The New Clinicopathologic and Molecular Findings in Myeloid Neoplasms With inv(3)(q21q26)/t(3;3)(q21;q26.2).
The New Clinicopathologic and Molecular Findings in Myeloid Neoplasms With inv(3)(q21q26)/t(3;3)(q21;q26.2).
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inv(3)(q21q26)/t(3;3)(q21;q26.2) 骨髓肿瘤的新临床病理学和分子学发现。
DOI：
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发表时间：
2016
影响因子：
4.6
通讯作者：
H. Rashidi
中科院分区：
文献类型：
--
作者：
Huan;H. Rashidi
上下文
- Inv（3）（q21 q26）/t（3;3）（q21;q26.2）是3q 21 q26综合征中最常见的遗传异常形式。具有3q 21 q26异常的髓系肿瘤包括急性髓系白血病（AML）、骨髓增生异常综合征（MDS）和骨髓增生性肿瘤的急变。近年来inv（3）/t（3;3）髓系肿瘤的临床病理特征和新的分子或基因组学研究进展值得我们对此进行综述。
目的
- 目的：探讨inv（3）/t（3;3）髓系肿瘤的临床病理特征、分子及基因组改变。
数据源
- 这些数据来自英语文学中发表的文章。
结论
- 在临床病理学方面，最近对inv（3）/t（3;3）MDS的研究强调了其与inv（3）/t（3;3）携带AML的重叠临床病理学特征和相似的总生存期，无论髓系母细胞的百分比如何。在分子方面，AML和MDS伴inv（3）/t（3;3）表现出基因突变，影响RAS/受体酪氨酸激酶途径。此外，使用基因组编辑和基因组工程的功能基因组研究表明，GATA 2远端造血增强子重新分配到异位病毒整合位点1（EVI 1）启动子附近，而不形成新的致癌融合转录物是这些inv（3）/t（3;3）骨髓肿瘤的分子机制。尽管AML和MDS伴inv（3）/t（3;3）在2008年世界卫生组织分类中被列为骨髓恶性肿瘤的单独类别，但AML和MDS伴inv（3）/t（3;3）患者之间重叠的临床病理学特征、相似的总生存率以及分子和基因组水平上的相同模式可能共同有利于AML和MDS伴inv（3）/t（3;3）的统一。3）AML或髓系肿瘤伴inv（3）/t（3;3），无论原始细胞计数如何。
CONTEXT
- Inv(3)(q21q26)/t(3;3)(q21;q26.2) is the most common form of genetic abnormality of the so-called 3q21q26 syndrome. Myeloid neoplasms with 3q21q26 aberrancies include acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and blast crisis of myeloproliferative neoplasms. Recent advances on myeloid neoplasms with inv(3)/t(3;3) with regard to clinicopathologic features and novel molecular or genomic findings warrant a comprehensive review on this topic.
OBJECTIVE
- To review the clinicopathologic features and molecular as well as genomic alterations in myeloid neoplasms with inv(3)/t(3;3).
DATA SOURCES
- The data came from published articles in English-language literature.
CONCLUSIONS
- At the clinicopathologic front, recent studies on MDS with inv(3)/t(3;3) have highlighted their overlapping clinicopathologic features with and similar overall survival to that of inv(3)/t(3;3)-harboring AML regardless of the percentage of myeloid blasts. On the molecular front, AML and MDS with inv(3)/t(3;3) exhibit gene mutations, which affect the RAS/receptor tyrosine kinase pathway. Furthermore, functional genomic studies using genomic editing and genome engineering have shown that the reallocation of the GATA2 distal hematopoietic enhancer to the proximity of the promoter of ectopic virus integration site 1 (EVI1) without the formation of a new oncogenic fusion transcript is the molecular mechanism underlying these inv(3)/t(3;3) myeloid neoplasms. Although the AML and MDS with inv(3)/t(3;3) are listed as a separate category of myeloid malignancies in the 2008 World Health Organization classification, the overlapping clinicopathologic features, similar overall survival, and identical patterns at the molecular and genomic levels between AML and MDS patients with inv(3)/t(3;3) may collectively favor a unification of AML and MDS with inv(3)/t(3;3) as AML or myeloid neoplasms with inv(3)/t(3;3) regardless of the blast count.
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影响因子：
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DOI：
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