Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency. © 2020 BioMed Central Ltd unless otherwise stated. 2006;108(1):28–37.Marin D, Ibrahim AR, Lucas C, Gerrard G, Wang L, Szydlo RM, et al.
2018;19(3):15.Goldberg SL, Savona M, Mauro MJ. Leukemia. 2014;38(1):10–20.Soverini S, Colarossi S, Gnani A, Rosti G, Castagnetti F, Poerio A, et al. Blood. Leukemia. It doesn’t seem to have any effect on prognosis whether you have the same fusion protein as in CML or the slightly different one.You’re also correct that the genetic mutation occurs in different cell lines in each disease: in CML it is in the myeloid cell line, whereas in Ph+ ALL it is in the lymphoid cell line. 2017;130(S1):2903 (abstract).Takahashi N, Nishiwaki K, Nakaseko C, Aotsuka N, Sano K, Ohwada C, et al. 2017;12(1):e0171041.Hughes TP, Kaeda J, Branford S, Rudzki Z, Hochhaus A, Hensley ML, et al. has shown that the cumulative incidence of (stable) MRA number of clinical studies addressing TKI cessation in patients with stable DMR have been conducted over the past years or are currently ongoing (Table Besides CML, the Ph translocation can be detected in acute leukemia patients. 47 yr old male.
e A. Seràgnoli’, Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138, Bologna, ItalyDivision of Hematology, Ospedale dell’Angelo, Mestre, Venice, ItalyChildren’s Cancer Research Institute (CCRI) and Medical University of Vienna, Vienna, AustriaYou can also search for this author in Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML. Blood Adv. At present, clinical research questions are different in Ph+ ALL as compared to CML. Use of tyrosine kinase inhibitors to prevent relapse after allogeneic hematopoietic stem cell transplantation for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia: a position statement of the Acute Leukemia Working Party of the European Society for blood and marrow transplantation. 2012;26(9):2096–102.Marin D, Hedgley C, Clark RE, Apperley J, Foroni L, Milojkovic D, et al. 2015;15:45.Simona Soverini, Renato Bassan, and Thomas Lion contributed equally to this paper.Hematology/Oncology ‘L.
Early molecular response predicts outcomes in patients with chronic myeloid leukemia in chronic phase treated with frontline nilotinib or imatinib. 2018. Blood. 2013;122(6):872–84.Hochhaus A, Saussele S, Rosti G, Mahon FX, Janssen J, Hjorth-Hansen H, et al. Treatment of young patients with Philadelphia chromosome-positive acute lymphoblastic leukaemia using increased dose of imatinib and deintensified chemotherapy before allogeneic stem cell transplantation. BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia. Haematologica. Search
Nilotinib vs nilotinib plus pegylated interferon-alpha2b induction and nilotinib or pegylated interferon-alpha2b maintenance therapy for newly diagnosed BCR-ABL+ chronic myeloid leukemia patients in chronic phase: interim analysis of the tiger (CML V)-study. Leukemia. Discontinuation of tyrosine kinase inhibitor therapy in chronic myeloid leukaemia (EURO-SKI): a prespecified interim analysis of a prospective, multicentre, non-randomised, trial. Achieving deeper molecular response is associated with a better clinical outcome in chronic myeloid leukemia patients on imatinib front-line therapy. Blood. 2016;1(3):250–9.Jabbour E, Short NJ, Ravandi F, Huang X, Daver N, Di Nardo C, et al. Bone Marrow Transplant. Haematologica. 2016;128(6):774–82.Chalandon Y, Rousselot P, Cayuela J-M, Thomas X, Clappier E, Havelange V, et al. The Philadelphia chromosome forms when chromosome 9 and chromosome 22 break and exchange portions. The fact that they have the same chromosomal translocation doesn’t really alter the disease process in either CML or ALL, in terms of chronic vs. acute. Clin Cancer Res.
The translocation is the same – t(9;22) – but the actual breakpoint is different in the two diseases.
Early BCR-ABL1 transcript decline after 1 month of tyrosine kinase inhibitor therapy as an indicator for treatment response in chronic myeloid leukemia. Moving treatment-free remission into mainstream clinical practice in CML. Ann Oncol. In CML, the Philadelphia chromosome is always present; in ALL, it is present only in some cases. Cancer. What about a pt that has both PH+ALL and PH+CML . An abnormal chromosome called the Philadelphia chromosome is associated with chronic myelogenous leukemia. Eur J Cancer. 2012;26(10):2172–5.Etienne G, Dulucq S, Nicolini FE, Morisset S, Fort MP, Schmitt A, et al.
Pharmacogenomics. Results from the U.S. life after stopping TKIs (LAST) study. 2015;29(5):999–1003.Cross NC, White HE, Muller MC, Saglio G, Hochhaus A. Standardized definitions of molecular response in chronic myeloid leukemia. I would say “had” at this point Hi Nada – I think it is due to the nature of each of the diseases. 2016;27(suppl 5):v69–82.Parker WT, Lawrence RM, Ho M, Irwin DL, Scott HS, Hughes TP, et al.
2016;30(8):1638–47.Hughes T, Deininger M, Hochhaus A, Branford S, Radich J, Kaeda J, et al. Cancer Cell. Comparable results of autologous and allogeneic haematopoietic stem cell transplantation for adults with Philadelphia-positive acute lymphoblastic leukaemia in first complete molecular remission: an analysis by the Acute Leukemia Working Party of the EBMT. BMC Cancer. Blood. The Philadelphia chromosome is present in chronic myeloid leukemia.A. Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia. Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline. Final report of a phase II study of imatinib mesylate with Hyper-CVAD for the front-line treatment of adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia.
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