References

1. George P, Bali P, Annavarapu S, et al. Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3. Blood 2005; 105:1768-1776.

2. Schulte TW, Neckers LM. The benzoquinone ansamycin 17-allylamino-17-demethoxy-geldanamycin binds to HSP90 and shares important biologic activities with geldanamy-cin. Cancer Chemother Pharmacol 1998; 42:273-279.

3. Nimmanapalli R, O'Bryan E, Bhalla K. Geldanamycin and its analogue 17-allylamino-17-demethoxygeldanamycin lowers Bcr-Abl levels and induces apoptosis and differentiation of Bcr- Abl-positive human leukemic blasts. Cancer Res 2001; 61:1799-1804.

4. Nimmanapalli R, O'Bryan E, Huang M, et al. Molecular Characterization and Sensitivity of STI-571 (Imatinib Mesylate, Gleevec)-resistant, Bcr-Abl-positive, Human Acute Leukemia Cells to SRC Kinase Inhibitor PD180970 and 17-Allylamino-17- demethoxygelda-namycin. Cancer Res 2002; 62:5761-5769.

5. Gorre ME, Ellwood-Yen K, Chiosis G, Rosen N, Sawyers CL. BCR-ABL point mutants isolated from patients with imatinib mesylate- resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90. Blood 2002; 100:3041-3044.

6. Hochhaus A, Kreil S, Corbin AS, et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia 2002; 16:2190-2196.

7. Radujkovic A, Schad M, Topaly J, et al. Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL - Inhibition of P-glycoprotein function by 17-AAG. Leukemia 2005; 19:1198-1206.

8. Rahmani M, Reese E, Dai Y, et al. Cotreatment with suberanoylanilide hydroxamic acid and 17-allylamino 17-demethoxygeldanamycin synergistically induces apoptosis in

Bcr-Abl+ Cells sensitive and resistant to STI571 (imatinib mesylate) in association with down-regulation of Bcr-Abl, abrogation of signal transducer and activator of transcription 5 activity, and Bax conformational change. Mol Pharmacol 2005; 67:1166-1176.

9. Banerji U, O'Donnell A, Scurr M, et al. Phase I pharmacokinetic and pharmacodynamic study of 17-allylamino, 17-demethoxygeldanamycin in patients with advanced malignancies. J Clin Oncol 2005; 23:4152-4161.

10. Svingen PA, Tefferi A, Kottke TJ, et al. Effects of the bcr/abl kinase inhibitors AG957 and NSC 680410 on chronic myelogenous leukemia cells in vitro. Clin Cancer Res 2000; 6:237-249.

11. Chandra J, Hackbarth J, Le S, et al. Involvement of reactive oxygen species in adaphos-tin-induced cytotoxicity in human leukemia cells. Blood 2003; 102:4512-4519.

12. Mow BM, Chandra J, Svingen PA, et al. Effects of the Bcr/abl kinase inhibitors STI571 and adaphostin (NSC 680410) on chronic myelogenous leukemia cells in vitro. Blood 2002; 99:664-671.

13. Chandra J, Tracy J, Loegering D, et al. Adaphostin-induced oxidative stress overcomes BCR/ABL mutation-dependent and -independent imatinib resistance. Blood 2006; 107:2501-2506.

14. Kaur G, Sausville EA. Altered physical state of p210bcr-abl in tyrphostin AG957-treated K562 cells. Anticancer Drugs 1996; 7:815-824.

15. Sattler M, Verma S, Shrikhande G, et al. The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells. J Biol Chem 2000; 275:2427324278.

16. Dasmahapatra G, Nguyen TK, Dent P, Grant S. Adaphostin and bortezomib induce oxi-dative injury and apoptosis in imatinib mesylate-resistant hematopoietic cells expressing mutant forms of Bcr/Abl. Leuk Res 2006.

17. Karp JE, Lancet JE, Kaufmann SH, et al. Clinical and biologic activity of the farnesyl-transferase inhibitor R115777 in adults with refractory and relapsed acute leukemias: a phase 1 clinical-laboratory correlative trial. Blood 2001; 97:3361-3369.

18. Peters DG, Hoover RR, Gerlach MJ, et al. Activity of the farnesyl protein transferase inhibitor SCH66336 against BCR/ABL-induced murine leukemia and primary cells from patients with chronic myeloid leukemia. Blood 2001; 97:1404-1412.

19. Cortes J, AlBitar M, Thomas D, et al. Efficacy of the farnesyl transferase inhibitor R115777 in chronic myeloid leukemia and other hematologic malignancies. Blood 2003; 101:1692-1697.

20. Hoover RR, Mahon FX, Melo JV, Daley GQ. Overcoming STI571 resistance with the far-nesyl transferase inhibitor SCH66336. Blood 2002; 100:1068-1071.

21. Borthakur G, Kantarjian H, Daley G, et al. Pilot study of lonafarnib, a farnesyl transferase inhibitor, in patients with chronic myeloid leukemia in the chronic or accelerated phase that is resistant or refractory to imatinib therapy. Cancer 2006; 106:346-352.

22. Jorgensen HG, Allan EK, Graham SM, et al. Lonafarnib reduces the resistance of primitive quiescent CML cells to imatinib mesylate in vitro. Leukemia. 2005; 19:1184-1191.

23. Kuroda J, Kimura S, Segawa H, et al. The third-generation bisphosphonate zoledronate synergistically augments the anti-Ph+ leukemia activity of imatinib mesylate. Blood 2003; 102:2229-2235.

24. Chuah C, Barnes DJ, Kwok M, et al. Zoledronate inhibits proliferation and induces apop-tosis of imatinib-resistant chronic myeloid leukaemia cells. Leukemia 2005; 19:18961904.

25. Segawa H, Kimura S, Kuroda J, et al. Zoledronate synergises with imatinib mesylate to inhibit Ph primary leukaemic cell growth. Br J Haematol 2005; 130:558-560.

26. Kang CD, Yoo SD, Hwang BW, et al. The inhibition of ERK/MAPK not the activation of JNK/SAPK is primarily required to induce apoptosis in chronic myelogenous leukemic K562 cells. Leuk Res 2000; 24:527-534.

27. Yu C, Krystal G, Varticovksi L, et al. Pharmacologic mitogen-activated protein/extracellular signal-regulated kinase kinase/mitogen-activated protein kinase inhibitors interact synergistically with STI571 to induce apoptosis in Bcr/Abl-expressing human leukemia cells. Cancer Res 2002; 62:188-199.

28. 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.

29. Yu C, Dasmahapatra G, Dent P, Grant S. Synergistic interactions between MEK1/2 and histone deacetylase inhibitors in BCR/ABL+ human leukemia cells. Leukemia 2005; 19:1579-1589.

30. Skorski T, Kanakaraj P, Nieborowska-Skorska M, et al. Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome-positive cells. Blood 1995; 86:726 - 736.

31. Marley SB, Lewis JL, Schneider H, Rudd CE, Gordon MY. Phosphatidylinositol-3 kinase inhibitors reproduce the selective antiproliferative effects of imatinib on chronic myeloid leukaemia progenitor cells. Br J Haematol 2004; 125:500-511.

32. Klejman A, Rushen L, Morrione A, Slupianek A, Skorski T. Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571. Oncogene 2002; 21: 5868-5876.

33. Yaguchi S, Fukui Y, Koshimizu I, et al. Antitumor activity of ZSTK474, a new phospha-tidylinositol 3-kinase inhibitor. J Natl Cancer Inst 2006; 98:545-556.

34. Walker EH, Pacold ME, Perisic O, et al. Structural determinants of phosphoinositide 3-kinase inhibition by wortmannin, LY294002, quercetin, myricetin, and staurosporine. Mol Cell 2000; 6:909-919.

35. Ly C, Arechiga AF, Melo JV, Walsh CM, Ong ST. Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycin. Cancer Res 2003; 63:5716-5722.

36. Dengler J, von Bubnoff N, Decker T, Peschel C, Duyster J. Combination of imatinib with rapamycin or RAD001 acts synergistically only in Bcr-Abl-positive cells with moderate resistance to imatinib. Leukemia 2005; 19:1835-1838.

37. Kim JH, Chu SC, Gramlich JL, et al. Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen species. Blood 2005; 105:17171723.

38. Mohi MG, Boulton C, Gu TL, et al. Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs. Proc Natl Acad Sci USA 2004; 101:3130-3135.

39. Mayerhofer M, Aichberger KJ, Florian S, et al. Identification of mTOR as a novel bifunc-tional target in chronic myeloid leukemia: dissection of growth-inhibitory and VEGF-suppressive effects of rapamycin in leukemic cells. FASEB J 2005; 19:960-962.

40. La Rosee P, Johnson K, Corbin AS, et al. In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl-positive cell lines. Blood 2004; 103:208-215.

41. Burchert A, Wang Y, Cai D, et al. Compensatory PI3-kinase/Akt/mTor activation regulates imatinib resistance development. Leukemia 2005; 19:1774-1782.

42. Nimmanapalli R, Fuino L, Stobaugh C, Richon V, Bhalla K. Cotreatment with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced apoptosis of Bcr-Abl-positive human acute leukemia cells. Blood 2003; 101:3236-3239.

43. Nimmanapalli R, Fuino L, Bali P, et al. Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apop-tosis of imatinib mesylate-sensitive or -refractory chronic myelogenous leukemia-blast crisis cells. Cancer Res 2003; 63:5126-5135.

44. Yu C, Rahmani M, Almenara J, et al. Histone deacetylase inhibitors promote STI571-mediated apoptosis in STI571-sensitive and -resistant Bcr/Abl+ human myeloid leukemia cells. Cancer Res 2003; 63:2118-2126.

45. Morotti A, Cilloni D, Messa F, et al. Valproate enhances imatinib-induced growth arrest and apoptosis in chronic myeloid leukemia cells. Cancer 2006; 106:1188-1196.

46. Yu C, Rahmani M, Conrad D, et al. The proteasome inhibitor bortezomib interacts syner-gistically with histone deacetylase inhibitors to induce apoptosis in Bcr/Abl+ cells sensitive and resistant to STI571. Blood 2003; 102:3765-3774.

47. Gatto S, Scappini B, Pham L, et al. The proteasome inhibitor PS-341 inhibits growth and induces apoptosis in Bcr/Abl-positive cell lines sensitive and resistant to imatinib mesylate. Haematologica 2003; 88:853-863.

48. Dai Y, Rahmani M, Pei XY, Dent P, Grant S. Bortezomib and flavopiridol interact syner-gistically to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate through both Bcr/Abl-dependent and -independent mechanisms. Blood 2004; 104:509-518.

49. Yu C, Krystal G, Dent P, Grant S. Flavopiridol potentiates STI571-induced mitochondrial damage and apoptosis in BCR-ABL-positive human leukemia cells. Clin Cancer Res 2002; 8:2976-2984.

50. Grant S, Karp JE, Koc ON, et al. Phase I Study of Flavopiridol in Combination with Imatinib Mesylate (STI571, Gleevec) in Bcr/Abl+ Hematological Malignancies [abstract]. Blood 2005; 106:1102.

51. Issa JP, Garcia-Manero G, Giles FJ, et al. Phase 1 study of low-dose prolonged exposure schedules of the hypomethylating agent 5-aza-2'-deoxycytidine (decitabine) in hemato-poietic malignancies. Blood 2004; 103:1635-1640.

52. Kantarjian HM, O'Brien S, Cortes J, et al. Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia. Cancer 2003; 98:522-528.

53. Puccetti E, Guller S, Orleth A, et al. BCR-ABL mediates arsenic trioxide-induced apoptosis independently of its aberrant kinase activity. Cancer Res 2000; 60:3409-3413.

54. Perkins C, Kim CN, Fang G, Bhalla KN. Arsenic induces apoptosis of multidrug-resist-ant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L). Blood 2000; 95:1014-1022.

55. Du Y, Wang K, Fang H, et al. Coordination of intrinsic, extrinsic, and endoplasmic reti-culum-mediated apoptosis by imatinib mesylate combined with arsenic trioxide in chronic myeloid leukemia. Blood 2006; 107:1582-1590.

56. Nimmanapalli R, Bali P, O'Bryan E, et al. Arsenic trioxide inhibits translation of mRNA of bcr-abl, resulting in attenuation of Bcr-Abl levels and apoptosis of human leukemia cells. Cancer Res. 2003; 63:7950 - 7958.

57. La Rosee P, Shen L, Stoffregen EP, Deininger M, Druker BJ. No correlation between the proliferative status of Bcr-Abl positive cell lines and the proapoptotic activity of imatinib mesylate (Gleevec/Glivec). Hematol J 2003; 4:413-419.

Was this article helpful?

0 0
10 Ways To Fight Off Cancer

10 Ways To Fight Off Cancer

Learning About 10 Ways Fight Off Cancer Can Have Amazing Benefits For Your Life The Best Tips On How To Keep This Killer At Bay Discovering that you or a loved one has cancer can be utterly terrifying. All the same, once you comprehend the causes of cancer and learn how to reverse those causes, you or your loved one may have more than a fighting chance of beating out cancer.

Get My Free Ebook


Post a comment