CD163-positive cancer cells are a predictor of a worse clinical course in lung adenocarcinoma.


Journal

Pathology international
ISSN: 1440-1827
Titre abrégé: Pathol Int
Pays: Australia
ID NLM: 9431380

Informations de publication

Date de publication:
Oct 2021
Historique:
revised: 09 06 2021
received: 26 04 2021
accepted: 12 06 2021
pubmed: 8 7 2021
medline: 9 2 2022
entrez: 7 7 2021
Statut: ppublish

Résumé

CD163 is one of the scavenger receptors expressed on macrophages. However, several immunohistochemical studies have demonstrated that CD163 is also detected on cancer cells, and is associated with a poor prognosis. In the present study, we detected CD163 staining on cancer cells in lung adenocarcinoma and squamous cell carcinoma (SCC), and investigated the relationship between CD163 on cancer cells and the clinical prognosis. CD163 staining was seen in 128 of 342 adenocarcinoma cases and 35 of 103 SCC cases. Among the lung adenocarcinoma cases, the progression-free survival and overall survival were significantly shorter in the CD163 high group than the CD163 low group. A similar trend was observed among the SCC cases, but the difference was not statistically significant. Additionally, a higher number of macrophages was detected in areas with CD163-positive cancer cells when compared to areas with CD163-negative cancer cells. In summary, we found that CD163-positive cancer cells are a predictor of a worse clinical course in lung adenocarcinoma and SCC.

Identifiants

pubmed: 34231937
doi: 10.1111/pin.13144
doi:

Substances chimiques

Antigens, CD 0
Antigens, Differentiation, Myelomonocytic 0
Biomarkers, Tumor 0
CD163 antigen 0
Receptors, Cell Surface 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

666-673

Subventions

Organisme : Japan Society for the Promotion of Science
ID : 20H03459

Informations de copyright

© 2021 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.

Références

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Auteurs

Eri Matsubara (E)

Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Department of Thoracic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Yoshihiro Komohara (Y)

Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Center for Metabolic Regulation of Healthy Aging, Kumamoto University, Kumamoto, Japan.

Yusuke Shinchi (Y)

Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Department of Thoracic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Remi Mito (R)

Department of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Yukio Fujiwara (Y)

Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Koei Ikeda (K)

Department of Thoracic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Toshiyuki Shima (T)

Department of Pathology, Keio University School of Medicine, Tokyo, Japan.

Masayuki Shimoda (M)

Department of Pathology, Keio University School of Medicine, Tokyo, Japan.

Yae Kanai (Y)

Department of Pathology, Keio University School of Medicine, Tokyo, Japan.

Takuro Sakagami (T)

Department of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Makoto Suzuki (M)

Department of Thoracic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

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