Evidence map›Paper›PMID 41826681›Full record

ArticleBJC reports2026

IL10RB expression in cancer cells is associated with evolutionary changes to solidify treatment resistance.

Chie Kudo-Saito, Hiroki Ozawa, Hiroshi Imazeki, Hitomi Masuda, Aki Takaiwa, Masayoshi Toyoura

Abstract read
In one paragraph

Article in BJC reports, 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
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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

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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

6 authors.

Chie Kudo-SaitoDepartment of Immune Medicine, National Cancer Center Research Institute, Tokyo, Japan. ckudo@ncc.go.jp.ORCID http://orcid.org/0000-0003-4644-9404
Hiroki OzawaDepartment of Immune Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Hiroshi ImazekiDepartment of Immune Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Hitomi MasudaChiome Bioscience Inc, Tokyo., Japan.
Aki TakaiwaChiome Bioscience Inc, Tokyo., Japan.
Masayoshi ToyouraChiome Bioscience Inc, Tokyo., Japan.

Funding

Chiome Bioscience Inc. C2017-143Japan Agency for Medical Research and Development 106209
6 · The paper itself

Abstract

backgroundMany molecular mechanisms underlying tumor escape, in which cancer cells undergo epithelial-to-mesenchymal transition (EMT) and thereby acquire metastatic potential and cancer stemness, have been reported. However, cancer metastasis and treatment resistance remain unconquerable for many cancer patients, probably due to diverse evolutionary changes in cancer cells.

methodsGene expressions in cancer cells with/without EMT-governing snail overexpression were compared using GeneChip microarray, and a gene was identified that was significantly increased with snail expression. The molecular functions were analyzed in vitro and in vivo using cancer cells overexpressing the identified gene, and the therapeutic efficacy induced by blocking the molecule was evaluated using mouse tumor models.

resultsSnail expression dramatically enhanced IL10RB expression in cancer cells, and IL10RB overexpression in cancer cells enhanced cellular adhesion, invasiveness, and chemoresistance. Treatment with anti-IL10RB blocking mAb attenuated such refractory properties of the IL10RB

conclusionThis study revealed that IL10RB is a key molecule in cancer intractability after achieving snail-induced EMT. Targeting IL10RB may be a promising strategy for improving clinical outcomes in the treatment of cancer.

Identifiers

PMID41826681
PMCPMC12988042

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.