Cardoso B A, Gírio A, Henriques C, Martins L R, Santos C, Silva A, Barata J T
Unidade de Biologia do Cancro, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Braz J Med Biol Res. 2008 May;41(5):344-50. doi: 10.1590/s0100-879x2008005000016. Epub 2008 Apr 30.
T-cell acute lymphoblastic leukemia (T-ALL) is a biologically heterogeneous disease with respect to phenotype, gene expression profile and activation of particular intracellular signaling pathways. Despite very significant improvements, current therapeutic regimens still fail to cure a portion of the patients and frequently implicate the use of aggressive protocols with long-term side effects. In this review, we focused on how deregulation of critical signaling pathways, in particular Notch, PI3K/Akt, MAPK, Jak/STAT and TGF-beta, may contribute to T-ALL. Identifying the alterations that affect intracellular pathways that regulate cell cycle and apoptosis is essential to understanding the biology of this malignancy, to define more effective markers for the correct stratification of patients into appropriate therapeutic regimens and to identify novel targets for the development of specific, less detrimental therapies for T-ALL.
T细胞急性淋巴细胞白血病(T-ALL)在表型、基因表达谱以及特定细胞内信号通路的激活方面是一种生物学上异质性的疾病。尽管有非常显著的改善,但目前的治疗方案仍无法治愈一部分患者,并且经常涉及使用具有长期副作用的激进方案。在本综述中,我们重点关注关键信号通路的失调,特别是Notch、PI3K/Akt、MAPK、Jak/STAT和TGF-β,如何导致T-ALL。识别影响调节细胞周期和凋亡的细胞内通路的改变,对于理解这种恶性肿瘤的生物学特性、定义更有效的标志物以将患者正确分层到合适的治疗方案中以及识别开发针对T-ALL的特异性、危害较小的疗法的新靶点至关重要。