Previous best responses can be re-achieved by resumption after imatinib discontinuation in patients with chronic myeloid leukemia: implication for intermittent imatinib therapy

被引:42
作者
Goh, Hyun-Gyung [1 ]
Kim, Yoo-Jin [2 ]
Kim, Dong-Wook [1 ,2 ]
Kim, Hyeoung-Joon [3 ]
Kim, Soo-Hyun [1 ]
Jang, Se-Eun [1 ]
Lee, Jeong [1 ]
Kim, Dongho [1 ]
Kim, Wan-Seok [1 ]
Park, Sa-Hee [1 ]
Kweon, Il-Young [1 ]
机构
[1] Catholic Univ Korea, Mol Genet Res Inst, Seoul, South Korea
[2] Catholic Univ Korea, Div Hematol, Seoul, South Korea
[3] Chonnam Natl Univ, Dept Hematol Oncol, Hwasun Hosp, Jeonnam, South Korea
关键词
Chronic myeloid leukemia; intermittent imatinib therapy; complete cytogenetic response; complete molecular response; COMPLETE MOLECULAR RESPONSE; INTERFERON; SURVIVAL; MESYLATE;
D O I
10.1080/10428190902926973
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Although imatinib is considered as a front line therapy in patients with chronic myeloid leukemia (CML), it is still unclear whether transient imatinib discontinuation may adversely affect the outcome. This study was conducted to investigate long-term outcome after discontinuation and resumption of imatinib, and to determine whether intermittent imatinib therapy can be employed in patients with CML. Twenty six Philadelphia chromosome positive (Ph+) patients with CML discontinued imatinib when they achieved complete cytogenetic response (CCyR) or complete molecular response (CMR), and they were retreated with imatinib in case of hematologic, cytogenetic or molecular relapse. Except one patient who progressed and two patients who are in persistent molecular remission without imatinib resumption, all of 23 patients are maintaining the best response achieved after imatinib resumption with a median follow-up of 44 months. This study shows that although imatinib cannot be discontinued completely, intermittent therapy can be considered for the treatment of patients with CML in particular situations.
引用
收藏
页码:944 / 951
页数:8
相关论文
共 16 条
[1]   Discontinuation of imatinib therapy after achievement of complete molecular response in a Ph plus CML patient treated while in long lasting complete cytogenetic remission (CCR) induced by interferon [J].
Breccia, M. ;
Diverio, D. ;
Pane, F. ;
Nanni, M. ;
Russo, E. ;
Biondo, F. ;
Frustaci, A. ;
Gentilini, F. ;
Alimena, G. .
LEUKEMIA RESEARCH, 2006, 30 (12) :1577-1579
[2]   To the editor: Discontinuation of imatinib therapy after achieving a molecular response [J].
Cortes, J ;
O'Brien, S ;
Kantarjian, H .
BLOOD, 2004, 104 (07) :2204-2205
[3]   The molecular biology of chronic myeloid leukemia [J].
Deininger, MWN ;
Goldman, JM ;
Melo, JV .
BLOOD, 2000, 96 (10) :3343-3356
[4]   Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells [J].
Druker, BJ ;
Tamura, S ;
Buchdunger, E ;
Ohno, S ;
Segal, GM ;
Fanning, S ;
Zimmermann, J ;
Lydon, NB .
NATURE MEDICINE, 1996, 2 (05) :561-566
[5]   How I treat chronic myeloid leukemia in the imatinib era [J].
Goldman, John M. .
BLOOD, 2007, 110 (08) :2828-2837
[6]   Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro [J].
Graham, SM ;
Jorgensen, HG ;
Allan, E ;
Pearson, C ;
Alcorn, MJ ;
Richmond, L ;
Holyoake, TL .
BLOOD, 2002, 99 (01) :319-325
[7]  
Hochhaus A, 2007, BLOOD, V110, p15A
[8]   Long-term survival benefit and improved complete cytogenetic and molecular response rates with imatinib mesylate in Philadelphia chromosome-positive chronic-phase chronic myeloid leukemia after failure of interferon-α [J].
Kantarjian, HM ;
Cortes, JE ;
O'Brien, S ;
Luthra, R ;
Giles, F ;
Verstovsek, S ;
Facerl, S ;
Thomas, D ;
Garcia-Manero, G ;
Rios, MB ;
Shan, J ;
Jones, D ;
Talpaz, M .
BLOOD, 2004, 104 (07) :1979-1988
[9]   The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype [J].
Melo, JV .
BLOOD, 1996, 88 (07) :2375-2384
[10]  
Merante S, 2005, HAEMATOLOGICA, V90, P979