ABL tyrosine kinase inhibitor-induced pulmonary alveolar proteinosis in chronic myeloid leukemia

2014 ◽  
Vol 100 (6) ◽  
pp. 611-614 ◽  
Author(s):  
Mariko Yoshimura ◽  
Kensuke Kojima ◽  
Rika Tomimasu ◽  
Noriyasu Fukushima ◽  
Shinichiro Hayashi ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor ◽  
Pulmonary Alveolar Proteinosis ◽  
Abl Tyrosine Kinase ◽  
Alveolar Proteinosis ◽  
Abl Tyrosine Kinase Inhibitor

scholarly journals CHRONIC MYELOID LEUKEMIA IN PATIENT WITH THE KLINEFELTER SYNDROME

2016 ◽  
Vol 38 (3) ◽  
pp. 195-197 ◽  
Author(s):  
S V Andreieva ◽  
K V Korets ◽  
O A Kyselova ◽  
O E Ruzhinska ◽  
I M Serbin
Keyword(s):  
Targeted Therapy ◽  
Chronic Myeloid Leukemia ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Chromosomal Abnormality ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor ◽  
Klinefelter Syndrome ◽  
Abl Tyrosine Kinase ◽  
Abl Tyrosine Kinase Inhibitor

Aim: Genetic inborn along with acquired diseases arise due to the lesions in genome of multipotent hematopoietic stem cells. The aim was to study an influence of constitutional anomaly, Klinefelter syndrome, and additional structural rearrangements on the BCR-ABL tyrosine kinase inhibitor targeted therapy efficacy. Material and Methods: We describe a 32-year-old male patient with chronic myeloid leukemia (CML) who was detected to have sex chromosomal abnormality during evaluation for Philadelphia chromosome. Results: At diagnosis of CML, two clones were detected by standard cytogenetic investigation of bone marrow cells: 1) clone with translocation t(9;22)(q34;q11), with two sex X chromosomes and absence sex chromosome Y; 2) clone with t(9;22) and unbalanced t(Y;20)(q11;q13). Analysis of blast transformed lymphocytes from peripheral blood showed karyotype 47,XXY. Monitoring of targeted therapy with second generation inhibitor of BCR-ABL tyrosine kinase indicated a cytogenetic remission and absence of BCR-ABL1 fusion signals after 11 months. Conclusions: Absence of translocation t(9;22)(q34;q11) in blast transformed T-lymphocytes at diagnosis of CML evidences that this translocation may appear not only at the level of multipotent haemopoietic cell progenitors but also may have oligo lineage myeloid origin. Presence of additional structural chromosomal abnormality in the clone with t(9;22)(q34;q11) does not affect the efficacy of therapy with the use of second generation BCR-ABL tyrosine kinase inhibitor.

scholarly journals Axl Blockade by BGB324 Inhibits BCR-ABL Tyrosine Kinase Inhibitor–Sensitive and -Resistant Chronic Myeloid Leukemia

2016 ◽  
Vol 23 (9) ◽  
pp. 2289-2300 ◽  
Author(s):  
Isabel Ben-Batalla ◽  
Robert Erdmann ◽  
Heather Jørgensen ◽  
Rebecca Mitchell ◽  
Thomas Ernst ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor ◽  
Abl Tyrosine Kinase ◽  
Abl Tyrosine Kinase Inhibitor

scholarly journals Is going for cure in chronic myeloid leukemia possible and justifiable?

Hematology ◽  
2012 ◽  
Vol 2012 (1) ◽  
pp. 122-128 ◽  
Author(s):  
François-Xavier Mahon
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Tyrosine Kinase ◽  
Myeloid Leukemia ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Clinical Results ◽  
Major Question ◽  
Abl Tyrosine Kinase ◽  
Show Evidence ◽  
Abl Tyrosine Kinase Inhibitor

Abstract After more than a decade of treatment of chronic myeloid leukemia (CML) patients with the BCR-ABL tyrosine kinase inhibitor imatinib, and despite the impressive clinical results of this targeted therapeutic, many questions remain unresolved. One major question is how to cure CML, and the next step for the future will be to address this key issue. CML is a good model of cancer. The fact that the majority of CML patients who respond very well but discontinue tyrosine kinase inhibitors later show evidence of molecular recurrence focuses attention on the need for further research on leukemic stem cells. The challenge now is to understand why, after stopping treatment, the leukemia recurs in some patients but not in others. If we win this battle, this progress will certainly benefit the treatment and management of other leukemias and solid tumors and will validate this new topic.

Treatment of Chronic Myeloid Leukemia Elderly Patients in the Tyrosine Kinase Inhibitor Era

2013 ◽  
Vol 13 (7) ◽  
pp. 755-767 ◽  
Author(s):  
Domenico Russo ◽  
Michele Malagola ◽  
Cristina Skert ◽  
Carla Filì ◽  
Cesare Bergonzi ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Elderly Patients ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor
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