Analysis on the Laboratory Examination Characteristics in 28 Patients with Acute Megakaryoblastic Leukemia

doi:10.13523/j.cb.20190901

China Biotechnology

2019, Vol. 39

Issue (9): 2-10 DOI: 10.13523/j.cb.20190901

Orginal Article

Analysis on the Laboratory Examination Characteristics in 28 Patients with Acute Megakaryoblastic Leukemia

HE Ling-ling,LUO Ting-ting,CHANG Yan,WANG Ya-zhe,YUAN Xiao-ying,SHI Wei-hua,LAI Yue-yun,SHI Hong-xia,QIN Ya-zhen,HUANG Xiao-jun,LIU Yan-rong(

)

Institute of Hematology,People Hospital,Peking University,Beijing 100044 ,China

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Abstract

Objective: To analyze the laboratory characteristics in patients with acute megakaryoblastic leukemia(AMKL).Methods: The immunophenotypes of leukemia cells in 28 patients with AMKL were analyzed by means of 4 tubes of 8 color panel. Meanwhile, bone marrow morphology,cell chemistry,chromosome karyotype and gene were examined.Results: Among 28 AMKL patients, the highest positive rates were macrokaryocyte-associated antibodies: CD41a, CD61, CD42b, CD36. The positive rates were 81.48%, 92.86%, 72.00% and 70.83%, respectively. Among them, 53.57% of the patients expressed CD41a, CD61 and CD42b, and 82.14% of the patients expressed at least two kinds of antibodies. The positive expression rates of CD117, CD34, CD38 and HLA-DR were 64.29%, 42.86%, 64.29% and 46.15% respectively, which were lower in AMKL patients than in non-APL patients (P< 0.01). There was no significant difference between the positive expression rates of CD13 and CD33 in AMKL and non-APL AML patients. CD15, CD64, CD14, CD300e and MPO, cCD79a and cCD3 were all negative. Compared with non-Down syndrome-related AMKL (non-DS-AMKL), the expression of CD7 and CD11b was higher in Down syndrome-related AMKL (DS-AMKL) (P < 0.05). Among AMKL patients, 17 (65.4%) had complex chromosome karyotypes and 5 had + 21 chromosome abnormalities; only 5 had normal karyotypes. Twenty-five leukemia patients were screened for fusion genes. WT1 gene expression increased in 24 patients (96%) and 12 patients (70.58%) with EVI1 gene expression increased (53.93 < 37.98%). Four patients were positive for fusion genes (2 MLL-AF9, 1 TLS-ERG and 1 P210 BCL/ABL).Conclusion: 82.14% of AMKL patients express at least two megakaryocyte-related markers. The expression of myeloid progenitor cell markers is relatively low, most of which are complex chromosomal karyotype abnormalities. The abnormal expression rates of WT1 and EVI1 are higher.

Key words： Acute megakaryoblastic leukemia Immunophenotype Flow cytometry

Received: 15 August 2019 Published: 20 September 2019

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Corresponding Authors: Yan-rong LIU E-mail: yrliu163@163.com

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	Ling-ling HE
	Ting-ting LUO
	Yan CHANG
	Ya-zhe WANG
	Xiao-ying YUAN
	Wei-hua SHI
	Yue-yun LAI
	Hong-xia SHI
	Ya-zhen QIN
	Xiao-jun HUANG
	Yan-rong LIU

Cite this article:

HE Ling-ling,LUO Ting-ting,CHANG Yan,WANG Ya-zhe,YUAN Xiao-ying,SHI Wei-hua,LAI Yue-yun,SHI Hong-xia,QIN Ya-zhen,HUANG Xiao-jun,LIU Yan-rong. Analysis on the Laboratory Examination Characteristics in 28 Patients with Acute Megakaryoblastic Leukemia. China Biotechnology, 2019, 39(9): 2-10.

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https://manu60.magtech.com.cn/biotech/10.13523/j.cb.20190901 OR https://manu60.magtech.com.cn/biotech/Y2019/V39/I9/2

Table 1 The positive expression rates of antibodies in 28 patients with AMKL

Table 2 The positive expression rates of different macrokaryocyte-associated antibody groups in 28 patients with AMKL

Table 3 The comparison of antigen expression in non-APL AML and AMKL patients

Fig.1 Blasts with megakaryocytes

序号		性别		年龄 (岁)		骨髓增生活跃程度			巨幼细胞 (%)	融合基因 X/abl(%)		染色体核型
1		女		0.1		Ⅲ			38	WT1 38.0 EVI1 78.9		47,XX,t(3;12;16)(q26;13;24),der(17)t(1;17)(q21;p13),+21 [4] /47,idem,t(1,3)(q25;q21)[19]
2		男		0.6		Ⅱ			83	WT1 32.1		46,XY[16]
3		女		0.9		Ⅳ			38	WT1 24.8		48,XX,+2,del(15)(q15;q24),+19[10]
4		男		1.0		Ⅲ			74	WT1 1.3 EVI1 49.8		46,Y,del(X)(q22),add(2)(q24),-7,del(9)(q22;q32),16qh+c,+mar1[3]/46,Y,-X,add(2)(q24),-7,del(9)(q22;q32),16qh+c,+mar1,+mar2[1]/46,XY, 16qh+c[7] 16qh+考虑为体质性异常
5		女		1.0		Ⅲ			86	WT1 16.6		47,XX,-7,+21,+21[5]/47,XX,der(7;18)(q10;q10),+21,+21[9]
6		男		1.0		Ⅲ			64	WT1 88.8		46,XY,add(9)(q34)[8]/46,idm,del(20)(p11)[2]
7		男		1.0		Ⅱ-Ⅲ			56	WT1 20.6		46,XY,del(13)(q12;q22)[2]/46,Y,t(X;12)(p11;q15),del(13)(q12;q22) [7]/46,XY, [1]
8		女		1.0		Ⅲ			31	WT1 20.4 EVI1 36.1		48,XX,del(7)(q31),del(8)(q21;q22),+9,der(9),del(9)(q11;q13),del(9)(q22;q34)X2,+19[6]/47,idem,-21[6] /46,XX[8]
序号	性别		年龄 (岁)		骨髓增生活跃程度		巨幼细胞 (%)	融合基因 X/abl(%)			染色体核型
9	男		1.0		Ⅱ		22	MLL-AF9 8.4 WT1 6.1 EVI1 122.6			46,XY[16]
10	男		1.1		Ⅱ		30	WT1 2.4 EVI1 61.9			48,XY,add(3)(p25),del(5)(q22;q35),+19,+mar[5]/48,idm,add(3)(q11)[8]/47,XY,add(3)(p25),del(5)(q22;q35),del(12)(p11),+19[2]/47,XY,der(3)add(3)(p25)add(3)(q11),del(5)(q22;q35),+19[5]/46,XY[4]
11	男		1.5		Ⅱ		56	MLL-AF9 0.17			46,XY [20]
12	男		1.9		Ⅴ		50	WT1 9.7 EVI1 101.3			49,XY,+4,+8,+10[1]/46,XY[2]
13	男		1.9		Ⅱ		56	WT1 185.6			46,XY, [20]
14	女		2.0		Ⅲ		39	WT1 16.0			50,XX,+8,+10,+21,+21[7]/46,XX[13]
15	男		2.0		Ⅱ-Ⅲ		35	WT1 10.0 EVI1 19.4			46,XY,t(1;11)(p32;q23),add(3)(q11),t(10;16)(q22;p13),inv(11)(p15;q13),del(20)(q11)[13]/47,XY,t(1;11),add(3),+8,t(10;16),inv(11) [4]/46,XY[3]
16	男		2.0		Ⅱ		76	WT1 20.0 EVI1 96.1			46,XY,add(19)(p13)[1]/46,XY,der(2;3)(q10;p10),+3,inv(12)(q22;q24),15ps+[1]/46,XY[18] 15ps+考虑为体质性异常
17	男		2.0		Ⅱ		31	WT1 57.2			47,XY,del(9)(q22;q32),+19[1]/46,XY[19]
18	女		2.0		Ⅱ		22	-			-
19	男		2.0		Ⅱ		89	WT1 217.3			46,XY
20	男		2.0		Ⅲ		81	WT1 33.8 EVI1 13.8			56,XY,+2,+2,+6,+7,+8,+10,+15,+19,+19,+20[10]
21	男		4.0		Ⅱ-Ⅲ		85	WT1 1.3 PRAME 244.7			45-50,XY,t(4;11)(q21;q23),+7,+8,+del(11)(q23),+del(11)(q23),del(20)(q11),+21 [cp6]
22	男		9.0		Ⅲ		52	-			47,XY,+3 [5]/46,XY [15]
23	男		27.0		Ⅲ		42	-			-
24	男		40.0		Ⅱ		97	TLS-ERG 342.2 WT1 141.7			48,Y,del(X)(q22),der(2)t(1;2)(q23;q37),del(9)(q22;q32),+10,-13,+14,t(16;21)(p11;q22),+mar[5]/46,XY, [4]
25	男		47.0		Ⅲ-Ⅳ		74	WT1 2.4 EVI1 15.7 PRAME 2.0			44-50,XY,+del(1)(p13),del(1)(q21),dic(1;2)(q21;p25),+2,add(4)(p16),+add(4)(p16),-5,+6,der(11),t(1;11)(q21;q23),add(13)(q34),add(15)(p13),+add(15)(p13),dic(17;19)(p13;q13),+18,add(19)(q13),+21,add(22)(p13),+mar\(cp5)/47,XY,+17 [1]/46,XY [9]
26	男		52.0		Ⅲ		71	WT1 5.1 PREAME 2.0 EVI1 14.3			41-42,XY,t(1;5)(q32;q31),t(3;22)(q21;p11),-6,-7,del(8)(q21),add(9)(q34),-12,-14,-17,add(19)(p13),-22,+2mar [cp3]/46,XY [7]
27	男		62.0		Ⅲ		61	WT1 11.2 EVI1 37.3			42-43,XY,+X,+Y,del(1),(q41),add(5)(q11),-7,-9,-13,add(14)(p13),-16,-18,add(18)(p11),-21,+mar1-mar3 [cp10]
28	女		69.0		Ⅲ		21	WT1 3.3 BCR/ABL(P210) 34.9			46,XX,t(9;22;22)(q34;q11;q13)[1]/46,xx,t(9;22)(q34;q11)[5]

Table 4 Morphological classification,immunophenotype , karyotype and gene of the 28 patients with AMKL


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