Health care of Kyrgyzstan
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Results of treatment of patients with chronic myeloid leukemia in the Kyrgyz Republic using tyrosine kinase inhibitors of different generations

https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
Results of treatment of patients with chronic myeloid leukemia in the Kyrgyz Republic using tyrosine kinase inhibitors of different generations
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Abstract About the authors References

Abstract

Introduction. Chronic myeloid leukemia (CML) is a myeloproliferative disorder occurring in 1-2 cases per 100,000 adults. CML is characterized by a balanced genetic translocation t(9;22)(q34;q11.2). This rearrangement is known as the Philadelphia chromosome (Ph chromosome). Objective of the study. To evaluate the results of treatment with tyrosine kinase inhibitors in 546 patients with Ph+ CML in the Kyrgyz Republic for the period from 2003 to 2023. Materials and methods. The results of molecular genetic studies of patients treated with drugs such as imatinib, nilotinib, dasatinib, ponatinib were used as materials. Results and discussion. The overall survival rate for 20 years was 83%. The mortality rate is 5.1%. The rates of major molecular responses and complete molecular responses were 49% and 32%, respectively. Conclusion. The use of different generations of tyrosine kinase inhibitors in CML can significantly increase the duration and quality of life of patients.

About the authors

Жусупова Шербет Колдошовна, соискатель, заведующая отделе нием Онкогематологии Национального центра онкологии и гематологии, Бишкек, Кыргызская Республика

Zhusupova Sherbet Koldoshovna, applicant, head of the Oncohematology Department of the National Center of Oncology and Hematology, Bishkek, Kyrgyz Republic

Жусупова Шербет Колдошовна, арыз ээси, Улуттук онкология жана гематология борборунун онкогематология бөлүмүнүн башчысы, Бишкек шаары, Кыргыз Республикасы

References

1. American Cancer Society. Cancer Facts & Figures 2017. Atlanta: American Cancer Society; 2017.
2. Huang X, Cortes J, Kantarjian H. Estimations of the increasing prevalence and plateau prevalence of chronic myeloid
leukemia in the era of tyrosine kinase inhibitor therapy. Cancer. 2012; 118(12): 3123–3127.
3. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine
fluorescence and Giemsa staining. Nature. 1973; 243(5405): 290–293.
4. Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid
cells. Blood. 1993; 82(6): 1838–1847.
5. Okuda K, Matulonis U, Salgia R, Kanakura Y, Druker B, Griffin JD. Factor independence of human myeloid leukemia
cell lines is associated with increased phosphorylation of the proto-oncogene Raf-1. Exp Hematol. 1994; 22(11): 1111–1117.
6. Raitano AB, Halpern JR, Hambuch TM, Sawyers CL. The Bcr-Abl leukemia oncogene activates Jun kinase and requires
Jun for transformation. Proc Natl Acad Sci USA. 1995; 92(25): 11746–11750.
7. Sawyers CL, Callahan W, Witte ON. Dominant negative MYC blocks transformation by ABL oncogenes. Cell.1992; 70(6): 
901–910.
8. Shuai K, Halpern J, ten Hoeve J, Rao X, Sawyers CL. Constitutive activation of STAT5 by the BCR-ABL oncogene in
chronic myelogenous leukemia. Oncogene. 1996; 13(2): 247–254.
9. Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators
of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996; 183(3): 811–820.
10. Guru Murthy GS, Atallah E. Treatment-Free Remission in CML: the US Perspective.Curr Hematol Malig Rep. 2019
Feb;14(1):56-61. doi: 10.1007/s11899-019-0496-8.
11. Narlı Özdemir Z, Kılıçaslan NA, Yılmaz M, Eşkazan AE.Guidelines for the treatment of chronic myeloid leukemia from the
NCCN and ELN: differences and similarities.Int J Hematol. 2023 Jan;117(1):3-15. doi: 10.1007/s12185-022-03446-1.
12. Braun TP, Eide CA, Druker BJ.Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell. 2020 Apr
13;37(4):530-542. doi: 10.1016/j.ccell.2020.03.006.

1. American Cancer Society. Cancer Facts & Figures 2017. Atlanta: American Cancer Society; 2017.
2. Huang X, Cortes J, Kantarjian H. Estimations of the increasing prevalence and plateau prevalence of chronic myeloid
leukemia in the era of tyrosine kinase inhibitor therapy. Cancer. 2012; 118(12): 3123–3127.
3. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine
fluorescence and Giemsa staining. Nature. 1973; 243(5405): 290–293.
4. Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid
cells. Blood. 1993; 82(6): 1838–1847.
5. Okuda K, Matulonis U, Salgia R, Kanakura Y, Druker B, Griffin JD. Factor independence of human myeloid leukemia
cell lines is associated with increased phosphorylation of the proto-oncogene Raf-1. Exp Hematol. 1994; 22(11): 1111–1117.
6. Raitano AB, Halpern JR, Hambuch TM, Sawyers CL. The Bcr-Abl leukemia oncogene activates Jun kinase and requires
Jun for transformation. Proc Natl Acad Sci USA. 1995; 92(25): 11746–11750.
7. Sawyers CL, Callahan W, Witte ON. Dominant negative MYC blocks transformation by ABL oncogenes. Cell.1992; 70(6): 
901–910.
8. Shuai K, Halpern J, ten Hoeve J, Rao X, Sawyers CL. Constitutive activation of STAT5 by the BCR-ABL oncogene in
chronic myelogenous leukemia. Oncogene. 1996; 13(2): 247–254.
9. Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators
of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996; 183(3): 811–820.
10. Guru Murthy GS, Atallah E. Treatment-Free Remission in CML: the US Perspective.Curr Hematol Malig Rep. 2019
Feb;14(1):56-61. doi: 10.1007/s11899-019-0496-8.
11. Narlı Özdemir Z, Kılıçaslan NA, Yılmaz M, Eşkazan AE.Guidelines for the treatment of chronic myeloid leukemia from the
NCCN and ELN: differences and similarities.Int J Hematol. 2023 Jan;117(1):3-15. doi: 10.1007/s12185-022-03446-1.
12. Braun TP, Eide CA, Druker BJ.Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell. 2020 Apr
13;37(4):530-542. doi: 10.1016/j.ccell.2020.03.006.

1. American Cancer Society. Cancer Facts & Figures 2017. Atlanta: American Cancer Society; 2017.
2. Huang X, Cortes J, Kantarjian H. Estimations of the increasing prevalence and plateau prevalence of chronic myeloid
leukemia in the era of tyrosine kinase inhibitor therapy. Cancer. 2012; 118(12): 3123–3127.
3. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine
fluorescence and Giemsa staining. Nature. 1973; 243(5405): 290–293.
4. Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid
cells. Blood. 1993; 82(6): 1838–1847.
5. Okuda K, Matulonis U, Salgia R, Kanakura Y, Druker B, Griffin JD. Factor independence of human myeloid leukemia
cell lines is associated with increased phosphorylation of the proto-oncogene Raf-1. Exp Hematol. 1994; 22(11): 1111–1117.
6. Raitano AB, Halpern JR, Hambuch TM, Sawyers CL. The Bcr-Abl leukemia oncogene activates Jun kinase and requires
Jun for transformation. Proc Natl Acad Sci USA. 1995; 92(25): 11746–11750.
7. Sawyers CL, Callahan W, Witte ON. Dominant negative MYC blocks transformation by ABL oncogenes. Cell.1992; 70(6): 
901–910.
8. Shuai K, Halpern J, ten Hoeve J, Rao X, Sawyers CL. Constitutive activation of STAT5 by the BCR-ABL oncogene in
chronic myelogenous leukemia. Oncogene. 1996; 13(2): 247–254.
9. Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators
of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996; 183(3): 811–820.
10. Guru Murthy GS, Atallah E. Treatment-Free Remission in CML: the US Perspective.Curr Hematol Malig Rep. 2019
Feb;14(1):56-61. doi: 10.1007/s11899-019-0496-8.
11. Narlı Özdemir Z, Kılıçaslan NA, Yılmaz M, Eşkazan AE.Guidelines for the treatment of chronic myeloid leukemia from the
NCCN and ELN: differences and similarities.Int J Hematol. 2023 Jan;117(1):3-15. doi: 10.1007/s12185-022-03446-1.
12. Braun TP, Eide CA, Druker BJ.Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell. 2020 Apr
13;37(4):530-542. doi: 10.1016/j.ccell.2020.03.006.

Keywords
Treatment , Survival , Chronic myelogenous leukemia , Diagnostics
Для цитирования

Жусупова Ш.К. Результаты лечения больных с хроническим миелоидным лейкозом в Кыргызской Республике с применением ингибиторов тирозинкиназ разных поколений. Научно-практический журнал «Здравоохранение Кыргызстана» 2025, № 3, с. 73-77. https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
For citation
 Zhusupova Sh.K. Results of treatment of patients with chro nic myeloid leukemia in the Kyrgyz Republic using tyrosine kinase inhibitors of different generations. Scientific practical journal “Health care of Kyrgyzstan” 2025, No.3, p. 73-77. https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
Цитата үчүн

Жусупова Ш.К. Кыргыз Республикасында өнөкөт миелолейкоз менен ооруган бейтаптарды ар кандай муундагы тирозинкиназа ингибиторлору менен дарылоонун жыйынтыктары. Кыргызстандын саламаттык сактоо
илимий-практикалык журналы 2025, № 3, б. 73-77. https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
Authors Zhusupova Sh.K.
Link doi.org https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
Pages 73-77
Keywords Treatment, Survival, Chronic myelogenous leukemia, Diagnostics
Russian
Об авторах

Жусупова Шербет Колдошовна, соискатель, заведующая отделе нием Онкогематологии Национального центра онкологии и гематологии, Бишкек, Кыргызская Республика
Полный текст

PDF (RUS)
Список литературы

1. American Cancer Society. Cancer Facts & Figures 2017. Atlanta: American Cancer Society; 2017.
2. Huang X, Cortes J, Kantarjian H. Estimations of the increasing prevalence and plateau prevalence of chronic myeloid
leukemia in the era of tyrosine kinase inhibitor therapy. Cancer. 2012; 118(12): 3123–3127.
3. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine
fluorescence and Giemsa staining. Nature. 1973; 243(5405): 290–293.
4. Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid
cells. Blood. 1993; 82(6): 1838–1847.
5. Okuda K, Matulonis U, Salgia R, Kanakura Y, Druker B, Griffin JD. Factor independence of human myeloid leukemia
cell lines is associated with increased phosphorylation of the proto-oncogene Raf-1. Exp Hematol. 1994; 22(11): 1111–1117.
6. Raitano AB, Halpern JR, Hambuch TM, Sawyers CL. The Bcr-Abl leukemia oncogene activates Jun kinase and requires
Jun for transformation. Proc Natl Acad Sci USA. 1995; 92(25): 11746–11750.
7. Sawyers CL, Callahan W, Witte ON. Dominant negative MYC blocks transformation by ABL oncogenes. Cell.1992; 70(6): 
901–910.
8. Shuai K, Halpern J, ten Hoeve J, Rao X, Sawyers CL. Constitutive activation of STAT5 by the BCR-ABL oncogene in
chronic myelogenous leukemia. Oncogene. 1996; 13(2): 247–254.
9. Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators
of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996; 183(3): 811–820.
10. Guru Murthy GS, Atallah E. Treatment-Free Remission in CML: the US Perspective.Curr Hematol Malig Rep. 2019
Feb;14(1):56-61. doi: 10.1007/s11899-019-0496-8.
11. Narlı Özdemir Z, Kılıçaslan NA, Yılmaz M, Eşkazan AE.Guidelines for the treatment of chronic myeloid leukemia from the
NCCN and ELN: differences and similarities.Int J Hematol. 2023 Jan;117(1):3-15. doi: 10.1007/s12185-022-03446-1.
12. Braun TP, Eide CA, Druker BJ.Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell. 2020 Apr
13;37(4):530-542. doi: 10.1016/j.ccell.2020.03.006.
Для цитирования

Жусупова Ш.К. Результаты лечения больных с хроническим миелоидным лейкозом в Кыргызской Республике с применением ингибиторов тирозинкиназ разных поколений. Научно-практический журнал «Здравоохранение Кыргызстана» 2025, № 3, с. 73-77. https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
English
About authors

Zhusupova Sherbet Koldoshovna, applicant, head of the Oncohematology Department of the National Center of Oncology and Hematology, Bishkek, Kyrgyz Republic
Full text

PDF (RUS)
References

1. American Cancer Society. Cancer Facts & Figures 2017. Atlanta: American Cancer Society; 2017.
2. Huang X, Cortes J, Kantarjian H. Estimations of the increasing prevalence and plateau prevalence of chronic myeloid
leukemia in the era of tyrosine kinase inhibitor therapy. Cancer. 2012; 118(12): 3123–3127.
3. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine
fluorescence and Giemsa staining. Nature. 1973; 243(5405): 290–293.
4. Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid
cells. Blood. 1993; 82(6): 1838–1847.
5. Okuda K, Matulonis U, Salgia R, Kanakura Y, Druker B, Griffin JD. Factor independence of human myeloid leukemia
cell lines is associated with increased phosphorylation of the proto-oncogene Raf-1. Exp Hematol. 1994; 22(11): 1111–1117.
6. Raitano AB, Halpern JR, Hambuch TM, Sawyers CL. The Bcr-Abl leukemia oncogene activates Jun kinase and requires
Jun for transformation. Proc Natl Acad Sci USA. 1995; 92(25): 11746–11750.
7. Sawyers CL, Callahan W, Witte ON. Dominant negative MYC blocks transformation by ABL oncogenes. Cell.1992; 70(6): 
901–910.
8. Shuai K, Halpern J, ten Hoeve J, Rao X, Sawyers CL. Constitutive activation of STAT5 by the BCR-ABL oncogene in
chronic myelogenous leukemia. Oncogene. 1996; 13(2): 247–254.
9. Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators
of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996; 183(3): 811–820.
10. Guru Murthy GS, Atallah E. Treatment-Free Remission in CML: the US Perspective.Curr Hematol Malig Rep. 2019
Feb;14(1):56-61. doi: 10.1007/s11899-019-0496-8.
11. Narlı Özdemir Z, Kılıçaslan NA, Yılmaz M, Eşkazan AE.Guidelines for the treatment of chronic myeloid leukemia from the
NCCN and ELN: differences and similarities.Int J Hematol. 2023 Jan;117(1):3-15. doi: 10.1007/s12185-022-03446-1.
12. Braun TP, Eide CA, Druker BJ.Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell. 2020 Apr
13;37(4):530-542. doi: 10.1016/j.ccell.2020.03.006.
For citation
 Zhusupova Sh.K. Results of treatment of patients with chro nic myeloid leukemia in the Kyrgyz Republic using tyrosine kinase inhibitors of different generations. Scientific practical journal “Health care of Kyrgyzstan” 2025, No.3, p. 73-77. https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
Kyrgyz
Авторлор жөнүндө

Жусупова Шербет Колдошовна, арыз ээси, Улуттук онкология жана гематология борборунун онкогематология бөлүмүнүн башчысы, Бишкек шаары, Кыргыз Республикасы
Шилтемелер

1. American Cancer Society. Cancer Facts & Figures 2017. Atlanta: American Cancer Society; 2017.
2. Huang X, Cortes J, Kantarjian H. Estimations of the increasing prevalence and plateau prevalence of chronic myeloid
leukemia in the era of tyrosine kinase inhibitor therapy. Cancer. 2012; 118(12): 3123–3127.
3. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine
fluorescence and Giemsa staining. Nature. 1973; 243(5405): 290–293.
4. Mandanas RA, Leibowitz DS, Gharehbaghi K, et al. Role of p21 RAS in p210 bcr-abl transformation of murine myeloid
cells. Blood. 1993; 82(6): 1838–1847.
5. Okuda K, Matulonis U, Salgia R, Kanakura Y, Druker B, Griffin JD. Factor independence of human myeloid leukemia
cell lines is associated with increased phosphorylation of the proto-oncogene Raf-1. Exp Hematol. 1994; 22(11): 1111–1117.
6. Raitano AB, Halpern JR, Hambuch TM, Sawyers CL. The Bcr-Abl leukemia oncogene activates Jun kinase and requires
Jun for transformation. Proc Natl Acad Sci USA. 1995; 92(25): 11746–11750.
7. Sawyers CL, Callahan W, Witte ON. Dominant negative MYC blocks transformation by ABL oncogenes. Cell.1992; 70(6): 
901–910.
8. Shuai K, Halpern J, ten Hoeve J, Rao X, Sawyers CL. Constitutive activation of STAT5 by the BCR-ABL oncogene in
chronic myelogenous leukemia. Oncogene. 1996; 13(2): 247–254.
9. Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators
of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 1996; 183(3): 811–820.
10. Guru Murthy GS, Atallah E. Treatment-Free Remission in CML: the US Perspective.Curr Hematol Malig Rep. 2019
Feb;14(1):56-61. doi: 10.1007/s11899-019-0496-8.
11. Narlı Özdemir Z, Kılıçaslan NA, Yılmaz M, Eşkazan AE.Guidelines for the treatment of chronic myeloid leukemia from the
NCCN and ELN: differences and similarities.Int J Hematol. 2023 Jan;117(1):3-15. doi: 10.1007/s12185-022-03446-1.
12. Braun TP, Eide CA, Druker BJ.Response and Resistance to BCR-ABL1-Targeted Therapies. Cancer Cell. 2020 Apr
13;37(4):530-542. doi: 10.1016/j.ccell.2020.03.006.
Цитата үчүн

Жусупова Ш.К. Кыргыз Республикасында өнөкөт миелолейкоз менен ооруган бейтаптарды ар кандай муундагы тирозинкиназа ингибиторлору менен дарылоонун жыйынтыктары. Кыргызстандын саламаттык сактоо
илимий-практикалык журналы 2025, № 3, б. 73-77. https://dx.doi.org/10.51350/zdravkg2025.3.9.10.73.77
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