Browsing by Author "Vidovic, A. (6701313789)"
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Publication Central nervous system relapse in CD56+, FLT3/ITD+ promyelocytic leukemia(2012) ;Colovic, N. (6701607753) ;Tomin, D. (6603497854) ;Vidovic, A. (6701313789) ;Tosic, N. (15729686900) ;Atkinson, H.D. (7101883648)Colovic, Milica D. (21639151700)Central nervous system (CNS) involvement in acute promyelocytic leukemia (APL) is rare and tends to be seen mostly following treatment with all-trans retinoic acid (ATRA), due to prolonged patient survival and poor penetration of the drug in the CNS. At least 10% of extramedullary relapses in APL involve the CNS, and associated factors include an increased age, the BCR isoform, the development of differentiation syndrome, a high white cell count at presentation and hemorrhage into the CNS during induction therapy. We present the case of a patient with high-risk APL, CD56+, CD2+ in whom a CNS relapse was diagnosed through the presence of a PML/RARα rearrangement on PCR of the cerebrospinal fluid (CSF). © 2011 Springer Science+Business Media, LLC. - Some of the metrics are blocked by yourconsent settings
Publication Central nervous system relapse in CD56+, FLT3/ITD+ promyelocytic leukemia(2012) ;Colovic, N. (6701607753) ;Tomin, D. (6603497854) ;Vidovic, A. (6701313789) ;Tosic, N. (15729686900) ;Atkinson, H.D. (7101883648)Colovic, Milica D. (21639151700)Central nervous system (CNS) involvement in acute promyelocytic leukemia (APL) is rare and tends to be seen mostly following treatment with all-trans retinoic acid (ATRA), due to prolonged patient survival and poor penetration of the drug in the CNS. At least 10% of extramedullary relapses in APL involve the CNS, and associated factors include an increased age, the BCR isoform, the development of differentiation syndrome, a high white cell count at presentation and hemorrhage into the CNS during induction therapy. We present the case of a patient with high-risk APL, CD56+, CD2+ in whom a CNS relapse was diagnosed through the presence of a PML/RARα rearrangement on PCR of the cerebrospinal fluid (CSF). © 2011 Springer Science+Business Media, LLC. - Some of the metrics are blocked by yourconsent settings
Publication Mixed phenotype acute leukemia of T/myeloid type with a prominent cellular heterogeneity and unique karyotypic aberration 45,XY, dic(11;17)(2012) ;Colovic, M. (21639151700) ;Colovic, N. (6701607753) ;Jankovic, G. (7005387173) ;Kraguljac Kurtovic, N. (37037758700) ;Vidovic, A. (6701313789) ;Djordjevic, V. (57215460423)Bogdanovic, A. (6603686934)Introduction. A 26-yr-old male patient with mixed phenotype acute leukemia of T/myeloid type with prominent leukemic cell heterogeneity, and the presence of a so far unreported karyotype aberration in this type of acute leukemia 45,XY, dic(11;17)(11qter→11p11.2::17p11.2→17qter) is presented. Methods. Flow immunocytometry was performed by direct multicolor immunofluorescent technique on bone marrow aspirates. Cytogenetic analyses were performed using G-banding method by direct preparation of unstimulated bone marrow cells and following 24hours of culture in RPMI 1540 culture medium with 25% fetal calf serum at 37°C Results. The flow immunocytometry of bone marrow nucleated cells revealed the existance of three distinct blast cell populations with overlapping immunophenotypes. Predominant blast cell population had an early myeloid phenotype and aberrant expression of CD7 antigen (HLA-DR +, CD34 +, anti-MPO +, CD117 +, CD33 +, CD13 +, CD7 +low, cyCD3 -, TdT -). The other two blast cell populations, smaller in cell diameter and less sizable in cell proportion, both shared the T-lymphoid features. The patient was treated with ADE protocol (etoposide, cytarabine and doxorubicine). A complete remission was achieved and lasted 5months. Conclusion. A case of MPAL with complex biological features, 45,XY, dic(11;17)(11qter→11p11.2::17p11.2→17qter) karyotype and an aggressive, therapy-resistant clinical course, is presented. © 2011 Blackwell Publishing Ltd. - Some of the metrics are blocked by yourconsent settings
Publication Mixed phenotype acute leukemia of T/myeloid type with a prominent cellular heterogeneity and unique karyotypic aberration 45,XY, dic(11;17)(2012) ;Colovic, M. (21639151700) ;Colovic, N. (6701607753) ;Jankovic, G. (7005387173) ;Kraguljac Kurtovic, N. (37037758700) ;Vidovic, A. (6701313789) ;Djordjevic, V. (57215460423)Bogdanovic, A. (6603686934)Introduction. A 26-yr-old male patient with mixed phenotype acute leukemia of T/myeloid type with prominent leukemic cell heterogeneity, and the presence of a so far unreported karyotype aberration in this type of acute leukemia 45,XY, dic(11;17)(11qter→11p11.2::17p11.2→17qter) is presented. Methods. Flow immunocytometry was performed by direct multicolor immunofluorescent technique on bone marrow aspirates. Cytogenetic analyses were performed using G-banding method by direct preparation of unstimulated bone marrow cells and following 24hours of culture in RPMI 1540 culture medium with 25% fetal calf serum at 37°C Results. The flow immunocytometry of bone marrow nucleated cells revealed the existance of three distinct blast cell populations with overlapping immunophenotypes. Predominant blast cell population had an early myeloid phenotype and aberrant expression of CD7 antigen (HLA-DR +, CD34 +, anti-MPO +, CD117 +, CD33 +, CD13 +, CD7 +low, cyCD3 -, TdT -). The other two blast cell populations, smaller in cell diameter and less sizable in cell proportion, both shared the T-lymphoid features. The patient was treated with ADE protocol (etoposide, cytarabine and doxorubicine). A complete remission was achieved and lasted 5months. Conclusion. A case of MPAL with complex biological features, 45,XY, dic(11;17)(11qter→11p11.2::17p11.2→17qter) karyotype and an aggressive, therapy-resistant clinical course, is presented. © 2011 Blackwell Publishing Ltd.
