[Ara-c induced apoptosis in human myeloid leukemia cell line HL-60].
OBJECTIVE
To elucidate the pattern of chemotherapy drugs induced apoptosis and its role in chemotherapy of acute leukemia.


METHODS
Apoptosis induced by Ara-c in human myeloid leukemia cell line HL-60 was investigated by applying light microscopy, electron microscopy combined with DNA electrophoresis and flow cytometry analysis techniques.


RESULTS
Apoptosis persisted throughout 36 hours following addition of Ara-c with a gradual augmentation. Efficiency of apoptosis was enhanced in a dose-dependent pattern, HL-60 treated with six other chemotherapy drugs and perpherial white blood cells from a AML case undergoing DA protocol chemotherapy exhibited typical DNA ladder pattern. Further investigation indicated that chemotherapy drugs induced apoptosis came into being possibly by downregulation the oncogenes expression of c-myc and bcl-2.


CONCLUSIONS
Chemotherapy induced apoptosis is a primary mechanism in chemotherapy.
Zhou
J
J
Institute of Hematology, Tongji Medical University, Wuhan.
Chen
Y
Y
Li
C
C
D000964:Antimetabolites, Antineoplastic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D003561:Cytarabine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D018922:HL-60 Cells / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis
D000964:Antimetabolites, Antineoplastic; D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D003561:Cytarabine