T-cell acute lymphoblastic leukemia (T-ALL) is characterized by a variable response to steroids during induction and/or consolidation therapy. Notably, recent work suggested that these differences in glucocorticoid sensitivity might, at least in part, be mediated by hyperactivation of specific oncogenic pathways such as RAS/MEK/ERK, PI3K/AKT and IL7R/JAK/STAT. In this review, we elaborate on putative associations between aberrant signaling, therapy resistance, incidence of relapse and clinical outcome in human T-ALL. Furthermore, we emphasize that this potential association with clinical parameters might also be mediated by the tumor microenvironment as a result of increased sensitivity of leukemic T-cells towards cytokine induced signaling pathway activation. With this in mind, we provide an overview of small molecule inhibitors that might have clinical potential for the treatment of human T-ALL in the near future as a result of their ability to overcome steroid resistance thereby potentially increasing survival rates in this aggressive hematological neoplasm.

T细胞急性淋巴细胞白血病（T-ALL）的特征是诱导和/或巩固治疗期间对类固醇的反应不同。值得注意的是，最近的研究表明，糖皮质激素敏感性的这些差异可能至少部分地由特定致癌途径（如RAS / MEK / ERK，PI3K / AKT和IL7R / JAK / STAT）的过度激活介导。在这篇综述中，我们详细阐述了人类T-ALL中异常信号传导，治疗耐药性，复发率和临床结局之间的假定关联。此外，我们强调，由于白血病T细胞对细胞因子诱导的信号通路激活的敏感性增加，肿瘤微环境也可能介导了这种与临床参数的潜在关联。考虑到这一点，