Novel therapies for chronic myelogenous leukemia

被引:34
作者
Jahagirdar, BN [1 ]
Miller, JS [1 ]
Shet, A [1 ]
Verfaillie, CM [1 ]
机构
[1] Univ Minnesota, Div Hematol Oncol & Transplantat, Stem Cell Inst, Minneapolis, MN 55455 USA
关键词
D O I
10.1016/S0301-472X(01)00633-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The BCR-ABL oncogene is essential to the pathogenesis of chronic myelogenous leukemia, and immune mechanisms play an important role in control of this disease. Understanding of the molecular pathogenesis of chronic myelogenous leukemia has led to the development of several novel therapies, which can be broadly divided into therapies based on 1) inhibition of the BCR-ABL oncogene expression, 2) inhibition of other genes important to the pathogenesis of chronic myelogenous leukemia, 3) inhibition of BCR-ABL protein function, and 4) immunomodulation, We have systematically review-ed each of these novel therapeutic approaches in this article. (C) 2001 International Society for Experimental Hematology, Published by Elsevier Science Inc.
引用
收藏
页码:543 / 556
页数:14
相关论文
共 213 条
[1]   Efficient retrovirus-mediated transfer of the multidrug resistance 1 gene into autologous human long-term repopulating hematopoietic stem cells [J].
Abonour, R ;
Williams, DA ;
Einhorn, L ;
Hall, KM ;
Chen, J ;
Coffman, J ;
Traycoff, CM ;
Bank, A ;
Kato, I ;
Ward, M ;
Williams, SD ;
Hromas, R ;
Robertson, MJ ;
Smith, FO ;
Woo, D ;
Mills, B ;
Srour, EF ;
Cornetta, K .
NATURE MEDICINE, 2000, 6 (06) :652-658
[2]   SIGNALING BY ABL ONCOGENES THROUGH CYCLIN D1 [J].
AFAR, DEH ;
MCLAUGHLIN, J ;
SHERR, CJ ;
WITTE, ON ;
ROUSSEL, MF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (21) :9540-9544
[3]   GENETIC APPROACHES TO DEFINING SIGNALING BY THE CML-ASSOCIATED TYROSINE KINASE BCR-ABL [J].
AFAR, DEH ;
GOGA, A ;
COHEN, L ;
SAWYERS, CL ;
MCLAUGHLIN, J ;
MOHR, RN ;
WITTE, ON .
COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY, 1994, 59 :589-594
[4]   DIFFERENTIAL COMPLEMENTATION OF BCR-ABL POINT MUTANTS WITH C-MYC [J].
AFAR, DEH ;
GOGA, A ;
MCLAUGHLIN, J ;
WITTE, ON ;
SAWYERS, CL .
SCIENCE, 1994, 264 (5157) :424-426
[5]   Primary proliferating immature myeloid cells from CML patients are not resistant to induction of apoptosis by DNA damage and growth factor withdrawal [J].
Albrecht, T ;
Schwab, R ;
Henkes, M ;
Peschel, C ;
Huber, C ;
Aulitzky, WE .
BRITISH JOURNAL OF HAEMATOLOGY, 1996, 95 (03) :501-507
[6]   UK MEDICAL-RESEARCH-COUNCIL RANDOMIZED, MULTICENTER TRIAL OF INTERFERON-ALPHA-N1 FOR CHRONIC MYELOID-LEUKEMIA - IMPROVED SURVIVAL IRRESPECTIVE OF CYTOGENETIC RESPONSE [J].
ALLAN, NC ;
RICHARDS, SM ;
SHEPHERD, PCA .
LANCET, 1995, 345 (8962) :1392-1397
[7]   APOPTOSIS IN CHRONIC MYELOID-LEUKEMIA - NORMAL RESPONSES BY PROGENITOR CELLS TO GROWTH-FACTOR DEPRIVATION, X-IRRADIATION AND GLUCOCORTICOIDS [J].
AMOS, TAS ;
LEWIS, JL ;
GRAND, FH ;
GOODING, RP ;
GOLDMAN, JM ;
GORDON, MY .
BRITISH JOURNAL OF HAEMATOLOGY, 1995, 91 (02) :387-393
[8]  
ANAFI M, 1993, BLOOD, V82, P3524
[9]   AN OLIGOMER COMPLEMENTARY TO C-MYB-ENCODED MESSENGER-RNA INHIBITS PROLIFERATION OF HUMAN MYELOID-LEUKEMIA CELL-LINES [J].
ANFOSSI, G ;
GEWIRTZ, AM ;
CALABRETTA, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (09) :3379-3383
[10]  
Bayever E, 1993, Antisense Res Dev, V3, P383