 12 days (2-41) before candidaemia. The patients received caspofungin for a median duration of 12 days (range 6-26), obtaining a favourable overall response of 58%. At 30 days, 11 patients had died (46%); candidaemia was responsible for mortality in six patients (25%). These results suggest that treatment of candidaemia with caspofungin in neutropenic HM was efficacious, as it is in non-haematological subgroups.

Dasatinib restores full donor chimerism in a patient with imatinib-resistant Ph+ ALL relapsing after unrelated cord blood transplantation

The t(9;22) translocation, known as the Philadelphia (Ph) chromosome, represents the most adverse prognostic factor for adult acute lymphoblastic leukemia (ALL) and, until recently, conventional chemotherapy programs have not been effective in patients with this diagnosis [1], allogeneic stem cell transplantation (SCT) being therefore considered the only option for a cure [2]. Since imatinib was introduced as the first molecularly targeted therapy, the treatment for Phþ ALL has been rapidly changing [3], but unfortunately the emergence of resistance to imatinib remains a major problem in the treatment of Phþ leukemias [4,5]. The need for alternative approaches for imatinib-resistant Phþ leukemias has led to the development of a second generation of targeted therapies, such as AMN107 (nilotinib) and BMS354825 (dasatinib). The progression-free survival (PFS) achieved to date with dasatinib is clinically relevant, considering the very poor prognosis of this difficult-to-treat population, and may open a window of opportunity for many of these patients [6,7]. Here we describe the case of a Phþ ALL patient who received salvage therapy with dasatinib, achieving a durable molecular remission for more than 8 months, after failure of both imatinib-based treatment and subsequent allogeneic cord blood transplantation (CBT). A 37-year-old woman was referred to our hospital in May 2005 with a history of night-sweats and tiredness. The initial laboratory evaluation revealed haemoglobin 12.7 g/dl, WBC 25610/l, platelet count 150610/l, LDH 3500 UI/l, and 72% blast cells in the blood smear. A bone marrow aspirate showed 89% blast cells and the immunophenotype was consistent with a pre-B ALL. The karyotype was 46,XX,t(9;22) 7q7 in 100% of metaphases, and presence of the Bcr/Abl fusion gene was demonstrated using reverse transcriptase polymerase chain reaction (RT-PCR). She was treated with induction therapy according to GIMEMA LAL 0904 protocol, including prednisone, vincristine, daunoblastine, and asparaginase. Imatinib 800 mg per day was added to standard induction chemotherapy according to the presence of Ph chromosome. The patient achieved a hematologic and cytogenetic complete remission (CR) after induction, without any major complication, and in July 2005 she was started on maintenance treatment with imatinib 400 mg per day. She had no HLA-matched sibling and search for an unrelated donor was initiated. At more than 6 months after diagnosis, a bone marrow aspirate revealed 29% of blasts and cytogenetic response was lost (30% Phþ metaphases). Imatinib was escalated to 800 mg per day and prednisone and weekly vincristine were administered, but blast cell percentage increased to 38%; the patient underwent a standard salvage treatment (HAM), obtaining a hematologic CR, whereas her bone marrow remained positive for the t(9;22) translocation.

Eradication of JAK2 V617F mutation after allogeneic transplantation in a patient with myelofibrosis with myeloid metaplasia

Eradication of JAK2 V617F mutation after allogeneic transplantation in a patient with myelofibrosis with myeloid metaplasia

Reply to ‘Absence of JAK-2 (Val617Phe) point mutations in multiple myeloma’ by Dr Qin Huang et al. referred to ‘Screening of JAK2 V617F mutation in multiple myeloma’ from Fiorini A et al. published in Leukemia 2006, October 20

Reply to ‘Absence of JAK-2 (Val617Phe) point mutations in multiple myeloma’ by Dr Qin Huang et al. referred to ‘Screening of JAK2 V617F mutation in multiple myeloma’ from Fiorini A et al. published in Leukemia 2006, October 20