Evidence map›Paper›PMID 38600426›Full record

ArticleInternational journal of clinical oncology2024

Progressive changes in the protein expression profile of alveolar septa in early-stage lung adenocarcinoma.

Toru Kimura, Takashi Akazawa, Yu Mizote, Harumi Nakamura, Miki Sakaue, Tomohiro Maniwa, Yasushi Shintani, Keiichiro Honma, Hideaki Tahara, Jiro Okami

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Article in International journal of clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

What it found

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Toru KimuraDepartment of General Thoracic Surgery, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan. kimura@thoracic.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-4504-232X
Takashi AkazawaDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Yu MizoteDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Harumi NakamuraLaboratory of Genomic Pathology, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Miki SakaueDepartment of General Thoracic Surgery, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Tomohiro ManiwaDepartment of General Thoracic Surgery, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Yasushi ShintaniDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, 2-2-L5, Yamadaoka, , Suita, 565-0871, Japan.
Keiichiro HonmaDepartment of Pathology, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Hideaki TaharaDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.
Jiro OkamiDepartment of General Thoracic Surgery, Osaka International Cancer Institute, 3-1-69, Otemae, Chuo-Ku, Osaka, 541-8567, Japan.

Funding

JSPS KAKENHI JP19K09314
6 · The paper itself

Abstract

backgroundAdenocarcinomas show a stepwise progression from atypical adenomatous hyperplasia (AAH) through adenocarcinoma in situ (AIS) to invasive adenocarcinoma (IA). Immunoglobulin superfamily containing leucine-rich repeat (ISLR) is a marker of tumor-restraining cancer-associated fibroblasts (CAFs), which are distinct from conventional, strongly α-smooth muscle actin (αSMA)-positive CAFs. Fibroblast activation protein (FAP) has been focused on as a potential therapeutic and diagnostic target of CAFs.

methodsWe investigated the changes in protein expression during adenocarcinoma progression in the pre-existing alveolar septa by assessing ISLR, αSMA, and FAP expression in normal lung, AAH, AIS, and IA. Fourteen AAH, seventeen AIS, and twenty IA lesions were identified and randomly sampled. Immunohistochemical analysis was performed to evaluate cancer-associated changes and FAP expression in the pre-existing alveolar structures.

resultsNormal alveolar septa expressed ISLR. The ISLR level in the alveolar septa decreased in AAH and AIS tissues when compared with that in normal lung tissue. The αSMA-positive area gradually increased from the adjacent lung tissue (13.3% ± 15%) to AIS (87.7% ± 14%), through AAH (70.2% ± 21%). Moreover, the FAP-positive area gradually increased from AAH (1.69% ± 1.4%) to IA (11.8% ± 7.1%), through AIS (6.11% ± 5.3%). Protein expression changes are a feature of CAFs in the pre-existing alveolar septa that begin in AAH. These changes gradually progressed from AAH to IA through AIS.

conclusionsFAP-positive fibroblasts may contribute to tumor stroma formation in early-stage lung adenocarcinoma, and this could influence the development of therapeutic strategies targeting FAP-positive CAFs for disrupting extracellular matrix formation.

Indexed as

Adenocarcinoma of LungDisease ProgressionEndopeptidasesLung NeoplasmsMembrane ProteinsActinsAdenocarcinomaAdenocarcinoma in SituAdultAgedBiomarkers, TumorCancer-Associated FibroblastsFemaleFibroblast Activation Protein AlphaGelatinasesHumansActinsBiomarkers, TumorEndopeptidasesFibroblast Activation Protein AlphaGelatinasesMembrane ProteinsSerine EndopeptidasesCancer-associated fibroblastFibroblast-activation proteinLepidic growthLung adenocarcinomaTumor stroma

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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.