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  • Author: Cătălin Dănăilă x
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Open access

Georgiana E. Grigore, Angela Dascalescu, Mihaela Zlei, Iuliu C. Ivanov, Catalin Danaila, Tudor Petreus and Eugen Carasevici

Abstract

Background/aim: T lymphocytes are important players of the immune response. B-CLL is characterized by several immune defects. Our study aims to characterize the distinct maturational and functional T/NK cell subsets within B-cell chronic lymphocytic leukemia disease Rai stages. Patients and methods: Peripheral blood mononuclear cells from 43 patients enrolled in the study (16 females and 27 males, aged 68±10, 8 Rai 0, 22 Rai 1/2 and 13 Rai 3/4) were analyzed by multiparameter flow cytometry. Distinct subsets within the CD4+ (naive, central memory, effector/peripheral memory, regulatory-Tregs, follicular-TFH, CXCR3+ and/or CCR4+), CD8+ (naive+memory, effector, senescent) and NK (CD57+ and/or CD94+) were identified and compared between disease Rai stages. Results: Total numbers of T lymphocytes increase with disease stage. Both CD4+ and CD8+ T cells are elevated in absolute counts. The majority of CD4+ T cells are antigen-experienced, with increased Tregs, TFH and CXCR3+ (Th1-associated profile) T cell counts. The CD8+ T cells expansion is due mostly to the senescent CD57+ subset. No significant difference within NK subsets was observed among different disease stages. Conclusions: B-CLL behaviour seems to be associated with increased numbers of TFH and Tregs. The therapeutic modulation of T cell response in B-CLL patients may play an important role in the disease behaviour and may be a key event compensating for the immunodeficiency occurring mostly in advanced stages of the disease.

Open access

Roxana Popescu, Angela Dăscălescu, Cătălin Dănăilă, Doramina Ghiorghiu, Mihaela Zlei, Anca Ivanov, Adriana Sireteanu, Eusebiu Vlad Gorduza and Doina Azoicăi

Abstract

The coexistence of t(9;22) and inv(16) has been described in a very limited number of cases of CML, de novo or therapy-related AML. We report a patient with CML who presented both inversion of chromosome 16 and Philadelphia chromosome and evolved towards the blast phase under treatment with Imatinib. Laboratory diagnosis and monitoring was made by flow cytometry, conventional cytogenetics and molecular genetics techniques. The inv(16), detected by karyotyping in the Philadelphia chromosome positive clone at the moment of the blast transformation, was retrospectively assessed by means of real-time PCR, and was proved to have been present since diagnosis. The bone marrow biopsy performed in the blast phase of CML confirmed the presence of blasts belonging to the myeloid lineage, with indications of monocytic differentiation, frequently associated with inv(16). Moreover, the case also associated a F359V tyrosine kinase domain mutation, resulting in intermediate resistance to Imatinib and Nilotinib, which imposed therapy-switch to Dasatinib. In our case the evolution was progressive, followed by death due to lack of response to tyrosine kinase inhibitors, 18 months after diagnosis. The coexistence of t(9;22) and inv(16) in CML seems to be associated with an aggressive clinical evolution and resistance to tyrosine kinase inhibitor therapy. Due to the very small number of cases described in literature, therapeutic decisions are still difficult for patients displaying these abnormalities

Open access

Ion Antohe, Angela Dăscălescu, Cătălin Dănăilă, Mihaela Zlei, Iuliu Ivanov, Adriana Sireteanu, Oana Boca, Raluca Oană and Petru Cianga

Abstract

Background: Acute basophilic leukemia is a rare subtype of acute myeloid leukemia, as categorized by the 2008 World Health Organization classification of myeloid neoplasms. Acute basophilic leukemia diagnosis requires thorough morphological, cytochemical, immunophenotypic, molecular, and cytogenetic studies and exclusion of other hematological neoplasms associating basophilia. The disease course is defined by histamine driven, occasionally life-threatening respiratory, cardiovascular, cutaneous or digestive complications, as well as primary refractoriness to standard therapy. Clinical presentation: We herein report a case of a 63-year-old asthmatic female patient diagnosed with acute basophilic leukemia, associated with previously unpublished cytogenetic features and FLT-3 ITD mutation, pulmonary leukostasis and spontaneous pulmonary capillary leak syndrome, which worsened immediately following chemotherapy initiation. Respiratory complications were successfully managed, but recrudesced upon emergence of refractory disease and were ultimately fatal. We highlight the likelihood of pulmonary complications induced by basophil degranulation and tumor lysis in hypercellular acute basophilic leukemia and the potential benefit of histamine receptor blockade in this setting.