Type T Large Granular Lymphocyte Leukemia (T-LGLL) is a chronic disorder characterized by the abnormal proliferation of clonal cytotoxic T cells. The intriguing association of T-LGLL with autoimmune and inflammatory diseases, the most prominent example being rheumatoid arthritis, raises questions about the underlying pathophysiologic relationships between these disorders which share several biological and clinical features, most notably neutropenia, which is considered as a clinical hallmark. Recent progress in molecular genetics has contributed to a better understanding of pathogenetic mechanisms, thus moving our knowledge in the field of LGL leukemias forward. Focusing on the constitutive activation of STAT3 pathway and the well-established role of STAT3 mutations in T-LGLL, we herein discuss whether the T cell clones occurring in comorbid conditions are the cause or the consequence of the immune-inflammatory associated events. Overall, this review sheds light on the intricate relationships between inflammation and cancer, emphasizing the importance of the STAT3 gene and its activation in the pathophysiology of these conditions. Gaining a deeper understanding of these underlying mechanisms seeks to pave the way for the development of novel targeted therapies for patients affected by inflammation-related cancers.
T大颗粒淋巴细胞白血病（T-LGLL）是一种以克隆性细胞毒性T细胞异常增殖为特征的慢性疾病。该病与自身免疫性及炎症性疾病存在引人关注的关联性，其中最显著的例子是类风湿关节炎。这种关联引发了对疾病间潜在病理生理关系的探讨——这些疾病具有多种共同的生物学和临床特征，尤其是作为临床标志的中性粒细胞减少症。分子遗传学的最新进展促进了对发病机制的深入理解，从而推动了我们在LGL白血病领域的认知发展。本文聚焦于STAT3通路的持续性激活以及STAT3突变在T-LGLL中的明确作用，探讨了共存疾病中出现的T细胞克隆究竟是免疫炎症相关事件的原因还是结果。总体而言，本综述揭示了炎症与癌症之间复杂的相互作用关系，强调了STAT3基因及其激活在这些疾病病理生理过程中的重要性。深化对这些潜在机制的理解，有望为炎症相关癌症患者开发新型靶向疗法铺平道路。
肿瘤(癌症)患者之家