An Overview of Translocation-Related Oncogenesis in the Chronic Myeloid Leukaemias
An Overview of Translocation-Related Oncogenesis in the Chronic Myeloid Leukaemias
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慢性粒细胞白血病易位相关肿瘤发生概述
作者：
B. Bain
在慢性粒细胞白血病和t（9;22）（q34;q11）患者中证实了BCR-ABL融合基因，这代表了在人类肿瘤中首次识别出导致致癌融合基因形成的易位。从最初的观察开始，这种白血病发生机制在慢性粒细胞白血病中得到越来越多的认识。融合基因通常已掺入编码受体或细胞质酪氨酸激酶，特别是ABL、PDGFRB和FGFR 1的基因的一部分。这与编码转录因子或其他核蛋白的基因在急性髓性白血病中的频繁参与形成对比。然而，编码酪氨酸激酶的基因也与某些急性白血病病例有关。除慢性粒细胞白血病中的BCR-ABL融合基因外，所有这些融合基因在慢性髓性白血病病例中均不常见或罕见。大部分费城阴性慢性髓细胞白血病病例的分子机制仍有待发现。
The demonstration of the BCR-ABL fusion gene in patients with chronic granulocytic leukaemia and t(9;22)(q34;q11) represents the first recognition, in a human neoplasm, of a translocation leading to formation of an oncogenic fusion gene. Since this initial observation, this leukaemogenic mechanism has been increasingly recognized in chronic myeloid leukaemias. The fusion gene has often incorporated part of a gene encoding a receptor or cytoplasmic tyrosine kinase, particularly ABL, PDGFRB and FGFR1. This contrasts with the frequent involvement of genes encoding transcription factors or other nuclear proteins in acute myeloid leukaemia. Nevertheless, genes encoding tyrosine kinases have also been implicated in some cases of acute leukaemia. With the exception of the BCR-ABL fusion gene in chronic granulocytic leukaemia, all these fusion genes are uncommon or rare among cases of chronic myeloid leukaemia. The molecular mechanisms underlying the great majority of cases of Philadelphia-negative chronic myeloid leukaemia remain to be discovered.
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影响因子：
20.3
作者：
M. K. Magnússon;K. Meade;K. E. Brown;D. Arthur;Lisa A. Krueger;A. Barrett;C. Dunbar
通讯作者：
M. K. Magnússon;K. Meade;K. E. Brown;D. Arthur;Lisa A. Krueger;A. Barrett;C. Dunbar
影响因子：
56.9
作者：
DALEY, GQ;VANETTEN, RA;BALTIMORE, D
通讯作者：
BALTIMORE, D
影响因子：
20.3
作者：
Schwaller, J;Anastasiadou, E;Gilliland, DG
通讯作者：
Gilliland, DG
影响因子：
20.3
作者：
Sillaber, C;Gesbert, F;Griffin, JD
通讯作者：
Griffin, JD