{"entity": "researcher", "timestamp": "2026-09-03T05:16:29.227Z", "family": "Zhang", "given": "Lei", "initials": "L", "orcid": "0000-0001-7438-0489", "affiliations": ["Key Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China. lei.zhang@snnu.edu.cn.", "Department of Spine Surgery, Huaihua No.2 Hospital, Hunan University of Medicine, Huaihua, 418000, China. lei.zhang@snnu.edu.cn."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/204e83e68d0e4ec9ba875b997e5bf8f4.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/204e83e68d0e4ec9ba875b997e5bf8f4"}}, "publications": [{"entity": "publication", "iuid": "e9e1aec439f84da8a530c84d6f65f8d4", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/e9e1aec439f84da8a530c84d6f65f8d4.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/e9e1aec439f84da8a530c84d6f65f8d4"}}, "title": "1p/19q co-deletion status is associated with distinct tumor-associated macrophage infiltration in IDH mutated lower-grade gliomas.", "authors": [{"family": "Zhang", "given": "Yanyu", "initials": "Y"}, {"family": "Xie", "given": "Yuan", "initials": "Y"}, {"family": "He", "given": "Liqun", "initials": "L"}, {"family": "Tang", "given": "Jiefu", "initials": "J"}, {"family": "He", "given": "Qiyuan", "initials": "Q"}, {"family": "Cao", "given": "Qingze", "initials": "Q"}, {"family": "Cui", "given": "Langjun", "initials": "L"}, {"family": "Guo", "given": "Wei", "initials": "W"}, {"family": "Hua", "given": "Kai", "initials": "K"}, {"family": "Dimberg", "given": "Anna", "initials": "A"}, {"family": "Wang", "given": "Liang", "initials": "L"}, {"family": "Zhang", "given": "Lei", "initials": "L", "orcid": "0000-0001-7438-0489", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/204e83e68d0e4ec9ba875b997e5bf8f4.json"}}], "type": "journal article", "published": "2021-02-00", "journal": {"title": "Cell Oncol (Dordr)", "issn": "2211-3436", "volume": "44", "issue": "1", "pages": "193-204", "issn-l": null}, "abstract": "Tumor-associated macrophages (TAM)s are critical regulators of glioma progression. As yet, however, TAMs in isocitrate dehydrogenase (IDH) mutated lower-grade gliomas (LGGs) have not been thoroughly investigated. The aim of this study was to determine whether 1p/19q co-deletion status affects the TAM phenotype or its prevalence in IDH mutated LGGs.\n\nTAMs in IDH mutated LGGs were analyzed using transcriptome data from 230 samples in the TCGA database in combination with transcriptome data from single-cell RNA sequencing of IDH-mutated LGGs. Proteins potentially involved in TAM regulation were examined by immuno-staining in primary LGG samples harboring IDH mutations. Essential signaling pathways regulating TAM phenotypes were investigated in a glioma mouse model using small molecule inhibitors.\n\nMost of the TAMs in IDH-mutated LGGs expressed the M1 activation markers CD86 and TNF, whereas a subset of individual TAMs co-expressed both M1 and M2-related markers. Bioinformatics analysis in combination with immuno-staining of IDH-mutated patient samples revealed higher amounts of TAMs expressing M2-related markers in 1p/19q non-codeletion IDH-mutated LGGs compared to 1p/19q codeletion LGGs. The levels of transforming growth factor beta 1 (TGF\u03b21) and macrophage colony-stimulating factor (M-CSF) were significantly higher in 1p/19q non-codeletion LGGs than in 1p/19q codeletion LGGs. M-CSF and TGF\u03b21 signal inhibition decreased tumor growth and modulated the TAM phenotype in a glioma mouse model.\n\nOur data indicate that 1p/19q co-deletion status relates to distinct TAM infiltration in gliomas, which is likely mediated by M-CSF and TGF\u03b21 signaling. M-CSF and TGF\u03b21 signaling may play a pivotal role in regulating the TAM phenotype in glioma.", "doi": "10.1007/s13402-020-00561-1", "pmid": "32915415", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12980690"}, {"db": "pii", "key": "10.1007/s13402-020-00561-1"}], "notes": [], "created": "2026-08-20T06:40:50.356Z", "modified": "2026-08-20T06:40:50.449Z"}]}