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Vol. 11, Art. 21 (pp. 268-283)    |    2010       

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The apoptotic activity cells of bone marrow at patients chronic myelogenous leukemia during treatment with imatinib mesylate (glivec)

Kozlov A.V., Syasina T.V., Bessmeltsev S.S.*, Udalieva V.U.*, Zaritzkiy A., Yu.**

St-Petersburg Medical Academy of Postgraduate Studies, Russia;
*- Russian Research Institute of Hematology and Transfusiology;
**- St-Petersburg Pavlov State Medical University.

Brief summary

The article presents the results of studying of action of a preparation imatinib mesylate (glivec) on апоптотическую activity of cells of a bone marrow at patients chronic myelogenous leukemia. It is established that glivec in a dose 400mg. at patients with complete hematologic response, the complete cytogenetic and major cytogenetic response provides high activity apoptotic processes in bone marrow cells. As it is revealed that glivec leads to stabilisation of apoptosis in cells of bone marrow about 6 months of therapy.


Key words

apoptosis, imatinib mesylate (glivec), chronic myelogenous leukemia.

Reference list

1. Abdylkadirov K.M., Bessmelcev S.S., Rykavicin O.A. Hronicheskii mieloleikoz. – SPb: “Specialnaya Literatyra”, 1998.- 464 s.


2. Daley G.Q., van Etten R.A., Baltimore D. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science 1990;247:824-30.


3. Sattler M., Salgia R. Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABL. Cytokine Growth Factor Rev 1997; 8:63-79.


4. Kopnin B. P. Misheni deistviya onkogenov i opyholevih sypressorov: kluch k ponimaniu bazovih mehanizmov kancerogeneza// Biohimiya. – 2000 – T.65. – Vip. 1. – S. 5–33.


5. Vladimirskaya E. B. Apoptoz i ego rol v regylyacii kletochnogo ravnovesiya // Klinicheskaya laboratornaya diagnostika. – 2002. – №11. – S.25 – 32.


6. Sturm I., Bosanquet A. G., Hermann S., Gurner D., Dorken B., Daniel P. T. Mutation of p53 and consecutive selective drug resistance in B-CLL occurs as a consequence of prior DNAdamaging chemotherapy // Cell. Death Differ.—2003.—Vol.10, №4.—P. 477—484.


7. Vladimirskaya E.B. Mehanizmi apoptoza kletok krovi.// Laboratornaya medicina.- 2001. – T.121. - №4. – s. 47-54.


8. Gambacorti-Passerini C, le Coutre P, Mologni L, et al. Inhibition of the ABL kinase activity blocks the proliferation of BCR/ABL+ leukemic cells and induces apoptosis. //Blood Cells Mol Dis. — 1997. — Vol.23. — P. 380-394.


9. Baccarani M., Cortes G., at al: Chronic Myeloid Leukemia: An Update of Concepts and Management Recommendations of European LeukemiaNet.// J. Clin. Oncol.—2009.—V. 27. —P.6041-6051.


10. Baccarani M, Saglio G, Goldman J, et al: Evolving concepts in the management of chronic myeloid leukemia: Recommendations from an expert panel on behalf of the European LeukemiaNet. Blood 108:1809-1820, 2006


11. Zimina V.A. Osobennosti apoptoticheskoi aktivnosti kletok kostnogo mozga y bolnih nehodjkinskimi zlokachestvennimi limfomami: dis. kand. med. nayk. – SPb.2003. – S.61 – 62., 78 – 79.


12. Lasynskaya E.B., Kravcov V.D., Freidlin I.S. Vzaimodeistvie makrofagov i stvolovih krovetvornih kletok mishei in vitro // Citologiya. – 1989. – T.31, №3. – S. 359-363.


13. Tronov V.A., Konstantinov E.M. Reparaciya DNK i gibel pokoyashihsya limfocitov krovi cheloveka, indycirovannie perekisu vodoroda //Biohimiya. – 2000. – T.65 – Vip. 11. – S.1516 – 1524.


14. Mayerhofer M, Valent P, Sperr W.R, Griffin J.D, Sillaber C. BCR/ABL induces expression of vascular endothelial growth factor and its transcriptional activator, hypoxia inducible factor-1 alpha, through a pathway involving phosphoinositide 3-kinase and the mammalian target of rapamycin. // Blood. — 2002. — Vol.100(10). — P.3767-3775.


15. Parmar S, Smith J, Sassano A, Uddin S, Katsoulidis E, Majchrzak B, Kambhampati S, Eklund E.A, Tallman M.S., Fish E.N, Platanias L.C. Differential regulation of the p70 S6 kinase pathway by interferon alpha (IFNalpha) and imatinib mesylate (STI571) in chronic myelogenous leukemia cells.// Blood. — 2005. — Vol. 106(7). — P.2436-2443.


16. Vigneri P, Wang J.Y. Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase.// Nat. Med. — 2001. — Vol.7. — P.228- 234.


17. Osipova E. U., Astrelina T. A., Rymyanceva S. A., Vladimirskaya E. B., Storojakov G. I. Prognosticheskoe znachenie yrovnya spontannogo apoptoza limfoblastov v ocenke otveta na indykcionnyu terapiu ostrogo limfoblastnogo leikoza y detei// Gematol. i transfyziol. – 2003. – T.48, №1. – S.16-19.


18. Blagosklonny M. //Leukemia. – 2000. – Vol.14. – P.1502 – 1518.


19. Smith B.D., Bambach B. J., Vala M. S., Barder J.P., Eger C., Brodsky R. A., Burke P. J., Gore S. D., Jones R. J. Inhibited apoptosis and drug resistance in acute myeloid leukemia // Br. J. Haematol. — 1998. — Vol. 102. — №4. — P. 1042—1049.


20. Pospelova T.I., Loseva M.I., Kovinev I.B. i dr. Osnovi opyholevoi progressii gemoblastozov // Bul. SO RAMN. – 2004. – T. 112, № 2. – S. 73—76.


21. Anthoney D.A., Mc Ilwrath A.J., Gallagher W.M., Edlin A.R. M., Brown R. Microsatellite Instability, Apoptosis and Loss of h53 Function in Drug-resistant Tumor Cells. // Cancer Res. 1996. — Vol.56. — N.6 — P.1374-1381.


22. Bible K.C. et al. // Clin. Cancer Research. —2000.—V.6. —P. 661–670.


23. Korystov Y.N. et al. // Eur. J. Pharmacol.—2004.—V. 493, N 13. —P. 57—64.


24. Reed J.C. Bcl-2 family proteins: regulators of apoptosis and chemoresistance in hematologic malignancies // Seminars in Hematology.—1997.—V. 34.—№ 4.—P.9—19.


25. Karen S. Ballard, Howard D., Homesley, Charles Hodson, Cary A. Presant, James Rutledge, Allan Hallquist, Mathieu Perree. Endometrial carcinoma in vitro chemosensitivity testing of single and combination chemotherapy regimens using the novel microculture kinetic apoptosis assay: implications for endometrisl cancer treatment.// J. Gynecol. Oncol. – 2010. - 21(1) 45-49.


26. Kravtsov VD, Priego V, Reilly GJ, Sethi H, Cooke J, Smith W, et al. Chemotherapy of myeloid leukemia directed by a microculture kinetic (MiCK) assay for apoptosis; The 42nd American Society of Hematology Meeting; 2000. Abstract 3129.


27. Barnes K, Mcintosh E, Whetton A.D, Daley G.Q, Bentley J, Baldwin S.A. Chronic myeloidleukaemia: an investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation.// Oncogene.—2005.—Vol.24,№20.—PP. 3257-3267.


28. Cullinane C, Dorow D.S, Kansara M, Conus N, Binns D, Hicks R.J, Ashman L.K, McArthurG.A, Thomas D.M. An in vivo tumor model exploiting metabolic response as a biomarker for targeted drug development.// Cancer Res.—2005.—Vol.65, №21.—PP. 9633-9636.


29. Geay J.F, Buet D, Zhang Y, Foudi A, Jarrier P, Berthebaud M, Turhan A.G, Vainchenker W, Louache F. p210BCR-ABL inhibits SDF-1 chemotactic response via alteration of CXCR4 signaling and down-regulation of CXCR4 expression.// Cancer Res.—2005.—Vol.65, №7.— P. 2676-2683.


30. Kantarjian H, Talpaz M, O'Brien S. Dose escalation of imatinib mesylate can overcome resistance to standard-dose therapy in patients with chronic myelogenous leukemia..- Blood.- 2003.-Vol. 101.PP.473-475.


31. Barnes D.J, Melo J.V. Primitive, quiescent and difficult to kill: the role of non- proliferating stem cells in chronic myeloid leukemia.// Cell Cycle.—2006.— Vol.5, №24.—P. 2862-2866.


32. Graham S.M, Jorgensen H.G, Allan E, Pearson C, Alcorn M.J, Richmond L, Holyoake T.L. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloidleukemia are insensitive to STI571 in vitro.//Blood.—2002. —Vol.99, №l.—P. 319-325.


33. Copland M, Jorgensen H.G, Holyoake T.L. Evolving molecular therapy for chronic myeloid leukaemia—are we on target?//Hematology.—2005.—Vol.10, №5.—P. 349-359.


34. Deininger M.W., Druker B.J. Specific targeted therapy of chronic myelogenous leukemia with imatinib.//Pharmacol. Rev.—2003.—Vol.55, №3.—P. 401-423.