Role of chemokines in T-cell acute lymphoblastic Leukemia: From pathogenesis to therapeutic options

T-cell acute lymphoblastic leukemia (T-ALL) is a highly heterogeneous and aggressive subtype of hematologic malignancy, with limited therapeutic options due to the complexity of its pathogenesis. Although high-dose chemotherapy and allogeneic hematopoietic stem cell transplantation have improved outcomes for T-ALL patients, there remains an urgent need for novel treatments in cases of refractory or relapsed disease. Recent research has demonstrated the potential of targeted therapies aimed at specific molecular pathways to improve patient outcomes. Chemokine-related signals, both upstream and downstream, modulate the composition of distinct tumor microenvironments, thereby regulating a multitude of intricate cellular processes such as proliferation, migration, invasion and homing. Furthermore, the progress in research has made significant contributions to precision medicine by targeting chemokine-related pathways. This review article summarizes the crucial roles of chemokines and their receptors in T-ALL pathogenesis. Moreover, it explores the advantages and disadvantages of current and potential therapeutic options that target chemokine axes, including small molecule antagonists, monoclonal antibodies, and chimeric antigen receptor T-cells.

Automated summary

T-cell acute lymphoblastic leukemia (T-ALL) is a highly heterogeneous and aggressive hematologic malignancy, with limited therapeutic options. Targeted therapies aimed at specific molecular pathways have shown potential in improving patient outcomes. Chemokine-related signals play crucial roles in T-ALL pathogenesis by modulating tumor microenvironments and cellular processes. This review explores the advantages and disadvantages of current and potential therapeutic options targeting chemokine axes.