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急性淋巴细胞白血病的分子生物学

Molecular biology of acute lymphocytic leukemia.

作者信息

Thandla S, Aplan P D

机构信息

Division of Pediatrics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

出版信息

Semin Oncol. 1997 Feb;24(1):45-56.

PMID:9045304
Abstract

Acute lymphoblastic leukemia (ALL) has been extensively studied and characterized at a molecular level. The identification and characterization of molecular lesions associated with ALL has led to advances in classification and prognosis of ALL, which in turn has been useful in stratifying ALL patients for treatment purposes. However, perhaps of greater long-term significance are insights into the mechanisms of leukemogenesis that have been provided by characterization of ALL at a molecular level. This review focuses on general themes and mechanisms of disease, concentrating on recent advances in the field, including the relationship of deregulated transcription factors to ALL, probable mechanisms of lymphoid translocations, and newly characterized genetic lesions, such as those involving tumor suppressor genes, 11q23 abnormalities, and 12p12 abnormalities.

摘要

急性淋巴细胞白血病(ALL)已在分子水平上得到广泛研究和表征。与ALL相关的分子病变的鉴定和表征推动了ALL分类和预后方面的进展,这反过来又有助于为治疗目的对ALL患者进行分层。然而,从分子水平对ALL进行表征所获得的白血病发生机制的见解可能具有更大的长期意义。本综述聚焦于疾病的一般主题和机制,重点关注该领域的最新进展,包括失调的转录因子与ALL的关系、淋巴易位的可能机制以及新发现的遗传病变,如涉及肿瘤抑制基因的病变、11q23异常和12p12异常。

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Molecular biology of acute lymphocytic leukemia.急性淋巴细胞白血病的分子生物学
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Id4 is deregulated by a t(6;14)(p22;q32) chromosomal translocation in a B-cell lineage acute lymphoblastic leukemia.在B细胞系急性淋巴细胞白血病中,Id4因t(6;14)(p22;q32)染色体易位而失调。
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引用本文的文献

1
The role of CALM-AF10 gene fusion in acute leukemia.CALM-AF10基因融合在急性白血病中的作用。
Leukemia. 2008 Apr;22(4):678-85. doi: 10.1038/sj.leu.2405074. Epub 2007 Dec 20.
2
The t(14;21)(q11.2;q22) chromosomal translocation associated with T-cell acute lymphoblastic leukemia activates the BHLHB1 gene.与T细胞急性淋巴细胞白血病相关的t(14;21)(q11.2;q22)染色体易位激活了BHLHB1基因。
Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3497-502. doi: 10.1073/pnas.97.7.3497.
3
Disordered T-cell development and T-cell malignancies in SCL LMO1 double-transgenic mice: parallels with E2A-deficient mice.
SCL LMO1双转基因小鼠中T细胞发育紊乱和T细胞恶性肿瘤:与E2A缺陷小鼠的相似之处。
Mol Cell Biol. 1999 Jul;19(7):5025-35. doi: 10.1128/MCB.19.7.5025.
4
The partial tandem duplication of ALL1 (MLL) is consistently generated by Alu-mediated homologous recombination in acute myeloid leukemia.急性髓系白血病中,ALL1(MLL)的部分串联重复是由Alu介导的同源重组持续产生的。
Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2390-5. doi: 10.1073/pnas.95.5.2390.