Evidence map›Paper›PMID 42785157›Full record

ReviewNeoplasia (New York, N.Y.)2026

Glucose-containing carriers in cancer therapy (GLUCOSE-ONC): A multistream critical review and quantitative exposure framework.

Shinichiro Kashiwagi, Chika Watanabe, Yuki Asaka, Saeko Henmi, Hanae Matsuda, Huixian Ding, Yuko Kikukawa, Ayako Gose, Mai Nishimoto, Asuka Kochi and 7 more

Abstract readReview
In one paragraph

Review in Neoplasia (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Shinichiro KashiwagiDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: spqv9ke9@view.ocn.ne.jp.
Chika WatanabeDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Yuki AsakaDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Saeko HenmiDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Hanae MatsudaDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Huixian DingDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Yuko KikukawaDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Ayako GoseDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Mai NishimotoDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Asuka KochiDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Koji TakadaDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Yukie TauchiDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Kana OgisawaDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Masatsune ShibutaniDepartment of Gastrointestinal Surgery, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Hisakazu FujitaDepartment of Scientific and Linguistic Fundamentals of Nursing, Osaka Metropolitan University Graduate School of Nursing, 1-5-17 Asahi-machi, Abeno-ku, Osaka 545-0051, Japan.
Tamami MorisakiDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Haruhito KinoshitaDepartment of Breast Surgical Oncology, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

ChemotherapyDextroseGlucoseInfusionMetabolismTumour progression

Identifiers

PMID42785157
PMCPMC13634770

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.