Clonal evolution of leukemia cells and chemoresistance
Abstract
Leukemic cells accumulate mutations and epigenetic changes in the process of disease development forming heterogeneous cell populations that are subject to selection and may respond differentially to therapy. Chemotherapy in turn damages new DNA generating mutations, and may kill leukemia cells most sensitive to drugs and select drug induced resistant subclones. Therefore, it is necessary to monitor changes in the subclonal composition during disease progression as such increased leukemia cell clonal evolution is the main reason for drug resistance and treatment insufficiency. Targeted treatment may be based on the molecular type of disease and on the tested cellular chemosensitivity of the individual patient at least for remission induction. Cellular drug sensitivity evaluation is not alternative to minimal residual disease estimation and whole exome sequencing. As it is not so easy to inhibit tumor evolution, diagnostics of cells sensitivity in the process of evolution may be of particular interest with remission induction. However, advantages of monitoring procedures sometimes are not so obvious.
About the Authors
A. . Svirnovski
Republican Research Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus
Russian Federation
Russian Federation
V. . Pasiukov
Republican Research Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus
Russian Federation
Russian Federation
D. . Kravchenko
Republican Research Center for Radiation Medicine and Human Ecology, Gomel, Belarus
Russian Federation
Russian Federation
N. . Feduro
Republican Research Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus
Russian Federation
Russian Federation
O. . Sergievich
Republican Research Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus
Russian Federation
Russian Federation
I. . Taras
Republican Research Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus
Russian Federation
Russian Federation
E. . Svirnovskaya
Republican Research Center for Transfusiology and Medical Biotechnologies, Minsk, Belarus
Russian Federation
Russian Federation
References
1. Youn, A. Using passenger mutations to estimate the timing of driver mutations and identify mutator alterations / A. Youn, R. Simon // BMC Bioinformatics. - 2013. - Vol. 14. - P. 363.
2. Cancer genome landscapes / B. Vogelstein [et al.] // Science. -2013. - P. 1546-1558.
3. Aberration in DNA methylation in B-cell lymphomas has a complex origin and increases the disease severity. De S. Shachnovich [et al.]. - PLoS Genet, 2013. - P. 145.
4. Clonal evolution in chronic lymphocytic leukemia: analysis of correlation with IGHV mutational status, NOTCH1 mutations and clinical significance. C. Lopez [et al.]. - Genes, Chromosomes and Cancer, 2013. - P. 7544-7545.
5. Clonal evolution in hematological malignancies and therapeutic implications. D.A. Landau [et al.]. - Leukemia, 2014. - P. 34-43.
6. Clonal evolution of preleukemic hematopoietic stem cells precedes human acute myeloid leukemia. M.I. Jan [et al.]. - Sci. Transl. Med., 2012. - P. 149.
7. The origin and evolution of mutations in acute myeloid leukemia. J.S. Welch [et al.]. - Cell, 2012. - P. 264-278.
8. Jan, M.I. Clone evolution of acute leukemia genomes / M.I. Jan, R. Majeti // Oncogene. - 2013. - Vol. 32. - P. 135-140.
9. Clonal origins in relapse in ETV6-RUNX1 acute lymphoblastic leukemia. F.W. van Delft [et al.]. - Blood, 2010. - P. 6247-6254.
10. Stable non-transforming minimal residual disease philadelphia-chromosome positive acute lymphoblastic leukemia after autologous transplantation: origin from neoplastic yet ‘preleukemic’ stem cells? A. Bohm [et al.]. - Leuk & Lymph, 2011. - P. 842-848.
11. Clonal heterogeneity in patients with cytogenetically normal acute myeloid leukemia with NPM1 mutations. D. Dvorakova [et al.]. - Leuk & Lymph, 2013. - P. 1056-?1060.
12. Bagby, G.C. Bone marrow failure as a risk factor for clonal evolution: prospects for leukemia prevention / G.C. Bagby, G. Meyers // Hematology. - 2007. - P. 40-46.
13. Clonal architecture of secondary acute myeloid leukemia / M.J. Walter [et al.] // N Engl J Med. - 2012. - P. 1090-1098.
14. Negrini, S. Genomic instability - an evolving hallmark of cancer / S. Negrini, V.G. Goroulis, T.D. Halazonetis // Nature Rev. Mol. Cell Biol. - 2010. - Vol. 11. - P. 228-?229.
15. Survival outcomes for clonal evolution in chronic myeloid leukemia patients on second generation tyrosine kinase inhibitor therapy / D. Verma [et al.] // Cancer. - 2010. - Vol. 116. - P. 2673-2681.
16. Clonal evolution in relapsed acute myeloid leukemia revealed by whole-genome sequencing / L. Ding [et al.] // Nature. - 2012. - Vol. 481. - P. 506.
17. Clonal evolution and devolution following chemotherapy in adult myelogenous leukemia / B. Parkin [et al.] // Blood. - 2012. - Vol. 121. - P. 369-377.
18. Relating human genetic variation to variation in drug responses / A.G. Madian [et al.] // Trends in genetics. - 2012. - Vol. 28. - P. 488-495.
19. The use of individualized tumor response testing in treatment selection: second randomization results from the LRF CLL4 trial and the predictive value of the test at trial entry / S. Matutes [et al.] // Leukemia. - 2013. - Vol. 27. - P. 307-310.
20. Flow cytometric chemosensitivity assay as a predictive tool of early clinical response in acute lymphoblastic leukemia / F. Galderisi [et al.] // Pediatr. Blood Cancer. - 2009. - Vol. 53. - P. 543-550.
21. The long-term impact of in vitro drug sensitivity testing on risk stratification and treatment outcome in acute lymphoblastic leukemia of childhood (CoALL 06-97) / G. Escherich [et al.] // Haematologica. - 2011. - Vol. 96. - P. 854-862.
22. Svirnovski, A.I. Leukemia therapy personalization: role of some laboratory technologies / A.I. Svirnovski // Meditsinskie novosti. - 2013. - Vol. 9. - P. 6-11.
Review
For citations:
Svirnovski A., Pasiukov V., Kravchenko D., Feduro N., Sergievich O., Taras I., Svirnovskaya E. Clonal evolution of leukemia cells and chemoresistance. Medical and Biological Problems of Life Activity. 2017;(1):24-28. (In Russ.)
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