13q12.2 deletions and FLT3 overexpression in acute leukemias.
作者信息
Poubel Caroline Pires, Boroni Mariana, Emerenciano Mariana
机构信息
Division of Clinical Research and.
Bioinformatics and Computational Biology Laboratory, Research Center, Instituto Nacional de Câncer (INCA), Rio de Janeiro, Brazil.
出版信息
Blood Adv. 2021 Apr 27;5(8):2075-2078. doi: 10.1182/bloodadvances.2020003643.
Abstract
摘要
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本文引用的文献
1
Deletions in BCP-ALL result in a TAD more FLT3.BCP-ALL 缺失导致 TAD 上更多的 FLT3。
Blood. 2020 Aug 20;136(8):919-920. doi: 10.1182/blood.2020006607.
2
13q12.2 deletions in acute lymphoblastic leukemia lead to upregulation of FLT3 through enhancer hijacking.急性淋巴细胞白血病中 13q12.2 的缺失导致 FLT3 通过增强子劫持而上调。
Blood. 2020 Aug 20;136(8):946-956. doi: 10.1182/blood.2019004684.
3
FLT3 overexpression in acute leukaemias: New insights into the search for molecular mechanisms.FLT3 过度表达在急性白血病中的研究：对分子机制探索的新见解。
Biochim Biophys Acta Rev Cancer. 2019 Aug;1872(1):80-88. doi: 10.1016/j.bbcan.2019.06.001. Epub 2019 Jun 12.
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Advances in biology of acute lymphoblastic leukemia (ALL) and therapeutic implications.急性淋巴细胞白血病（ALL）生物学进展及治疗意义
Am J Blood Res. 2018 Dec 10;8(4):29-56. eCollection 2018.
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FLT3 pathway is a potential therapeutic target for PRC2-mutated T-cell acute lymphoblastic leukemia.FLT3通路是PRC2突变型T细胞急性淋巴细胞白血病的一个潜在治疗靶点。
Blood. 2018 Dec 6;132(23):2520-2524. doi: 10.1182/blood-2018-04-845628. Epub 2018 Oct 3.
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