Apoptosis, haemopoiesis and leukaemogenesis

被引:14
作者
Ekert, PG [1 ]
Vaux, DL [1 ]
机构
[1] CANC RES INST, NEW YORK, NY USA
来源
BAILLIERES CLINICAL HAEMATOLOGY | 1997年 / 10卷 / 03期
关键词
apoptosis; caspase; bcl-2; CD95; programmed cell death;
D O I
10.1016/S0950-3536(97)80026-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Apoptosis, or physiological cell death, is the way in which unwanted cells are removed. The majority of cells formed during haemopoiesis are destined to die by apoptosis before they are fully differentiated, and homeostasis of cell number is maintained by a balance between mitosis and apoptosis. Many haematological malignancies are associated with changes in the number of cells undergoing apoptosis, which may be a direct or an indirect effect. Genetic mutations that prevent cell death cause cells to accumulate and can eventually lead to malignancy. Alternatively, oncogenic mutations that lead to increased cell production can indirectly cause a decrease in apoptosis in some populations and an increase in others. Chemotherapeutic drugs may kill cells directly, or indirectly by inducing apoptosis as a stress response. Therapeutic strategies are evolving to increase the propensity of malignant cells to die by either means and to mitigate side effects by reducing apoptosis in non-malignant cells.
引用
收藏
页码:561 / 576
页数:16
相关论文
共 69 条
[31]   REGULATION OF THE RAS SIGNALING NETWORK [J].
MARUTA, H ;
BURGESS, AW .
BIOESSAYS, 1994, 16 (07) :489-496
[33]   TP53 mutations in myelodysplastic syndrome [J].
Misawa, S ;
Horiike, S .
LEUKEMIA & LYMPHOMA, 1996, 23 (5-6) :417-422
[34]   INDUCTION OF APOPTOSIS IN FIBROBLASTS BY IL-1-BETA-CONVERTING ENZYME, A MAMMALIAN HOMOLOG OF THE C-ELEGANS CELL-DEATH GENE CED-3 [J].
MIURA, M ;
ZHU, H ;
ROTELLO, R ;
HARTWIEG, EA ;
YUAN, JY .
CELL, 1993, 75 (04) :653-660
[35]   ULTRASTRUCTURAL FEATURES OF FETAL ERYTHROID PRECURSORS INFECTED WITH PARVOVIRUS-B19 INVITRO - EVIDENCE OF CELL-DEATH BY APOPTOSIS [J].
MOREY, AL ;
FERGUSON, DJP ;
FLEMING, KA .
JOURNAL OF PATHOLOGY, 1993, 169 (02) :213-220
[36]   MASSIVE CELL-DEATH OF IMMATURE HEMATOPOIETIC-CELLS AND NEURONS IN BCL-X-DEFICIENT MICE [J].
MOTOYAMA, N ;
WANG, FP ;
ROTH, KA ;
SAWA, H ;
NAKAYAMA, K ;
NAKAYAMA, K ;
NEGISHI, I ;
SENJU, S ;
ZHANG, Q ;
FUJII, S ;
LOH, DY .
SCIENCE, 1995, 267 (5203) :1506-1510
[37]   FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex [J].
Muzio, M ;
Chinnaiyan, AM ;
Kischkel, FC ;
ORourke, K ;
Shevchenko, A ;
Ni, J ;
Scaffidi, C ;
Bretz, JD ;
Zhang, M ;
Gentz, R ;
Mann, M ;
Krammer, PH ;
Peter, ME ;
Dixit, VM .
CELL, 1996, 85 (06) :817-827
[38]   THE FAS DEATH FACTOR [J].
NAGATA, S ;
GOLSTEIN, P .
SCIENCE, 1995, 267 (5203) :1449-1456
[39]   CHROMOSOME-17 ABNORMALITIES AND INACTIVATION OF THE P53 GENE IN CHRONIC MYELOID-LEUKEMIA AND THEIR PROGNOSTIC-SIGNIFICANCE [J].
NAKAI, H ;
MISAWA, S .
LEUKEMIA & LYMPHOMA, 1995, 19 (3-4) :213-221
[40]   A unique spectrum of p53 mutations in B-cell chronic lymphocytic leukemia distinct from that of other lymphoid malignancies [J].
Newcomb, EW ;
ElRouby, S ;
Thomas, A .
MOLECULAR CARCINOGENESIS, 1995, 14 (04) :227-232