ZNF384融合亚型急性白血病的发病机制及预后研究进展

doi:10.3969/j.issn.1674-8115.2023.05.015

上海交通大学学报（医学版） ›› 2023, Vol. 43 ›› Issue (5): 631-640.doi: 10.3969/j.issn.1674-8115.2023.05.015

• 综述 • 上一篇

ZNF384融合亚型急性白血病的发病机制及预后研究进展

李瑛¹^,²(), 谭阳霞², 尹虹心², 蒋雁翎¹^,², 陈立¹, 蒙国宇²()

^1.昆明理工大学医学院基础医学系，昆明 650500
^2.上海交通大学医学院附属瑞金医院上海血液学研究所，医学基因组学国家重点实验室，国家转化医学研究中心（上海），上海 200025

收稿日期:2022-12-19 接受日期:2023-02-24 出版日期:2023-05-28 发布日期:2023-07-11
通讯作者: 蒙国宇 E-mail:3258414023@qq.com;guoyumeng@shsmu.edu.cn
作者简介:李　瑛（1994—），女，硕士生；电子信箱：3258414023@qq.com。
基金资助:
国家自然科学基金(81970132)

Research progress in the pathogenesis and prognosis of ZNF384 fusion subtype acute leukemia

LI Ying¹^,²(), TAN Yangxia², YIN Hongxin², JIANG Yanling¹^,², CHEN Li¹, MENG Guoyu²()

^1.Department of Basic Medicine, School of Medicine, Kunming University of Science and Technology, Kunming 650500, China
^2.Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine(Shanghai), RuiJin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

Received:2022-12-19 Accepted:2023-02-24 Online:2023-05-28 Published:2023-07-11
Contact: MENG Guoyu E-mail:3258414023@qq.com;guoyumeng@shsmu.edu.cn
Supported by:
National Natural Science Foundation of China(81970132)

摘要/Abstract

摘要：

由染色体易位引起的融合基因已成为白血病的主要致病因素。锌指蛋白384（zinc finger protein 384，ZNF384）融合作为急性白血病（acute leukemia，AL）中的非典型融合亚型，在不同的年龄群体中广泛发生。ZNF384具有丰富的融合伴侣，其中E1A结合蛋白p300（E1A binding protein p300，EP300）、转录因子3（transcription factor 3，TCF3）、TATA-box binding protein associated factor 15（TAF15）的融合频率最高。这些融合蛋白均保留了完整的ZNF384结构，但融合伴侣则有不同程度的缺失，说明不同的ZNF384融合亚型之间具有相似的致AL发生发展机制。现有研究主要认为ZNF384融合蛋白通过染色质重塑调控下游蛋白的转录表达，在造血干细胞的分化、癌细胞的增殖凋亡和基因组修复中发挥潜在作用。ZNF384融合患者同时表达淋系和髓系特有的抗原，在疾病的进展中具有谱系转化特性，丰富的免疫表型给治疗方式带来了不确定性，并与融合亚型、发病年龄一起影响患者的临床结局。该文通过对近10年已发表的案例和大型队列研究进行统计归纳分析，进一步确认了ZNF384融合及其各亚型AL在现有研究背景下的发生频率，总结了已有的机制信息，并对不同治疗方式下ZNF384融合患者的预后作了简要分析，以期为后续针对这一独特亚型AL的诊疗和研究提供参考。

关键词: ZNF384融合, 急性白血病, 免疫表型, 机制, 诊断, 预后

Abstract:

Gene fusions caused by chromosomal translocations have become the main pathogenic factors that initiate leukemogenesis. Zinc finger protein 384 (ZNF384) fusion, as an atypical fusion gene in acute leukemia (AL), has widely been identified in different age groups. ZNF384 rearranged 18 genes, with E1A binding protein p300 (EP300), transcription factor 3, (TCF3), and TATA-box binding protein-associated factor 15 (TAF15) being the most common fusion partners. These fusion proteins maintain the complete structure of ZNF384, but the fusion partners are missing in varying degrees, indicating that the mechanisms behind different subtypes of carcinogenesis have similarities. The mechanism of ZNF384-rearranged AL is also being actively investigated. It is mainly believed that the fusion protein regulates the transcription and expression of downstream proteins through chromatin remodeling, and plays a potential role in the differentiation of hematopoietic stem cells, the proliferation and apoptosis of cancer cells and genome repair. Patients with ZNF384 fusions express both lymphoid and myeloid-specific antigens, which have lineage-transforming properties during disease progression. The diversity of immunophenotypes leads to ambiguity in treatment options and diverse outcomes in prognosis studies, and affects the clinical outcome of patients together with fusion subtype and age of onset. Through the statistical analysis of published cases and large-scale cohort studies in the past 10 years, the incidence of ZNF384 fusion in AL and the frequency of each fusion subtype in the context of existing research were further confirmed. The impact of different treatment methods on the prognosis of patients was analyzed, and the identified mechanisms were summarized in order to provide reference for subsequent diagnosis, treatment and research of this unique AL subtype.

Key words: ZNF384 fusion, acute leukemia (AL), immunophenotype, mechanism, diagnosis, prognosis

中图分类号:

R733.71

李瑛, 谭阳霞, 尹虹心, 蒋雁翎, 陈立, 蒙国宇. ZNF384融合亚型急性白血病的发病机制及预后研究进展[J]. 上海交通大学学报（医学版）, 2023, 43(5): 631-640.

LI Ying, TAN Yangxia, YIN Hongxin, JIANG Yanling, CHEN Li, MENG Guoyu. Research progress in the pathogenesis and prognosis of ZNF384 fusion subtype acute leukemia[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2023, 43(5): 631-640.

图/表 4

表1 ZNF384 融合在AL中不同年龄段、不同免疫表型中的发生情况（n）

Tab 1 Frequency of ZNF384 fusion in different age groups and different immune phenotypes in AL （n）

Number	Total	Child (≤18 years)	Adult (>18 years)	ZNF384 fusion	ALL	MPAL	Publication year
1	173	4	‒	4	4	‒	2022^[26]
2	652	‒	11	11	11	‒	2022^[27]
3	643	17	‒	17	9	8	2021^[28]
4	242	‒	47	47	47	‒	2021^[7]
5	1 229	‒	9	9	9	‒	2021^[29]
6	598	6	1	7	7	‒	2021^[30]
7	56	1	9	10	9	1	2020^[22]
8	37	‒	3	3	3	‒	2020^[31]
9	115	15	‒	15	‒	15	2018^[12]
10	274	4	6	10	10	‒	2018^[15]
11	1 223	39	22	61	61	‒	2018^[2]
12	216	25	‒	25	25	‒	2017^[13]
13	240	7	‒	7	6	1	2016^[32]
14	401	6	‒	6	6	‒	2015^[8]
Summary	6 099	124	108	232	207	25

图1 ZNF384 融合各亚型在不同年龄群体中发生的频数分布

Fig 1 Occurrence frequency of ZNF384 fusion subtypes in different age groups

图2 ZNF384 部分融合亚型的断点统计以及融合蛋白结构图Note： The exon6/6-exon2/3 on the left side of the figure indicates that there are two types of fusion breakpoints between EP300 and ZNF384, exon6-exon2 and exon6-exon3. The small colored squares below the figure represent protein domains. TAZ1—transcriptional adapter zinc binding 1.

Fig 2 Breakpoint statistics and fusion protein structure diagram of some ZNF384 fusion subtypes

图3 ZNF384融合蛋白诱发AL的可能机制

Fig 3 Possible mechanism of ZNF384 fusion protein-induced AL

参考文献 68

1	QIAN M X, ZHANG H, KHAM S K, et al. Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP[J]. Genome Res, 2017, 27(2): 185-195.
2	LI J F, DAI Y T, LILLJEBJÖRN H, et al. Transcriptional landscape of B cell precursor acute lymphoblastic leukemia based on an international study of 1, 223 cases[J]. Proc Natl Acad Sci USA, 2018, 115(50): E11711-E11720.
3	ZALIOVA M, STUCHLY J, WINKOWSKA L, et al. Genomic landscape of pediatric B-other acute lymphoblastic leukemia in a consecutive European cohort[J]. Haematologica, 2019, 104(7): 1396-1406.
4	LI J F, DAI Y T, WU L, et al. Emerging molecular subtypes and therapeutic targets in B-cell precursor acute lymphoblastic leukemia[J]. Front Med, 2021, 15(3): 347-371.
5	MÄKINEN V P, REHN J, BREEN J, et al. Multi-cohort transcriptomic subtyping of B-cell acute lymphoblastic leukemia[J]. Int J Mol Sci, 2022, 23(9): 4574.
6	LIU Y F, WANG B Y, ZHANG W N, et al. Genomic profiling of adult and pediatric B-cell acute lymphoblastic leukemia[J]. EBioMedicine, 2016, 8: 173-183.
7	QIN Y Z, JIANG Q, XU L P, et al. The prognostic significance of ZNF384 fusions in adult ph-negative B-cell precursor acute lymphoblastic leukemia: a comprehensive cohort study from a single Chinese center[J]. Front Oncol, 2021, 11: 632532.
8	GOCHO Y, KIYOKAWA N, ICHIKAWA H, et al. A novel recurrent EP300-ZNF384 gene fusion in B-cell precursor acute lymphoblastic leukemia[J]. Leukemia, 2015, 29(12): 2445-2448.
9	DICKERSON K M, QU C X, GAO Q S, et al. ZNF384 fusion oncoproteins drive lineage aberrancy in acute leukemia[J]. Blood Cancer Discov, 2022, 3(3): 240-263.
10	WU Z Y, ZHANG F, LIU C Z, et al. Whole transcriptome sequencing reveals a TCF4-ZNF384 fusion in acute lymphoblastic leukemia[J]. Front Oncol, 2022, 12: 900054.
11	HIRABAYASHI S, BUTLER E R, OHKI K, et al. Clinical characteristics and outcomes of B-ALL with ZNF384 rearrangements: a retrospective analysis by the Ponte di Legno Childhood ALL Working Group[J]. Leukemia, 2021, 35(11): 3272-3277.
12	ALEXANDER T B, GU Z H, IACOBUCCI I, et al. The genetic basis and cell of origin of mixed phenotype acute leukaemia[J]. Nature, 2018, 562(7727): 373-379.
13	HIRABAYASHI S, OHKI K, NAKABAYASHI K, et al. ZNF384-related fusion genes define a subgroup of childhood B-cell precursor acute lymphoblastic leukemia with a characteristic immunotype[J]. Haematologica, 2017, 102(1): 118-129.
14	YAGUCHI A, ISHIBASHI T, TERADA K, et al. EP300-ZNF384 fusion gene product up-regulates GATA3 gene expression and induces hematopoietic stem cell gene expression signature in B-cell precursor acute lymphoblastic leukemia cells[J]. Int J Hematol, 2017, 106(2): 269-281.
15	MCCLURE B J, HEATLEY S L, KOK C H, et al. Pre-B acute lymphoblastic leukaemia recurrent fusion, EP300-ZNF384, is associated with a distinct gene expression[J]. Br J Cancer, 2018, 118(7): 1000-1004.
16	YAMAMOTO K, KAWAMOTO S, MIZUTANI Y, et al. Mixed phenotype acute leukemia with t (12;17) (p13;q21)/TAF15-ZNF384 and other chromosome abnormalities[J]. Cytogenet Genome Res, 2016, 149(3): 165-170.
17	PING N N, QIU H Y, WANG Q, et al. Establishment and genetic characterization of a novel mixed-phenotype acute leukemia cell line with EP300-ZNF384 fusion[J]. J Hematol Oncol, 2015, 8: 100.
18	MARTINI A, LA STARZA R, JANSSEN H, et al. Recurrent rearrangement of the Ewing′s sarcoma gene, EWSR1, or its homologue, TAF15, with the transcription factor CIZ/NMP4 in acute leukemia[J]. Cancer Res, 2002, 62(19): 5408-5412.
19	IACOBUCCI I, KIMURA S, MULLIGHAN C G. Biologic and therapeutic implications of genomic alterations in acute lymphoblastic leukemia[J]. J Clin Med, 2021, 10(17): 3792.
20	MA J, GUAN J, CHEN B. ZNF384 rearrangement in acute lymphocytic leukemia with renal involvement as the first manifestation is associated with a poor prognosis: a case report[J]. Mol Cytogenet, 2022, 15(1): 4.
21	NISHIMURA A, HASEGAWA D, HIRABAYASHI S, et al. Very late relapse cases of TCF3-ZNF384-positive acute lymphoblastic leukemia[J]. Pediatr Blood Cancer, 2019, 66(11): e27891.
22	JING Y, LI Y F, WAN H, et al. Detection of EP300-ZNF384 fusion in patients with acute lymphoblastic leukemia using RNA fusion gene panel sequencing[J]. Ann Hematol, 2020, 99(11): 2611-2617.
23	OBERLEY M J, GAYNON P S, BHOJWANI D, et al. Myeloid lineage switch following chimeric antigen receptor T-cell therapy in a patient with TCF3-ZNF384 fusion-positive B-lymphoblastic leukemia[J]. Pediatr Blood Cancer, 2018, 65(9): e27265.
24	SCHWAB C, HARRISON C J. Advances in B-cell precursor acute lymphoblastic leukemia genomics[J]. HemaSphere, 2018, 2(4): e53.
25	GERR H, ZIMMERMANN M, SCHRAPPE M, et al. Acute leukaemias of ambiguous lineage in children: characterization, prognosis and therapy recommendations[J]. Br J Haematol, 2010, 149(1): 84-92.
26	TRAN T H, LANGLOIS S, MELOCHE C, et al. Whole-transcriptome analysis in acute lymphoblastic leukemia: a report from the DFCI ALL Consortium Protocol 16-001[J]. Blood Adv, 2022, 6(4): 1329-1341.
27	MOORMAN A V, BARRETTA E, BUTLER E R, et al. Prognostic impact of chromosomal abnormalities and copy number alterations in adult B-cell precursor acute lymphoblastic leukaemia: a UKALL14 study[J]. Leukemia, 2022, 36(3): 625-636.
28	ZALIOVA M, WINKOWSKA L, STUCHLY J, et al. A novel class of ZNF384 aberrations in acute leukemia[J]. Blood Adv, 2021, 5(21): 4393-4397.
29	PAIETTA E, ROBERTS K G, WANG V, et al. Molecular classification improves risk assessment in adult BCR-ABL1-negative B-ALL[J]. Blood, 2021, 138(11): 948-958.
30	JEHA S, CHOI J, ROBERTS K G, et al. Clinical significance of novel subtypes of acute lymphoblastic leukemia in the context of minimal residual disease-directed therapy[J]. Blood Cancer Discov, 2021, 2(4): 326-337.
31	姚子龙, 李艳芬, 李猛, 等. 伴EP300-ZNF384融合基因阳性的急性B淋巴细胞白血病临床特点分析[J]. 中国实验血液学杂志, 2020, 28(1): 24-28.
	YAO Z L, LI Y F, LI M, et al. Analysis of clinical characteristics of acute B lymphoblastic leukemia with EP300-ZNF384 fusion gene positive [J]. Journal of Experimental Hematology, 2020, 28(1): 24-28.
32	SHAGO M, ABLA O, HITZLER J, et al. Frequency and outcome of pediatric acute lymphoblastic leukemia with ZNF384 gene rearrangements including a novel translocation resulting in an ARID1B/ZNF384 gene fusion[J]. Pediatr Blood Cancer, 2016, 63(11): 1915-1921.
33	OTA T, SUZUKI Y, NISHIKAWA T, et al. Complete sequencing and characterization of 21, 243 full-length human cDNAs[J]. Nat Genet, 2004, 36(1): 40-45.
34	SEETHARAM A, BAI Y, STUART G W. A survey of well conserved families of C₂H₂ zinc-finger genes in Daphnia[J]. BMC Genomics, 2010, 11: 276.
35	FEISTER H A, TORRUNGRUANG K, THUNYAKITPISAL P, et al. NP/NMP4 transcription factors have distinct osteoblast nuclear matrix subdomains[J]. J Cell Biochem, 2000, 79(3): 506-517.
36	FAN Z Y, TARDIF G, BOILEAU C, et al. Identification in human osteoarthritic chondrocytes of proteins binding to the novel regulatory site AGRE in the human matrix metalloprotease 13 proximal promoter[J]. Arthritis Rheum, 2006, 54(8): 2471-2480.
37	YOUNG S K, SHAO Y, BIDWELL J P, et al. Nuclear matrix protein 4 is a novel regulator of ribosome biogenesis and controls the unfolded protein response via repression of Gadd34 expression[J]. J Biol Chem, 2016, 291(26): 13780-13788.
38	JIN H L, VAN'T HOF R J, ALBAGHA O M, et al. Promoter and intron 1 polymorphisms of COL1A1 interact to regulate transcription and susceptibility to osteoporosis[J]. Hum Mol Genet, 2009, 18(15): 2729-2738.
39	SHAO Y, WICHERN E, CHILDRESS P J, et al. Loss of Nmp4 optimizes osteogenic metabolism and secretion to enhance bone quality[J]. Am J Physiol Endocrinol Metab, 2019, 316(5): E749-E772.
40	YAN Z H, ZHOU Y, YANG Y, et al. Zinc finger protein 384 enhances colorectal cancer metastasis by upregulating MMP2[J]. Oncol Rep, 2022, 47(3): 49.
41	GAO Y Y, LING Z Y, ZHU Y R, et al. The histone acetyltransferase HBO₁ functions as a novel oncogenic gene in osteosarcoma[J]. Theranostics, 2021, 11(10): 4599-4615.
42	WAN F, ZHOU J, CHEN X, et al. Overexpression and mutation of ZNF384 is associated with favorable prognosis in breast cancer patients[J]. Transl Cancer Res, 2019, 8(3): 779-787.
43	MENG Q X, WANG K N, LI J H, et al. ZNF384-ZEB1 feedback loop regulates breast cancer metastasis[J]. Mol Med, 2022, 28(1): 111.
44	CHEN G, CHEN J X, QIAO Y T, et al. ZNF830 mediates cancer chemoresistance through promoting homologous-recombination repair[J]. Nucleic Acids Res, 2018, 46(3): 1266-1279.
45	SINGH J K, SMITH R, ROTHER M B, et al. Zinc finger protein ZNF₃84 is an adaptor of Ku to DNA during classical non-homologous end-joining[J]. Nat Commun, 2021, 12(1): 6560.
46	CHILDRESS P, STAYROOK K R, ALVAREZ M B, et al. Genome-wide mapping and interrogation of the Nmp4 antianabolic bone axis[J]. Mol Endocrinol, 2015, 29(9): 1269-1285.
47	LIU S G, YUAN X Q, SU H, et al. ZNF384: a potential therapeutic target for psoriasis and alzheimer's disease through inflammation and metabolism[J]. Front Immunol, 2022, 13: 892368.
48	NYQUIST K B, THORSEN J, ZELLER B, et al. Identification of the TAF15-ZNF384 fusion gene in two new cases of acute lymphoblastic leukemia with a t (12;17) (p13;q12)[J]. Cancer Genet, 2011, 204(3): 147-152.
49	CHAN H M, LA THANGUE N B. p300/CBP proteins: hats for transcriptional bridges and scaffolds[J]. J Cell Sci, 2001, 114(pt 13): 2363-2373.
50	BLACK J C, CHOI J E, LOMBARDO S R, et al. A mechanism for coordinating chromatin modification and preinitiation complex assembly[J]. Mol Cell, 2006, 23(6): 809-818.
51	DUTTO I, SCALERA C, PROSPERI E. CREBBP and p300 lysine acetyl transferases in the DNA damage response[J]. Cell Mol Life Sci, 2018, 75(8): 1325-1338.
52	ATTAR N, KURDISTANI S K. Exploitation of EP300 and CREBBP lysine acetyltransferases by cancer[J]. Cold Spring Harb Perspect Med, 2017, 7(3): a026534.
53	ENGEL I, MURRE C. The function of E- and Id proteins in lymphocyte development[J]. Nat Rev Immunol, 2001, 1(3): 193-199.
54	ZHANG X, YUAN X, ZHU W, et al. SALL4: an emerging cancer biomarker and target[J]. Cancer Lett, 2015, 357(1): 55-62.
55	JIANG Y, JI Q K, LONG X Y, et al. CLCF1 is a novel potential immune-related target with predictive value for prognosis and immunotherapy response in glioma[J]. Front Immunol, 2022, 13: 810832.
56	DEMERLÉ C, GORVEL L, OLIVE D. BTLA-HVEM couple in health and diseases: insights for immunotherapy in lung cancer[J]. Front Oncol, 2021, 11: 682007.
57	ALVES J, WURDAK H, GARAY-MALPARTIDA H M, et al. TAF15 and the leukemia-associated fusion protein TAF15-CIZ/NMP4 are cleaved by caspases-3 and-7[J]. Biochem Biophys Res Commun, 2009, 384(4): 495-500.
58	ROSSOW K L, JANKNECHT R. The Ewing′s sarcoma gene product functions as a transcriptional activator[J]. Cancer Res, 2001, 61(6): 2690-2695.
59	GEORGAKOPOULOS N, DIAMANTOPOULOS P, MICCI F, et al. An adult patient with early pre-B acute lymphoblastic leukemia with t(12;17)(p13;q21)/ZNF384-TAF15[J]. In Vivo, 2018, 32(5): 1241-1245.
60	LIANG J J, PENG H, WANG J J, et al. Relationship between the structure and function of the transcriptional regulator E2A[J]. J Biol Res (Thessalon), 2021, 28(1): 15.
61	RAO C, MALAGUTI M, MASON J O, et al. The transcription factor E2A drives neural differentiation in pluripotent cells[J]. Development, 2020, 147(12): dev184093.
62	LÓPEZ-MENÉNDEZ C, VÁZQUEZ-NAHARRO A, SANTOS V, et al. E2A modulates stemness, metastasis, and therapeutic resistance of breast cancer[J]. Cancer Res, 2021, 81(17): 4529-4544.
63	ZHOU B Q, CHU X R, TIAN H, et al. The clinical outcomes and genomic landscapes of acute lymphoblastic leukemia patients with E2A-PBX1: a 10-year retrospective study[J]. Am J Hematol, 2021, 96(11): 1461-1471.
64	BRAMBILLASCA F, MOSNA G, BALLABIO E, et al. Promoter analysis of TFPT (FB1), a molecular partner of TCF3 (E2A) in childhood acute lymphoblastic leukemia[J]. Biochem Biophys Res Commun, 2001, 288(5): 1250-1257.
65	BAUDIS M, PRIMA V, TUNG Y H, et al. ABCB1 over-expression and drug-efflux in acute lymphoblastic leukemia cell lines with t(17;19) and E2A-HLF expression[J]. Pediatr Blood Cancer, 2006, 47(6): 757-764.
66	ZHAO X J, WANG P, DIEDRICH J D, et al. Epigenetic activation of the FLT3 gene by ZNF384 fusion confers a therapeutic susceptibility in acute lymphoblastic leukemia[J]. Nat Commun, 2022, 13(1): 5401.
67	GRIFFITH M, GRIFFITH O L, KRYSIAK K, et al. Comprehensive genomic analysis reveals FLT3 activation and a therapeutic strategy for a patient with relapsed adult B-lymphoblastic leukemia[J]. Exp Hematol, 2016, 44(7): 603-613.
68	UNIPROT CONSORTIUM. UniProt: the universal protein knowledgebase in 2021[J]. Nucleic Acids Res, 2021, 49(d1): D480-D489.

[1]	门如, 朱旻霞, 张伟明. 维持性血液透析患者血钾水平及其对预后影响[J]. 上海交通大学学报（医学版）, 2023, 43(4): 507-513.
[2]	王安君, 刘宁宁. 放疗对行化疗和手术的直肠癌患者的效果分析：一项基于SEER数据库的回顾性研究[J]. 上海交通大学学报（医学版）, 2023, 43(3): 320-332.
[3]	李芳, 李凯杨, 王珏, 晏睿阳, 沈慧, 刘敏. PLA2G2A在肾乳头状细胞癌中的表达及临床意义[J]. 上海交通大学学报（医学版）, 2023, 43(2): 152-161.
[4]	冯佳丽, 彭宇, 段君凯. 川崎病相关微RNA的功能机制及生物标志物研究进展[J]. 上海交通大学学报（医学版）, 2023, 43(2): 256-260.
[5]	后书敏, 邵静波. TdT阴性的淋巴母细胞淋巴瘤/急性淋巴细胞白血病临床特点、诊断及预后研究进展[J]. 上海交通大学学报（医学版）, 2023, 43(1): 120-124.
[6]	黄治物, 吴皓. 年龄相关性听力损失研究进展与临床干预策略[J]. 上海交通大学学报（医学版）, 2022, 42(9): 1182-1187.
[7]	邱佳辉, 蔡谦谦, 杨彦, 程非池, 裘正军, 黄陈. 神经脉管浸润联合肿瘤间质比对结直肠癌预后的预测价值[J]. 上海交通大学学报（医学版）, 2022, 42(8): 1070-1080.
[8]	沙攀, 赵雪雯, 朱浩天, 高崇洲, 刘珅. 肌腱粘连的机制及干预研究进展[J]. 上海交通大学学报（医学版）, 2022, 42(8): 1116-1121.
[9]	卫雪敏, 高成金. ASPECT评分在急性缺血性脑卒中临床应用中的研究进展[J]. 上海交通大学学报（医学版）, 2022, 42(7): 919-924.
[10]	张琳程, 钟华. 结节病的发病机制与临床治疗研究进展[J]. 上海交通大学学报（医学版）, 2022, 42(7): 931-938.
[11]	王杨, 程佳月, 王振. 经颅直流电刺激作用机制的研究进展[J]. 上海交通大学学报（医学版）, 2022, 42(7): 952-957.
[12]	何冬梅, 杨驰. 下颌骨髁突骨折的诊治方案：基于上海交通大学医学院附属第九人民医院颞下颌关节中心的经验[J]. 上海交通大学学报（医学版）, 2022, 42(6): 695-701.
[13]	何冬梅, 杨驰. 颞下颌关节强直的诊治方案：基于上海交通大学医学院附属第九人民医院颞下颌关节中心的经验[J]. 上海交通大学学报（医学版）, 2022, 42(6): 702-708.
[14]	张善勇, 杨驰. 颞下颌关节骨关节炎的诊治方案：基于上海交通大学医学院附属第九人民医院颞下颌关节中心的经验[J]. 上海交通大学学报（医学版）, 2022, 42(6): 709-716.
[15]	董亚兵, 郝昀博, 张文豪, 王轶雯, 陈敏洁. 下颌第三磨牙拔除术后下牙槽神经损伤的功能检测及预后分析[J]. 上海交通大学学报（医学版）, 2022, 42(6): 717-722.

ZNF384融合亚型急性白血病的发病机制及预后研究进展

Research progress in the pathogenesis and prognosis of ZNF384 fusion subtype acute leukemia

RichHTML

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

图/表 4

参考文献 68

相关文章 15

编辑推荐

Metrics