Evidence map›Paper›PMID 42710618›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

B-Cell Lymphoma-Extra Large Promotes Gastric Tumorigenesis via Apoptosis-Independent Wnt-β-Catenin Activation and Peroxisome Proliferator-Activated Receptor γ Suppression.

Yukiko Oya, Junya Arai, Yoku Hayakawa, Toshiro Shiokawa, Shintaro Shinohara, Masahiro Hata, Yuki Matsushita, Hiroto Kinoshita, Chie Uekura, Ken Kurokawa and 8 more

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In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 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

18 authors.

Yukiko OyaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Junya AraiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Division of Gastroenterology, The Institute of Medical Science, Asahi Life Foundation, Tokyo, Japan; Division of Digestive and Liver Disease, Department of Medicine, Columbia University, New York, New York.
Yoku HayakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address: yhayakawa-tky@umin.ac.jp.
Toshiro ShiokawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shintaro ShinoharaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masahiro HataDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yuki MatsushitaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroto KinoshitaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Chie UekuraDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Ken KurokawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Sohei AbeDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Mayo TsuboiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Sozaburo IharaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Nobumi SuzukiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hayato HikitaDepartment of Gastroenterology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Tetsuo TakeharaDepartment of Gastroenterology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Timothy C WangDivision of Digestive and Liver Disease, Department of Medicine, Columbia University, New York, New York.
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Funding

The Role of Stem Cells and the Microenvironment in Gastrointestinal CancersR35CA210088 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Timothy Cragin Wang · 2017 to 2026
$10.2M
THE FUNCTION AND REGULATION OF HISTIDINE DECARBOXYLASE IN GUT INFLAMMATIONR01DK048077 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WANG, TIMOTHY CRAGIN · 1995 to 2020
$5.9M
NCI NIH HHS R35 CA210088NIDDK NIH HHS R01 DK048077
6 · The paper itself

Abstract

BACKGROUND &

aimsThe Wnt-β-catenin and Yes-associated protein pathways cooperatively drive gastrointestinal tumor progression. BCL2L1, a Yes-associated protein target gene, encodes the anti-apoptotic isoform B-cell lymphoma-extra-large, which is highly expressed in multiple cancers, but its role in gastric cancer remains unclear.

methodsWe generated Mist1-CreERT; Apc

resultsDeletion of B-cell lymphoma-extra-large significantly reduced tumor growth and proliferation in Apc-deficient tumors, organoids, and xenografts. Nuclear β-catenin and Wnt target gene expression were attenuated, partly through derepression of Hnf4a and Pparg, indicating that B-cell lymphoma-extra-large promotes Wnt signaling. Concurrently, downregulation of Hnf4a and Pparg contributes to the inhibition of multiple metabolic pathways. In human gastric cancer, high BCL2L1 expression correlated with elevated Wnt target genes and poor prognosis, whereas PPARG expression inversely correlated with BCL2L1 and associated with favorable outcomes. Epidemiologic analysis suggested that pioglitazone, a peroxisome proliferator-activated receptor γ agonist, reduced gastric cancer incidence in diabetic patients.

conclusionsB-cell lymphoma-extra-large promotes gastric tumorigenesis through dual mechanisms-enhancing Wnt signaling and suppressing peroxisome proliferator-activated receptor γ-and highlight B-cell lymphoma-extra-large as a potential therapeutic target while suggesting peroxisome proliferator-activated receptor γ activation may be protective.

Indexed as

Bcl-xLGastric CancerPPARγWnt–β-catenin

Identifiers

PMID42710618
PMCPMC13685607

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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 OpenQuestion graph.