Combining BCR-ABL1 transcript levels at 3 and 6 months in chronic myeloid leukemia: implications for early intervention strategies

被引:79
作者
Neelakantan, Pratap [1 ]
Gerrard, Gareth [1 ]
Lucas, Claire [2 ]
Milojkovic, Dragana [1 ]
May, Philippa [1 ]
Wang, Lihui [2 ]
Paliompeis, Christos [1 ]
Bua, Marco [1 ]
Reid, Alistair [1 ]
Rezvani, Katayoun [1 ]
O'Brien, Stephen [3 ]
Clark, Richard [2 ]
Goldman, John [1 ]
Marin, David [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Dept Haematol, Hammersmith Hosp, London W12 0NN, England
[2] Royal Liverpool Univ Hosp, Dept Haematol, Liverpool, Merseyside, England
[3] Newcastle Univ, Northern Inst Canc Res, Dept Haematol, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England
关键词
STEM-CELLS; COMPETING RISK; IMATINIB; DASATINIB; QUIESCENT;
D O I
10.1182/blood-2012-11-466037
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Several groups have shown that that the BCR-ABL1 transcript level measured at 3 or 6 months after starting treatment with tyrosine kinase inhibitors strongly predicts clinical outcomes for patients with chronic myeloid leukemia. In this work, we asked whether the prognostic value of the 3-month transcript level could be improved by combining the 3- and 6-month results. We classified patients treated with imatinib and patients treated with dasatinib according to their transcript levels at 3 months and 6 months. The patients who met the 3-month landmark but failed the 6-month one had outcomes identical to those of patients who met both landmarks, whereas the patients who failed the first landmark but met the second one had prognoses similar to those who failed both landmarks. In summary, early intervention strategies can be based robustly just on the transcript level at 3 months. This trial was registered at www.clinicaltrials.gov as # NCT01460693. (Blood. 2013;121(14):2739-2742)
引用
收藏
页码:2739 / 2742
页数:4
相关论文
共 15 条
[1]   Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction [J].
Copland, Mhairi ;
Hamilton, Ashley ;
EIrick, Lucy J. ;
Baird, Janet W. ;
Allan, Elaine K. ;
Jordanides, Niove ;
Barow, Martin ;
Mountford, Joanne C. ;
Holyoake, Tessa L. .
BLOOD, 2006, 107 (11) :4532-4539
[2]   Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity [J].
Corbin, Amie S. ;
Agarwal, Anupriya ;
Loriaux, Marc ;
Cortes, Jorge ;
Deininger, Michael W. ;
Druker, Brian J. .
JOURNAL OF CLINICAL INVESTIGATION, 2011, 121 (01) :396-409
[3]   Imatinib for newly diagnosed patients with chronic myeloid leukemia: Incidence of sustained responses in an intention-to-treat analysis [J].
de Lavallade, Hugues ;
Apperley, Jane F. ;
Khorashad, Jamshid S. ;
Milojkovic, Dragana ;
Reid, Alistair G. ;
Bua, Marco ;
Szydlo, Richard ;
Olavarria, Eduardo ;
Kaeda, Jaspal ;
Goldman, John M. ;
Marin, David .
JOURNAL OF CLINICAL ONCOLOGY, 2008, 26 (20) :3358-3363
[4]  
Domenech JM, 2011, ANALISIS EVENTOS REC
[5]   A proportional hazards model for the subdistribution of a competing risk [J].
Fine, JP ;
Gray, RJ .
JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION, 1999, 94 (446) :496-509
[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]   A CLASS OF K-SAMPLE TESTS FOR COMPARING THE CUMULATIVE INCIDENCE OF A COMPETING RISK [J].
GRAY, RJ .
ANNALS OF STATISTICS, 1988, 16 (03) :1141-1154
[8]   Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival [J].
Hamilton, Ashley ;
Helgason, G. Vignir ;
Schemionek, Mirle ;
Zhang, Bin ;
Myssina, Svetlana ;
Allan, Elaine K. ;
Nicolini, Franck E. ;
Mueller-Tidow, Carsten ;
Bhatia, Ravi ;
Brunton, Valerie G. ;
Koschmieder, Steffen ;
Holyoake, Tessa L. .
BLOOD, 2012, 119 (06) :1501-1510
[9]   Early molecular and cytogenetic response is predictive for long-term progression-free and overall survival in chronic myeloid leukemia (CML) [J].
Hanfstein, B. ;
Mueller, M. C. ;
Hehlmann, R. ;
Erben, P. ;
Lauseker, M. ;
Fabarius, A. ;
Schnittger, S. ;
Haferlach, C. ;
Goehring, G. ;
Proetel, U. ;
Kolb, H-J ;
Krause, S. W. ;
Hofmann, W-K ;
Schubert, J. ;
Einsele, H. ;
Dengler, J. ;
Haenel, M. ;
Falge, C. ;
Kanz, L. ;
Neubauer, A. ;
Kneba, M. ;
Stegelmann, F. ;
Pfreundschuh, M. ;
Waller, C. F. ;
Branford, S. ;
Hughes, T. P. ;
Spiekermann, K. ;
Baerlocher, G. M. ;
Pfirrmann, M. ;
Hasford, J. ;
Saussele, S. ;
Hochhaus, A. .
LEUKEMIA, 2012, 26 (09) :2096-2102
[10]   Dasatinib versus Imatinib in Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia [J].
Kantarjian, Hagop ;
Shah, Neil P. ;
Hochhaus, Andreas ;
Cortes, Jorge ;
Shah, Sandip ;
Ayala, Manuel ;
Moiraghi, Beatriz ;
Shen, Zhixiang ;
Mayer, Jiri ;
Pasquini, Ricardo ;
Nakamae, Hirohisa ;
Huguet, Francoise ;
Boque, Concepcion ;
Chuah, Charles ;
Bleickardt, Eric ;
Bradley-Garelik, M. Brigid ;
Zhu, Chao ;
Szatrowski, Ted ;
Shapiro, David ;
Baccarani, Michele .
NEW ENGLAND JOURNAL OF MEDICINE, 2010, 362 (24) :2260-2270