The study of resistant mechanisms and reversal in an imatinib resistant Ph+ acute lymphoblastic leukemia cell line

Leukemia Research

Volumn 36, Issue 4, 2012, Pages 509-513

  Xing, Hongyun ^a,b   Yang, Xi ^a   Liu, Ting ^a   Lin, Juan ^a   Chen, Xiaoyi ^a   Gong, Yuping ^a  

^a SICHUAN UNIVERSITY   (China)

^b SOUTHWEST MEDICAL UNIVERSITY   (China)

Author keywords

Imatinib resistance; MTOR signaling pathway; Ph+ acute lymphoblastic leukemia; Proteasome inhibitor; Tyrosine kinase inhibitor

Indexed keywords

ABELSON KINASE; BCR ABL PROTEIN; BORTEZOMIB; DASATINIB; IMATINIB; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INITIATION FACTOR 4E BINDING PROTEIN 1; MAMMALIAN TARGET OF RAPAMYCIN; MITOGEN ACTIVATED PROTEIN KINASE; MULTIDRUG RESISTANCE PROTEIN 1; NILOTINIB; PHOSPHATIDYLINOSITOL 3 KINASE; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE; PROTEASOME; PROTEIN KINASE B; RAF PROTEIN; RAPAMYCIN; RAS PROTEIN; S6 KINASE; STAT PROTEIN; STRESS ACTIVATED PROTEIN KINASE; UBIQUITIN;

ACUTE LYMPHOBLASTIC LEUKEMIA; ARTICLE; BCR ABL1 GENE; CONTROLLED STUDY; CORRELATION ANALYSIS; DRUG POTENTIATION; ENZYME PHOSPHORYLATION; FUSION GENE; GENE; GENE MUTATION; GENE OVEREXPRESSION; HOCT1 GENE; HUMAN; HUMAN CELL; IN VITRO STUDY; LEUKEMIA CELL LINE; MDR1 GENE; PHILADELPHIA CHROMOSOME POSITIVE CELL; PRIORITY JOURNAL; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; UPREGULATION;

ANTINEOPLASTIC AGENTS; CELL LINE, TUMOR; CELL PROLIFERATION; DRUG RESISTANCE, NEOPLASM; FUSION PROTEINS, BCR-ABL; GENES, MDR; HUMANS; IMMUNOBLOTTING; MUTATION; PIPERAZINES; PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA; PYRIMIDINES; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION;

EID: 84862785354     PISSN: 01452126     EISSN: 18735835     Source Type: Journal    
DOI: 10.1016/j.leukres.2011.12.018     Document Type: Article

References (34)

1. Moorman A.V., Harrison C.J., Buck G.A., et al. Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALL-XII/Eastern Cooperative Oncology Group (ECOG) 2993 trial. Blood 2007, 109:3189-3197.
2. Ottmann O.G., Wassmann B. Treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia. Hematol Am Soc Hematol Educ Program 2005, 1:118-122.
3. Druker B.J. Imatinib as a paradigm of targeted therapies. Adv Cancer Res 2004, 91:1-30.
4. Nimmanapalli R., Bhalla K. Mechanisms of resistance to imatinib mesylate in BCR-ABL1-positive leukemias. Curr Opin Oncol 2002, 14:616-620.
5. Ottmann O.G., Wassmann B., Pfeifer H., et al. Imatinib compared with chemotherapy as front-line treatment of elderly patients with Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL). Cancer 2007, 109:2068-2076.
6. Gorre M.E., Mohammed M., Ellwood K., et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL1 gene mutation or amplification. Science 2001, 293:876-880.
7. Shah N.P., Nicoll J.M., Nagar B., et al. Multiple BCR-ABL1 kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell 2002, 2:117-125.
8. Thomas J., Wang L., Clark R.E., Pirmohamed M. Active transport of imatinib into and out of cells: implications for drug resistance. Blood 2004, 104:3739-3745.
9. White D.L., Saunders V.A., Dang P., et al. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood 2007, 110:4064-4072.
10. Ozaki K., Kosugi M., Baba N., et al. Blockade of the ERK or PI3K-Akt signaling pathway enhances the cytotoxicity of histone deacetylase inhibitors in tumor cells resistant to gefitinib or imatinib. Biochem Biophys Res Commun 2010, 391:1610-1615.
11. Aceves-Luquero C.I., Agarwal A., Callejas-Valera J.L., et al. ERK2, but not ERK1, mediates acquired and denovo resistance to imatinib mesylate: implication for CML therapy. PLoS One 2009, 4:e6124.
12. Chu S., Holtz M., Gupta M., Bhatia R. BCR/ABL kinase inhibition by imatinib mesylate enhances MAP kinase activity in chronic myelogenous leukemia CD34+ cells. Blood 2004, 103:3167-3174.
13. Coppo P., Flamant S., De Mas V., et al. BCR-ABL1 activates STAT3 via JAK and MEK pathways in human cells. Br J Haematol 2006, 134:171-179.
14. Dai Y., Rahmani M., Corey S.J., et al. A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2. J Biol Chem 2004, 279:34227-34239.
15. Pfeifer H., Wassmann B., Pavlova A., et al. Kinase domain mutations of BCR-ABL1 frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL). Blood 2007, 110:727-734.
16. Le Coutre P., Tassi E., Varella-Garcia M., et al. Induction of resistance to the Abelson inhibitor STI571 in human leukemic cells through gene amplification. Blood 2000, 95:1758-1766.
17. Mahon F.X., Belloc F., Lagarde V., et al. MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Blood 2003, 101:2368-2373.
18. Crossman L.C., Druker B.J., Deininger M.W., et al. hOCT 1 and resistance to imatinib. Blood 2005, 106:1133-1134. author reply 1134.
19. Soverini S., Colarossi S., Gnani A., et al. Resistance to dasatinib in Philadelphia-positive leukemia patients and the presence or the selection of mutations at residues 315 and 317 in the BCR-ABL1 kinase domain. Haematologica 2007, 92:401-404.
20. Jones D., Thomas D., Yin C.C., et al. Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL1 kinase inhibitors. Cancer 2008, 113:985-994.
21. Pfeifer H., Wystub S., Wassmann B., et al. Minimal residual disease and mutational status prior to and after SCT for patients with philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL). Blood 2008, 112:261. [abstract].
22. Deininger M.W., Goldman J.M., Melo J.V. The molecular biology of chronic myeloid leukemia. Blood 2000, 96:3343-3356.
23. O'Hare T., Walters D.K., Stoffregen E.P., et al. In vitro activity of BCR-ABL1 inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. Cancer Res 2005, 65:4500-4505.
24. Shah N.P., Tran C., Lee F.Y., et al. Overriding imatinib resistance with a novel AB kinase inhibitor. Science 2004, 305:399-401.
25. Kantarjian H., Giles F., Bhalla K., et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med 2006, 354:2542-2551.
26. Rix U., Hantschel O., Du rnberger M., et al. Chemical proteomic profiles of the BCR-ABL1 inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets. Blood 2007, 110:4055-4063.
27. Panwalkar A., Verstovsek S., Giles F.J. Mammalian target of rapamycin inhibition as therapy for hematologic malignancies. Cancer 2004, 100:657-666.
28. Hirase C., Maeda Y., Takai S., Kanamaru A. Hypersensitivity of Ph-positive lymphoid cell lines to rapamycin: possible clinical application of mTOR inhibitor. Leuk Res 2008, 33:450-459.
29. Saunders R., Metcalfe M.S., Nicholson M.L. Rapamycin in transplantation: a review of the evidence. Kidney Int 2001, 59:3-16.
30. Calne R., Collier D.S., Thiru S., et al. Rapamycin for immunosuppression in organ allografting. Lancet 1989, 2:227-230.
31. Schreibers S. Chemistry and biology of the immunophilins and their immunosuppressive ligands. Science 1991, 251:283-287.
32. Chen Y., Chen H., Molnar-Kimber K.L., et al. A putative sirolimus (rapamycin) effector protein. Biochem Biophys Res Commun 1994, 203:1-7.
33. Brown E., Albers M.W., Schreiber S.L., et al. A mammalian protein targeted by G1-arresting rapamycin-receptor complex. Nature 1994, 369:756-758.
34. Takeuchi J., Kyo T., Ohno R., et al. Induction therapy by frequent administration of doxorubicin with four other drugs, followed by intensive consolidation and maintenance therapy for adult acute lym phoblastic leukemia: the JALSG-ALL93 study. Leukemia 2002, 16:1259-1266.