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Items: 1 to 20 of 127

1.

Cytokine-dependent imatinib resistance in mouse BCR-ABL+, Arf-null lymphoblastic leukemia.

Williams RT, den Besten W, Sherr CJ.

Genes Dev. 2007 Sep 15;21(18):2283-7. Epub 2007 Aug 30.

2.

Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.

Williams RT, Roussel MF, Sherr CJ.

Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6688-93. Epub 2006 Apr 17.

3.

Chemotherapeutic agents circumvent emergence of dasatinib-resistant BCR-ABL kinase mutations in a precise mouse model of Philadelphia chromosome-positive acute lymphoblastic leukemia.

Boulos N, Mulder HL, Calabrese CR, Morrison JB, Rehg JE, Relling MV, Sherr CJ, Williams RT.

Blood. 2011 Mar 31;117(13):3585-95. doi: 10.1182/blood-2010-08-301267. Epub 2011 Jan 24.

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Imatinib resistant BCR-ABL1 mutations at relapse in children with Ph+ ALL: a Children's Oncology Group (COG) study.

Chang BH, Willis SG, Stork L, Hunger SP, Carroll WL, Camitta BM, Winick NJ, Druker BJ, Schultz KR.

Br J Haematol. 2012 May;157(4):507-10. doi: 10.1111/j.1365-2141.2012.09039.x. Epub 2012 Feb 2. No abstract available.

7.

PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia.

Wolff NC, Veach DR, Tong WP, Bornmann WG, Clarkson B, Ilaria RL Jr.

Blood. 2005 May 15;105(10):3995-4003. Epub 2005 Jan 18.

8.

Drug resistance and BCR-ABL kinase domain mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia from the imatinib to the second-generation tyrosine kinase inhibitor era: The main changes are in the type of mutations, but not in the frequency of mutation involvement.

Soverini S, De Benedittis C, Papayannidis C, Paolini S, Venturi C, Iacobucci I, Luppi M, Bresciani P, Salvucci M, Russo D, Sica S, Orlandi E, Intermesoli T, Gozzini A, Bonifacio M, Rigolin GM, Pane F, Baccarani M, Cavo M, Martinelli G.

Cancer. 2014 Apr 1;120(7):1002-9. doi: 10.1002/cncr.28522. Epub 2013 Dec 30.

9.

High-risk acute lymphoblastic leukemia cells with bcr-abl and INK4A/ARF mutations retain susceptibility to alloreactive T cells.

Young FM, Campbell A, Emo KL, Jansson J, Wang PY, Jordan CT, Mullen CA.

Biol Blood Marrow Transplant. 2008 Jun;14(6):622-30. doi: 10.1016/j.bbmt.2008.02.015. Epub 2008 Apr 14.

10.

Prevalence and dynamics of bcr-abl kinase domain mutations during imatinib treatment differ in patients with newly diagnosed and recurrent bcr-abl positive acute lymphoblastic leukemia.

Pfeifer H, Lange T, Wystub S, Wassmann B, Maier J, Binckebanck A, Giagounidis A, Stelljes M, Schmalzing M, Dührsen U, Wunderle L, Serve H, Brück P, Schmidt A, Hoelzer D, Ottmann OG.

Leukemia. 2012 Jul;26(7):1475-81. doi: 10.1038/leu.2012.5. Epub 2012 Jan 9.

PMID:
22230800
11.

Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice.

Hu Y, Swerdlow S, Duffy TM, Weinmann R, Lee FY, Li S.

Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16870-5. Epub 2006 Oct 31.

12.

Low BCR-ABL expression levels in hematopoietic precursor cells enable persistence of chronic myeloid leukemia under imatinib.

Kumari A, Brendel C, Hochhaus A, Neubauer A, Burchert A.

Blood. 2012 Jan 12;119(2):530-9. doi: 10.1182/blood-2010-08-303495. Epub 2011 Nov 18.

13.

Roots of imatinib resistance: a question of self-renewal?

Burchert A.

Drug Resist Updat. 2007 Aug-Oct;10(4-5):152-61. Epub 2007 Aug 1. Review.

PMID:
17683977
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Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era.

Iqbal Z, Aleem A, Iqbal M, Naqvi MI, Gill A, Taj AS, Qayyum A, ur-Rehman N, Khalid AM, Shah IH, Khalid M, Haq R, Khan M, Baig SM, Jamil A, Abbas MN, Absar M, Mahmood A, Rasool M, Akhtar T.

PLoS One. 2013;8(2):e55717. doi: 10.1371/journal.pone.0055717. Epub 2013 Feb 8.

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Increasing the BCR-ABL expression levels and/or the occurrence of ABL point mutations does not always predict resistance to Imatinib Mesylate in BCR-ABL positive acute lymphoblastic leukemia.

Grammatico S, Elia L, Peluso AL, Pedace L, Matarazzo M, Vitale A, Rago A, Pane F, Foà R, Cimino G.

Leuk Res. 2009 Jul;33(7):e73-4. doi: 10.1016/j.leukres.2008.11.009. Epub 2008 Dec 23. No abstract available.

PMID:
19108887
18.

PLK1 inhibitors synergistically potentiate HDAC inhibitor lethality in imatinib mesylate-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivo.

Dasmahapatra G, Patel H, Nguyen T, Attkisson E, Grant S.

Clin Cancer Res. 2013 Jan 15;19(2):404-14. doi: 10.1158/1078-0432.CCR-12-2799. Epub 2012 Nov 30.

19.

Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.

Hofmann WK, Komor M, Wassmann B, Jones LC, Gschaidmeier H, Hoelzer D, Koeffler HP, Ottmann OG.

Blood. 2003 Jul 15;102(2):659-61. Epub 2003 Mar 27.

20.

Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL).

Pfeifer H, Wassmann B, Pavlova A, Wunderle L, Oldenburg J, Binckebanck A, Lange T, Hochhaus A, Wystub S, Brück P, Hoelzer D, Ottmann OG.

Blood. 2007 Jul 15;110(2):727-34. Epub 2007 Apr 3.

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