| Background and aims: The abnormality of proliferation andapoptosis is a basic biological feature of acute leukemia, for whichchemotheraPy still is the main therapeutic method. Recent researcheshave found that the occurrence of leukemia and leukemic cell deathinduced by chemotheraPeutic drugs both have close relation toapoptosis. Some in vitro experiments indicated that nearly all kinds ofchemotherapeutic drugs couId induce aPoptosis of leukemic cells. Butthere are few researches on aPoptosis in vivo during chemotheraPy andthe reIation of aPoptosis to clinical response at present, because thelapoptotic ce1ls are easily eliminated by phagocytes so that detecting invivo apoptosis with cIassical methods becomes difficult. Clinically,there also lack early indexes to predict the clinical response ofchemotheraPy for individualizing theraPy Although there is close4$X 2002 SffA1$k*t ax$$M Ki-67 otg$8ktedS 24,J'otWAm%gtNWgttA1$#aMffRrelationship between cell proliferation and the effects ofchemotherapeutic drugs, little is known about the relation of cell' proliferation activity to in vivo aPoptosis induced by chemotheraPeuticagents. In order to provide early indexes fOr the prediction of clinicalchemotheraPy resPonse so that doctors can adjust theraPy regimens intime to reach better tfeatffient results, the in vivo aPoptosis before and24 hours after chemotheraPy and the eXPression of nuclear proliferationantigen KI-67 in acute leukemic cells were inveStigated and theirrelations to the clinical efficacy of chemotheraPy were analyzed in thisstudy.MateriaIs and methods: The samPles were from 29 cases withacute leukemia (25 cases untreated, 4 cases refractory or relaPsed),l6males and l3 females, the median age 35 years (range l5~74 years).20 cases with acute myeloid leukemia (AML, l Mo' 3 Ml, l0 M2, 2M., 3 Ms, l M,) and 9 cases with acut lymPhoblastic leukemia (ALL, lin blast crisis from chronic myelocytic leukemia) were involved. Theperipheral blood white cell count is all above 7 X l09/L and blast cells>30%. ChemotheraPy regimens included DA (DNR, Ara-C), HA (H,AIa-C), AA (ACR, Ara-C ), IDA (IDR, AIaC ), VDCP (VCR, DNR,CTX, Pred) and MEA (MXT VP-l6, AIaC). The aPOPtOsis ofleukemic ce1ls collected from blood before and 24 hours afterchemotheraPy was detected with flow cytometer by an early aPoPtOsis$X 2()02 affnl$n&Z enmmm Ki-67 fi&$isWfe#g 24 d'rtWNmmRtM$ISttA&mffMMffnmarker Annexin V, and the expression of Ki-67 anigen was measuredwith SP immunocytochemistry assay.ResuIts: (l ) The apoptosis ofleukemic cells before chemotherapywas 5.74% i 2.47% and obviously increased 24 hours afterchemotheraPy (9.77%f3,54%, P<0.001). (2) Of 29 cases, 2 casesexPired and 2 cases lost. l2 patients achieved comPlete remission (CR),1 partial remission (PR) and l2 non-remission (NR. CR and PRpatients were defined as efficient grouP and NR patients as failuregroup. The aPoptosis rate of efficient group before chemotheraPy was5.54% f 1.88%, increased 5.9l% t 3.48% 24 hours afterchemotherapy(l.45% i 3.09%); the apoptOsis rate of failure grouPbefOre and 24 hours after chemotherapy was 5.88% f 2.94% and 8. l5%I3.66% respectively, with the increment of apoptosis cells 2.28%f3.58%. Apoptosis induced by chemotherapeutics was significanlyincreased in the efficient group compared with the failure group(P<0.05), but there was no relationship betWeen the aPoPtosis beforechemotheraPy and clinical response (P>0.05). (3) The Ki-67 positivecells was 48.4% f 19.5% before chemotheraPy, 53.6%I 16.5% inefficient group and 38.4%f22.3% in the failure group. There was nosignificant diffience between the efficieflt grouP and failure group(P>0.05). No correlation was fOund between the expression of Ki-67antigen and the cell aPoptosis induced by chemotheraPy (rr0.003,P>0.05). (4) By multiple cut-off points analysis, when apoptosis increment =^3.50% was used as cut-off point, the high... |
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