Pediatric leukemia: what if everything happens at the cell surface?

By Ana Espino | Published on February 10, 2026 | 3 min read


Acute lymphoblastic leukemia (ALL) is the most common cancer in children, accounting for approximately 80% of pediatric leukemias. It is characterized by the massive proliferation of immature lymphoblasts in the bone marrow, disrupting normal hematopoiesis and leading to potentially fatal complications without prompt treatment. Owing to therapeutic advances, survival rates now exceed 85%. However, this success still conceals significant limitations in disease management.

Nearly one-third of high-risk patients develop refractory or relapsing disease, often associated with complex molecular alterations and immune escape mechanisms. Current strategies, based on intensive chemotherapy or targeted immunotherapies, face limitations related to toxicity, resistance, and insufficient patient stratification. A critical unmet need remains: the identification of novel molecular biomarkers to refine prognosis and enable more personalized therapeutic approaches.

In this context, sialic acids—terminal components of glycans on the cell surface—are emerging as potential modulators of tumor progression. Their role in cell adhesion, signaling, and immune evasion may position them as innovative therapeutic targets. This study was designed to assess the functional involvement of sialic acids in pediatric ALL by analyzing their expression, biological impact, and potential value as therapeutic targets or biomarkers in aggressive disease forms.  

Are sialic acids invisible accomplices?

The authors conducted a structured narrative review based on in vitro studies, animal models, and clinical data analyses. They examined the expression of different forms of sialic acids (Neu5Ac, Neu5Gc) and their transporters (such as SLC17A5), as well as enzymes regulating their metabolism, particularly sialyltransferases (STs).

The findings indicate that leukemic cells exhibit membrane hypersialylation, notably through increased α2,3- and α2,6-linked sialic acids. This alteration of the tumor glycocalyx promotes abnormal adhesion to the bone marrow microenvironment, enhances tissue invasion, and suppresses immune responses, particularly by inhibiting natural killer (NK) cell activation.

The study also highlights the role of specific transporters, such as SLC17A5, involved in intracellular sialic acid accumulation, which may disrupt cellular metabolism and lymphoblast differentiation. Transcriptomic database analyses (TCGA, GEO) reveal overexpression of these enzymes in aggressive ALL subtypes.

Experimental studies further suggest that inhibitors of sialyltransferases or enzymes capable of modifying glycosylated structures could help restore anti-tumor immune responses, paving the way for innovative combination therapies.

Can one excess sugar alter prognosis?