Comparative evaluation of bone marrow cells morpho-functional activity in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors of the first and second generation
AbstractThe efficiency of using the culture techniques of research for monitoring the patient’s response to the treatment by tyrosine kinase inhibitors of the first and second generation is shown. Thus, the functional activity of bone marrow cells in patients having the optimal treatment response to inhibitors of tyrosine kinases was significantly lower compared with patients with the acquired resistance to the drug, and patients who had CML diagnosed for first time. Furthermore, for patients with the optimal response to the nilotinib therapy, numbers of colonies in semi-solid agar in vitro was lower, than in patients with the optimal response to imatinib. When the leukaemic cell clone becomes resistant to tyrosine kinase inhibitors, the prevalence of early cells of granulocyte-macrophage hematopoietic stem cells is observed in CFU culture which can be an important prognostic factor for choosing the appropriate treatment strategy.
Bacco Di, A., Keeshan, K., McKenna, S.L., 2000. Molecular abnormalities in chronic myeloid leukemia: Deregulation of cell growth and apoptosis. Oncologist 5, 405–415.
Baran, Y., Saydam, G., 2012. Cumulative clinical experience from a decade of use: Imatinib as first-line treatment of chronic myeloid leukemia. J. Blood Med. 3, 139–150. >>doi: 10.2147/JBM.S29132
Belle, L., Bruck, F., Foguenne, J., 2012. Imatinib and nilotinib inhibit hematopoietic progenitor cell growth, but do not prevent adhesion, migration and engraftment of human cord blood CD34+ cells. PLoS One 7(12), e52564. >>doi: 10.1371/journal.pone.0052564
Chen, Y., Peng, C., Sullivan, C., 2010. Critical molecular pathways in cancer stem cells of chronic myeloid leukemia. Leukemia 24(9), 1545–1554. >>doi: 10.1038/leu.2010.143
Helgason, C.D., Helgason, C.L.M., 2012. Basic cell culture protocols. 3rd ed. Vol. 290. Humana Press Inc., Totowa, NJ.
Corbin, A.S., Agarwal, A., Loriaux, M., 2011. Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. J. Clin. Invest. 121, 396–409. >>doi: 10.1172/JCI35721
Falder, S., Talpaz, M., Estrov, Z., 1999. The biology of chronic myeloid leukemia. N. Engl. J. Med. 15, 164–172.
Frazer, R., Irvine, A., McMullin, M.F., 2007. Chronic myeloid leukaemia in the 21st century. Ulster Med. J. 76(1), 8–17.
Grineva, N.I., Ahlynina, T.V., Gerasimova, L.P., 2009. Razlichija v proliferacii i differencirovke Ph+ kletok ot individual'nyh bol'nyh HML v suspenzionnoj kul'ture. Ph+ kletki s vysokoj skorost'ju proliferacii [Differences in proliferation and differentiation of Ph+ cells from CML patients in individual suspension culture. Ph+ cells with high proliferation rates]. Jeksperimental'naja Onkologija 8, 53–68 (in Russian).
Jamieson, C.H.M., Ailles, L.E., Dylla, S.J., Muijtjens, M., Jones, C., Zehnder, J.L., Gotlib, J., Li, K., Manz, M.G., Keating, A., Sawyers, C.L., Weissman, I.L., 2004. Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N. Engl. J. Med. 351(7), 657–667. >>doi: 10.1056/NEJMoa040258
Jorgensen, H.G., Allan, E.K., Jordanides, N.E., 2007. Nilotinib exerts equipotent antiproliferative effects to imatinib and does not induce apoptosis in CD34+ CML cells. Blood 109, 4016–4019. >>doi: 10.1182/blood-2006-11-057521
Lenaerts, T., Castagnetti, F., Traulsen, A., 2011. Explaining the in vitro and in vivo differences in leukemia therapy. Cell Cycle 15, 1540–1544. >>doi: 10.4161/cc.10.10.15518
Mayani, H., Flores-Figueroa, E., Chavez-Gonzalez, A., 2009. In vitro biology of human myeloid leukemia. Leukemia Res. 33, 634–637. >>doi: 10.1016/j.leukres.2008.11.011
Deininger, M.W.N., Goldman, J.M., Melo, J.V., 2000. The molecular biology of chronic myeloid leukemia. Blood 96(10), 3343–3355.
Mughal, A., Aslam, M., Khan, A.M.H., Saleem, S., Umar, R., Saleem, M., 2013. Bcr-Abl tyrosine kinase inhibitors – current status. Infect. Agents Cancer 8(1), 23. >>doi: 10.1186/1750-9378-8-23
Mukhopadhyay, A., Dasgupta, S., Mukhopadhyay, S., 2012. Imatinib mesylate therapy in patients of chronic myeloid leukemia with philadelphia chromosome positive: An experience from Eastern India. Indian J. Hematol. Blood Transfus. 28(2), 82–88. >>doi: 10.1007/s12288-011-0108-9
O’Sullivan, S., Lin, J.M., Watson, M., 2011. The skeletal effects of the tyrosine kinase inhibitor nilotinib. Bone 49, 281–289. >>doi: 10.1016/j.bone.2011.04.014
Rosti, V., Bergamaschi, G., Lucotti, C., 1995. Oligodeoxynucleotides antisense to c-abl specifically inhibit entry into S-phase of CD34+ hematopoietic cells and their differentiation to granulocyte-macrophage progenitors. Blood 86, 3387–3393.
Ruibao, R., 2005. Mechanisms of BCR–ABL in the pathogenesis of chronic myelogenous leukemia. Nat. Rev. Cancer 5, 172–183.
Weisberg, E., Catley, L., Renee, D., 2007. Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL leukemias. Blood 109, 2112–2120. >>doi: 10.1182/blood-2006-06-026377
Zhang, B., Strauss, A.C., Chu, S., 2010. Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate. Cancer Cell 17(5), 427–442. >>doi: 10.1016/j.ccr.2010.03.011
Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons «Attribution» 4.0 License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.