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Items: 1 to 20 of 94

1.

Retention of CD34+ CML stem/progenitor cells during imatinib treatment and rapid decline after treatment with second-generation BCR-ABL inhibitors.

Minami Y, Abe A, Minami M, Kitamura K, Hiraga J, Mizuno S, Ymamoto K, Sawa M, Inagaki Y, Miyamura K, Naoe T.

Leukemia. 2012 Sep;26(9):2142-3. doi: 10.1038/leu.2012.73. No abstract available.

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Evaluation of residual CD34(+) Ph(+) progenitor cells in chronic myeloid leukemia patients who have complete cytogenetic response during first-line nilotinib therapy.

Defina M, Ippoliti M, Gozzetti A, Abruzzese E, Castagnetti F, Crupi R, Tiribelli M, Breccia M, Salvucci M, Aprile L, Baratè C, Gozzini A, Rosti G, Lauria F, Bocchia M.

Cancer. 2012 Nov 1;118(21):5265-9. doi: 10.1002/cncr.27506.

4.

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.

Corbin AS, Agarwal A, Loriaux M, Cortes J, Deininger MW, Druker BJ.

J Clin Invest. 2011 Jan;121(1):396-409. doi: 10.1172/JCI35721. Erratum in: J Clin Invest. 2011 Mar 1;121(3):1222.

5.

Effect of imatinib mesylate on chronic myelogenous leukemia hematopoietic progenitor cells.

Holtz MS, Bhatia R.

Leuk Lymphoma. 2004 Feb;45(2):237-45. Review.

PMID:
15101707
6.

Chronic myeloid leukemia stem cells possess multiple unique features of resistance to BCR-ABL targeted therapies.

Jiang X, Zhao Y, Smith C, Gasparetto M, Turhan A, Eaves A, Eaves C.

Leukemia. 2007 May;21(5):926-35.

PMID:
17330101
7.

Targeting chronic myeloid leukemia stem cells.

Helgason GV, Young GA, Holyoake TL.

Curr Hematol Malig Rep. 2010 Apr;5(2):81-7. doi: 10.1007/s11899-010-0043-0. Review.

PMID:
20425400
8.

Persistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatment.

Chu S, McDonald T, Lin A, Chakraborty S, Huang Q, Snyder DS, Bhatia R.

Blood. 2011 Nov 17;118(20):5565-72. doi: 10.1182/blood-2010-12-327437.

9.

Apoptosis in chronic myeloid leukemia cells transiently treated with imatinib or dasatinib is caused by residual BCR-ABL kinase inhibition.

Simara P, Stejskal S, Koutna I, Potesil D, Tesarova L, Potesilova M, Zdrahal Z, Mayer J.

Am J Hematol. 2013 May;88(5):385-93. doi: 10.1002/ajh.23419.

10.

Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment.

Bhatia R, Holtz M, Niu N, Gray R, Snyder DS, Sawyers CL, Arber DA, Slovak ML, Forman SJ.

Blood. 2003 Jun 15;101(12):4701-7.

11.

Properties of CD34+ CML stem/progenitor cells that correlate with different clinical responses to imatinib mesylate.

Jiang X, Forrest D, Nicolini F, Turhan A, Guilhot J, Yip C, Holyoake T, Jorgensen H, Lambie K, Saw KM, Pang E, Vukovic R, Lehn P, Ringrose A, Yu M, Brinkman RR, Smith C, Eaves A, Eaves C.

Blood. 2010 Sep 23;116(12):2112-21. doi: 10.1182/blood-2009-05-222471.

13.

Double minutes containing amplified bcr-abl fusion gene in a case of chronic myeloid leukemia treated by imatinib.

Morel F, Bris MJ, Herry A, Calvez GL, Marion V, Abgrall JF, Berthou C, Braekeleer MD.

Eur J Haematol. 2003 Apr;70(4):235-9.

PMID:
12656747
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15.

Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.

Härtel N, Klag T, Hanfstein B, Mueller MC, Schenk T, Erben P, Hochhaus A, La Rosée P.

J Cancer Res Clin Oncol. 2012 Feb;138(2):203-12. doi: 10.1007/s00432-011-1086-x.

PMID:
22089930
16.

Molecular and functional analysis of the stem cell compartment of chronic myelogenous leukemia reveals the presence of a CD34- cell population with intrinsic resistance to imatinib.

Lemoli RM, Salvestrini V, Bianchi E, Bertolini F, Fogli M, Amabile M, Tafuri A, Salati S, Zini R, Testoni N, Rabascio C, Rossi L, Martin-Padura I, Castagnetti F, Marighetti P, Martinelli G, Baccarani M, Ferrari S, Manfredini R.

Blood. 2009 Dec 10;114(25):5191-200. doi: 10.1182/blood-2008-08-176016.

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Molecular monitoring of response to imatinib (Glivec) in CML patients pretreated with interferon alpha. Low levels of residual disease are associated with continuous remission.

Paschka P, Müller MC, Merx K, Kreil S, Schoch C, Lahaye T, Weisser A, Petzold A, König H, Berger U, Gschaidmeier H, Hehlmann R, Hochhaus A.

Leukemia. 2003 Sep;17(9):1687-94.

PMID:
12970765
19.

BCR-ABL transcript dynamics support the hypothesis that leukemic stem cells are reduced during imatinib treatment.

Stein AM, Bottino D, Modur V, Branford S, Kaeda J, Goldman JM, Hughes TP, Radich JP, Hochhaus A.

Clin Cancer Res. 2011 Nov 1;17(21):6812-21. doi: 10.1158/1078-0432.CCR-11-0396.

20.

The poor response to imatinib observed in CML patients with low OCT-1 activity is not attributable to lower uptake of imatinib into their CD34+ cells.

Engler JR, Frede A, Saunders V, Zannettino A, White DL, Hughes TP.

Blood. 2010 Oct 14;116(15):2776-8. doi: 10.1182/blood-2010-01-267013.

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