Potential anti-lymphoma effect of M-CSFR inhibitor in adult T-cell leukemia/lymphoma

The c-fms proto-oncogene is also known as macrophage colony stimulating factor receptor (M-CSFR) or colony-stimulating factor-1 receptor (CSF-1R), and is expressed on several types of malignant tumor cells and myeloid cells. In the present study, we found that overexpression of M-CSFR was present in...

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Published inJournal of Clinical and Experimental Hematopathology Vol. 58; no. 4; pp. 152 - 160
Main Authors Komohara, Yoshihiro, Noyori, Osamu, Saito, Yoichi, Takeya, Hiroto, Baghdadi, Muhammad, Kitagawa, Fumihito, Hama, Naoki, Ishikawa, Kozo, Okuno, Yutaka, Nosaka, Kisato, Seino, Ken-ichiro, Matsuoka, Masao, Suzu, Shinya
Format Journal Article
LanguageEnglish
Published Japan The Japanese Society for Lymphoreticular Tissue Research 01.01.2018
JSLRT
Subjects
Adult
Apoptosis
ATLL
B7-H1 Antigen - biosynthesis
Cell Line, Tumor
CSF-1R
Cytokines - biosynthesis
Female
Gene Expression Regulation, Leukemic
Humans
Leukemia-Lymphoma, Adult T-Cell - drug therapy
Leukemia-Lymphoma, Adult T-Cell - metabolism
Leukemia-Lymphoma, Adult T-Cell - pathology
M-CSFR
macrophage
Male
Original
PD-L1
Receptor, Macrophage Colony-Stimulating Factor - antagonists & inhibitors
Receptor, Macrophage Colony-Stimulating Factor - biosynthesis
PD-L1
macrophage
M-CSFR
ATLL
CSF-1R
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Summary:The c-fms proto-oncogene is also known as macrophage colony stimulating factor receptor (M-CSFR) or colony-stimulating factor-1 receptor (CSF-1R), and is expressed on several types of malignant tumor cells and myeloid cells. In the present study, we found that overexpression of M-CSFR was present in adult T-cell leukemia/lymphoma (ATLL) cases. M-CSFR signaling was associated with lymphoma cell proliferation, and M-CSFR inhibition induced apoptosis in lymphoma cells. The ATLL cell line ATL-T expressed M-CSF/CSF-1 and interleukin (IL)-34, which are both M-CSFR ligands. M-CSF and IL-34 expression was seen in ATLL cases, and co-expression of these ligands was detected in 11 of 13 ATLL cases. M-CSFR inhibition suppressed programmed death-1 and -2 ligand in ATL-T cells and macrophages stimulated with conditioned medium from ATL-T cells. Thus, an M-CSFR inhibitor may be useful as additional therapy against ATLL due to direct and indirect mechanisms.
Bibliography:First two authors equally contributed to this work.
ISSN:1346-4280
1880-9952
DOI:10.3960/jslrt.18034