Кыргыз Республикасында өнөкөт миелолейкоз менен ооруган бейтаптарды ар кандай муундагы тирозинкиназа ингибиторлору менен дарылоонун жыйынтыктары

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

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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.

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

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

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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.

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

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.

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