دورية أكاديمية
Integrated analysis reveals distinct molecular, clinical, and immunological features of B7‐H3 in acute myeloid leukemia
العنوان: | Integrated analysis reveals distinct molecular, clinical, and immunological features of B7‐H3 in acute myeloid leukemia |
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المؤلفون: | Ling‐yi Zhang, Ye Jin, Pei‐hui Xia, Jiang Lin, Ji‐chun Ma, Ting Li, Zi‐qi Liu, He‐lin Xiang, Chen Cheng, Zi‐jun Xu, Hong Zhou, Jun Qian |
المصدر: | Cancer Medicine, Vol 10, Iss 21, Pp 7831-7846 (2021) |
بيانات النشر: | Wiley, 2021. |
سنة النشر: | 2021 |
المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
مصطلحات موضوعية: | acute myeloid leukemia, B7‐H3, immune checkpoint, prognosis, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282 |
الوصف: | Abstract The role of B7‐H3 in acute myeloid leukemia (AML) is not fully understood. Two previous studies investigating its expression and significances in AML are partially different. In this study, we aimed to systematically characterize the genomic and immune landscape in AML patients with altered B7‐H3 expression using multi‐omics data in the public domain. We found significantly increased B7‐H3 expression in AML compared to either other hematological malignancies or healthy controls. Clinically, high B7‐H3 expression was associated with old age, TP53 mutations, wild‐type WT1 and CEBPA, and the M3 and M5 FAB subtypes. Moreover, we observed that increased B7‐H3 expression correlated significantly with a poor outcome of AML patients in four independent datasets. Gene set enrichment analysis (GSEA) revealed the enrichment of the “EMT” oncogenic gene signatures in high B7‐H3 expressers. Further investigation suggested that B7‐H3 was more likely to be associated with immune‐suppressive cells (macrophages, neutrophils, dendritic cells, and Th17 cells). B7‐H3 was also positively associated with a number of checkpoint genes, such as VISTA (B7‐H5), CD80 (B7‐1), CD86 (B7‐2), and CD70. In summary, we uncovered distinct genomic and immunologic features associated with B7‐H3 expression in AML. This may lead to a better understanding of the molecular mechanisms underlying B7‐H3 dysregulation in AML and to the development of novel therapeutic strategies. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2045-7634 32924895 |
Relation: | https://doaj.org/toc/2045-7634 |
DOI: | 10.1002/cam4.4284 |
URL الوصول: | https://doaj.org/article/9ad32924895f4fb18b848e1ee95e93d6 |
رقم الأكسشن: | edsdoj.9ad32924895f4fb18b848e1ee95e93d6 |
قاعدة البيانات: | Directory of Open Access Journals |
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