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Items: 1 to 20 of 282

1.

All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib.

Cassuto O, Dufies M, Jacquel A, Robert G, Ginet C, Dubois A, Hamouda A, Puissant A, Luciano F, Karsenti JM, Legros L, Cassuto JP, Lenain P, Auberger P.

Oncotarget. 2012 Dec;3(12):1557-65.

2.

Efficacy of ponatinib against ABL tyrosine kinase inhibitor-resistant leukemia cells.

Okabe S, Tauchi T, Tanaka Y, Ohyashiki K.

Biochem Biophys Res Commun. 2013 Jun 7;435(3):506-11. doi: 10.1016/j.bbrc.2013.05.022. Epub 2013 May 14.

PMID:
23684619
3.

Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment.

Oaxaca DM, Yang-Reid SA, Ross JA, Rodriguez G, Staniswalis JG, Kirken RA.

Tumour Biol. 2016 Sep;37(9):12643-12654. Epub 2016 Jul 21.

4.

Tyrosine kinase inhibitor resistance in chronic myeloid leukemia cell lines: investigating resistance pathways.

Tang C, Schafranek L, Watkins DB, Parker WT, Moore S, Prime JA, White DL, Hughes TP.

Leuk Lymphoma. 2011 Nov;52(11):2139-47. doi: 10.3109/10428194.2011.591013. Epub 2011 Jun 30.

PMID:
21718141
5.

Cotreatment with vorinostat (suberoylanilide hydroxamic acid) enhances activity of dasatinib (BMS-354825) against imatinib mesylate-sensitive or imatinib mesylate-resistant chronic myelogenous leukemia cells.

Fiskus W, Pranpat M, Balasis M, Bali P, Estrella V, Kumaraswamy S, Rao R, Rocha K, Herger B, Lee F, Richon V, Bhalla K.

Clin Cancer Res. 2006 Oct 1;12(19):5869-78.

6.

HS-438, a new inhibitor of imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia.

Yun SM, Jung KH, Kim SJ, Fang Z, Son MK, Yan HH, Lee H, Kim J, Shin S, Hong S, Hong SS.

Cancer Lett. 2014 Jun 28;348(1-2):50-60. doi: 10.1016/j.canlet.2014.03.012. Epub 2014 Mar 18.

PMID:
24657654
7.

A molecular and biophysical comparison of macromolecular changes in imatinib-sensitive and imatinib-resistant K562 cells exposed to ponatinib.

Yandim MK, Ceylan C, Elmas E, Baran Y.

Tumour Biol. 2016 Feb;37(2):2365-78. doi: 10.1007/s13277-015-4015-9. Epub 2015 Sep 15.

PMID:
26373734
8.

Three novel patient-derived BCR/ABL mutants show different sensitivity to second and third generation tyrosine kinase inhibitors.

Redaelli S, Mologni L, Rostagno R, Piazza R, Magistroni V, Ceccon M, Viltadi M, Flynn D, Gambacorti-Passerini C.

Am J Hematol. 2012 Nov;87(11):E125-8. doi: 10.1002/ajh.23338. Epub 2012 Oct 9.

9.

Curcumin derivative C817 inhibits proliferation of imatinib-resistant chronic myeloid leukemia cells with wild-type or mutant Bcr-Abl in vitro.

Wu LX, Wu Y, Chen RJ, Liu Y, Huang LS, Lou LG, Zheng ZH, Chen YZ, Xu JH.

Acta Pharmacol Sin. 2014 Mar;35(3):401-9. doi: 10.1038/aps.2013.180. Epub 2014 Feb 3.

10.

Frequency of ABL gene mutations in chronic myeloid leukemia patients resistant to imatinib and results of treatment switch to second-generation tyrosine kinase inhibitors.

Marcé S, Zamora L, Cabezón M, Xicoy B, Boqué C, Fernández C, Grau J, Navarro JT, Fernández de Sevilla A, Ribera JM, Feliu E, Millá F; Grupo ICO de estudio de mutaciones de ABL en pacientes afectos de LMC..

Med Clin (Barc). 2013 Aug 4;141(3):95-9. doi: 10.1016/j.medcli.2012.10.028. Epub 2013 Feb 22.

PMID:
23433665
11.

Long-term outcome of patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors after imatinib failure is predicted by the in vitro sensitivity of BCR-ABL kinase domain mutations.

Jabbour E, Jones D, Kantarjian HM, O'Brien S, Tam C, Koller C, Burger JA, Borthakur G, Wierda WG, Cortes J.

Blood. 2009 Sep 3;114(10):2037-43. doi: 10.1182/blood-2009-01-197715. Epub 2009 Jun 30.

12.

Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis.

O'Hare T, Eide CA, Agarwal A, Adrian LT, Zabriskie MS, Mackenzie RJ, Latocha DH, Johnson KJ, You H, Luo J, Riddle SM, Marks BD, Vogel KW, Koop DR, Apgar J, Tyner JW, Deininger MW, Druker BJ.

Cancer Res. 2013 Jun 1;73(11):3356-70. doi: 10.1158/0008-5472.CAN-12-3904. Epub 2013 Apr 10.

13.

Combination of panobinostat with ponatinib synergistically overcomes imatinib-resistant CML cells.

Matsuda Y, Yamauchi T, Hosono N, Uzui K, Negoro E, Morinaga K, Nishi R, Yoshida A, Kimura S, Maekawa T, Ueda T.

Cancer Sci. 2016 Jul;107(7):1029-38. doi: 10.1111/cas.12965. Epub 2016 Jun 21.

14.

Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with nilotinib against BCR-ABL-positive leukemia cells involves the ABL kinase domain mutation.

Okabe S, Tauchi T, Tanaka Y, Kitahara T, Kimura S, Maekawa T, Ohyashiki K.

Cancer Biol Ther. 2014 Feb;15(2):207-15. doi: 10.4161/cbt.26725. Epub 2013 Nov 8.

15.

Overcoming CML acquired resistance by specific inhibition of Aurora A kinase in the KCL-22 cell model.

Yuan H, Wang Z, Zhang H, Roth M, Bhatia R, Chen WY.

Carcinogenesis. 2012 Feb;33(2):285-93. doi: 10.1093/carcin/bgr278. Epub 2011 Nov 24.

16.

Structural mechanism of the Pan-BCR-ABL inhibitor ponatinib (AP24534): lessons for overcoming kinase inhibitor resistance.

Zhou T, Commodore L, Huang WS, Wang Y, Thomas M, Keats J, Xu Q, Rivera VM, Shakespeare WC, Clackson T, Dalgarno DC, Zhu X.

Chem Biol Drug Des. 2011 Jan;77(1):1-11. doi: 10.1111/j.1747-0285.2010.01054.x. Epub 2010 Nov 30.

PMID:
21118377
17.

Ponatinib circumvents all types of imatinib resistance in chronic myelogenous leukemia cell lines.

Dufies M, Cassuto O, Jacquel A, Robert G, Auberger P.

Cell Cycle. 2013 Jun 1;12(11):1645-6. doi: 10.4161/cc.24982. Epub 2013 May 10. No abstract available.

PMID:
23673326
18.

MEK1/2 inhibitors sensitize Bcr/Abl+ human leukemia cells to the dual Abl/Src inhibitor BMS-354/825.

Nguyen TK, Rahmani M, Harada H, Dent P, Grant S.

Blood. 2007 May 1;109(9):4006-15. Epub 2007 Jan 11.

19.

Aberrant signalling by protein kinase CK2 in imatinib-resistant chronic myeloid leukaemia cells: biochemical evidence and therapeutic perspectives.

Borgo C, Cesaro L, Salizzato V, Ruzzene M, Massimino ML, Pinna LA, Donella-Deana A.

Mol Oncol. 2013 Dec;7(6):1103-15. doi: 10.1016/j.molonc.2013.08.006. Epub 2013 Aug 22.

20.

Sequential inhibitor therapy in CML: in vitro simulation elucidates the pattern of resistance mutations after second- and third-line treatment.

Bauer RC, Sänger J, Peschel C, Duyster J, von Bubnoff N.

Clin Cancer Res. 2013 Jun 1;19(11):2962-72. doi: 10.1158/1078-0432.CCR-13-0052. Epub 2013 Apr 2.

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