Cancer Treatment and Research Communications · Published 2026-01-01 · DOI 10.1016/j.ctarc.2026.101324
Despite the evolution of targeted therapies, the clinical efficacy of multimodal treatments is frequently constrained by a persistent ‘therapeutic ceiling’, where dose-limiting toxicities necessitate involuntary interruptions in 20%–25% of patients. These disruptions severely compromise relative dose intensity (RDI) and survival outcomes while escalating financial toxicity. In this Personal View, we evaluate oligo-fucoidan, a refined marine-derived bioactive sulfated polysaccharide, as a potential investigational adjunct for supporting therapeutic continuity. Preclinical evidence suggests that oligo-fucoidan may influence redox responses, ER-stress signaling, ferroptosis-related pathways, and inflammatory injury; however, these pathways remain mechanistic hypotheses rather than clinically validated mechanisms. Exploratory clinical and preclinical data also suggest possible interactions with the host–microbiota–immune axis, although causality in human oncology cohorts remains unproven. Clinical evidence, including small randomized trials in metastatic colorectal cancer and unresectable hepatocellular carcinoma, suggests possible improvements in disease control or liver function preservation, but effects on ORR, PFS, OS, treatment completion, and relative dose intensity require further validation. We propose a future research roadmap in which biomarker-informed supportive oncology remains a hypothesis-generating framework requiring standardized formulations, evidence grading, pharmacokinetic assessment, drug–drug interaction monitoring, safety surveillance, and clinically meaningful endpoints.
Abstract from DOAJ. Public domain (CC0 1.0).
Read the article at the publisher →