Shinichiro Kashiwagi, Chika Watanabe, Yuki Asaka, Saeko Henmi, Hanae Matsuda, Huixian Ding, Yuko Kikukawa, Ayako Gose, Mai Nishimoto, Asuka Kochi, Koji Takada, Yukie Tauchi, Kana Ogisawa, Masatsune Shibutani, Hisakazu Fujita, Tamami Morisaki, Haruhito Kinoshita
Claims that glucose-containing anticancer infusions 'feed cancer' conflate a transient pharmaceutical carrier with chronic dysglycaemia and assume that glucose uptake equals tumour growth. We developed GLUCOSE-ONC, a multistream critical review separating direct systemic carrier comparisons, acute human glycaemia, parenteral nutrition as a high-exposure boundary, chronic dysglycaemia, and translational glucose-drug interactions. Four reproducible PubMed searches yielded 1,077 unique records; chronic dysglycaemia was handled as contextual evidence, and the clinically relevant set was curated with explicit causal-distance rules. Only one randomised systemic carrier comparison was identified: 5% glucose reduced gemcitabine vascular pain versus saline, but progression and survival were not measured. Dextrose-based hyperthermic intraperitoneal chemotherapy produced marked hyperglycaemia and inconsistent perioperative outcomes, but its large heated intraperitoneal exposure is not transportable to routine systemic carriers. Parenteral-nutrition trials, despite much larger and repeated nutrient exposure, showed mixed survival findings and no consistent neoplastic-acceleration pattern; infection and catheter effects contributed to net harm. Translational findings were bidirectional: high glucose induced resistance in some models but sensitised pancreatic and hepatocellular models, whereas glucose deprivation also induced resistance in selected endometrial and ovarian models. A 100-500 mL 5% dextrose bag contains 5-25 g; at 70 kg, 25 g over 2 h is 2.98 mg/kg/min, a transient flux subject to endogenous-production and disposal feedback. Standard glucose-containing infusion should not be conflated with chronic hyperglycaemia. Available evidence does not support the claim that transient carrier-level glucose exposure accelerates cancer progression, although direct outcome studies remain insufficient to prove exact equivalence.