Evidence map›Paper›PMID 41912380›Full record

ArticleThoracic cancer2026

Tumor-Bearing Status Accelerates Bleomycin-Induced Pulmonary Inflammation via Endothelial Activation.

Shoko Isoyama, Kakuhiro Yamaguchi, Hiroshi Iwamoto, Yasushi Horimasu, Kunihiko Funaishi, Kiyofumi Shimoji, Shinjiro Sakamoto, Takeshi Masuda, Taku Nakashima, Shinichiro Ohshimo and 2 more

Abstract read
In one paragraph

Article in Thoracic cancer, 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

12 authors.

Shoko IsoyamaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.
Kakuhiro YamaguchiDepartment of Respiratory Medicine, Hiroshima University Hospital, Hiroshima, Japan.ORCID https://orcid.org/0000-0002-9117-1934
Hiroshi IwamotoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.
Yasushi HorimasuDepartment of Respiratory Medicine, Hiroshima University Hospital, Hiroshima, Japan.
Kunihiko FunaishiDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.
Kiyofumi ShimojiDepartment of Respiratory Medicine, Hiroshima University Hospital, Hiroshima, Japan.
Shinjiro SakamotoDepartment of Respiratory Medicine, Hiroshima University Hospital, Hiroshima, Japan.
Takeshi MasudaDepartment of Respiratory Medicine, Hiroshima University Hospital, Hiroshima, Japan.
Taku NakashimaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.
Shinichiro OhshimoDepartment of Emergency and Critical Care Medicine, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.
Hironobu HamadaDepartment of Physical Analysis and Therapeutic Sciences, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.ORCID https://orcid.org/0000-0002-7979-0708
Noboru HattoriDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima, Japan.ORCID https://orcid.org/0000-0002-8234-942X

Funding

Japan Society for the Promotion of Science 18K15951Japan Society for the Promotion of Science 22K16194
6 · The paper itself

Abstract

backgroundDrug-induced lung disease (DILD) is a severe adverse event of cancer treatment. Several clinical reports have demonstrated an association between DILD and tumor progression. However, the underlying mechanism remains unclear. This study aimed to elucidate the role of tumor-bearing status in the development of DILD.

methodsWe prepared a subcutaneous Lewis lung carcinoma (LLC) and KLN205-bearing model. To trigger DILD, bleomycin (BLM) was administered subcutaneously. mRNA expression associated with endothelial activation (PAI-1, vWF, and ICAM-1), inflammatory cell infiltration, and alveolar wall thickness was assessed by using bronchioalveolar lavage fluid (BALF) and lung tissue. Additionally, the role of high-mobility group box 1 (HMGB1) in tumor-bearing status was examined.

resultsCompared with control mice, LLC- and KLN205-bearing mice showed a tendency toward increased expression of at least one of PAI-1, vWF, and ICAM-1 on endothelium, along with inflammatory cell infiltration in the lungs. BLM-treated mice with LLC showed more inflammatory cell infiltration than BLM-treated mice, accompanied by a significant increase in PAI-1, vWF, and ICAM-1 expression on endothelium. Moreover, BLM-treated mice with LLC exhibited pronounced alveolar wall thickening. In LLC-bearing mice, serum HMGB1 levels were significantly higher compared with control mice. Additionally, inflammatory cell infiltration in the lungs tended to be increased by the intraperitoneal injection of HMGB1, which was accompanied by increased expression of vWF and ICAM-1 on endothelium.

conclusionsThis study showed that tumor-bearing status elicits proinflammatory activation in endothelial cells and inflammatory cell infiltration into the lungs that aggravates DILD caused by BLM.

Indexed as

BleomycinCarcinoma, Lewis LungPneumoniaAnimalsDisease Models, AnimalHMGB1 ProteinIntercellular Adhesion Molecule-1MaleMiceMice, Inbred C57BLvon Willebrand FactorBleomycinHMGB1 ProteinIntercellular Adhesion Molecule-1von Willebrand Factordrug‐induced lung diseaseendothelial cellsHMGB1inflammationtumor

Identifiers

PMID41912380
PMCPMC13070733

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.