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基于 TARGET 数据库分析鉴定肾横纹肌样瘤的预后免疫相关基因。

Identification of prognostic immune-related genes in rhabdoid tumor of kidney based on TARGET database analysis.

机构信息

State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong 510060, P.R. China.

Department of Pediatric Oncology, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.

出版信息

Aging (Albany NY). 2021 Feb 11;13(4):5461-5474. doi: 10.18632/aging.202475.

DOI:10.18632/aging.202475
PMID:33588380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7950296/
Abstract

BACKGROUND

Malignant rhabdoid tumor of the kidney (RTK) is a rare and highly aggressive pediatric malignancy. Immune system dysfunction is significantly correlated with tumor initiation and progression.

METHODS

We integrated and analyzed the expression profiles of immune-related genes (IRGs) in 65 RTK patients based on the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database. Prognostic related IRGs in RTK patients were analyzed using univariate and multivariate analysis, based on which a prognostic model with IRGs was constructed. Correlation analysis between the risk score of our model and tumor-infiltrating cell were also investigated.

RESULTS

Twenty two IRGs were significantly associated with the clinical outcomes of RTK patients. Gene ontology (GO) analysis revealed that inflammatory pathways were most frequently implicated in RTK. A prognostic model was constructed using 7 IRGs (), which were independent prognostic indices that could differentiate patients based on their survival outcomes. Furthermore, the risk scores from our prognostic model was positively associated with cancer-associated fibroblasts (CAFs).

CONCLUSIONS

We screened seven IRGs of clinical significance to distinguish patients with different survival outcomes. This may enhance our understanding of the immune microenvironment of RTK, and could use to design individualized treatments for RTK patients.

BACKGROUND

Malignant rhabdoid tumor of the kidney (RTK) is a rare and highly aggressive pediatric malignancy. Immune system dysfunction is significantly correlated with tumor initiation and progression.

METHODS

We integrated and analyzed the expression profiles of immune-related genes (IRGs) in 65 RTK patients based on the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database. Prognostic related IRGs in RTK patients were analyzed using univariate and multivariate analysis, based on which a prognostic model with IRGs was constructed. Correlation analysis between the risk score of our model and tumor-infiltrating cell were also investigated.

RESULTS

Twenty two IRGs were significantly associated with the clinical outcomes of RTK patients. Gene ontology (GO) analysis revealed that inflammatory pathways were most frequently implicated in RTK. A prognostic model was constructed using 7 IRGs (), which were independent prognostic indices that could differentiate patients based on their survival outcomes. Furthermore, the risk scores from our prognostic model was positively associated with cancer-associated fibroblasts (CAFs).

CONCLUSIONS

We screened seven IRGs of clinical significance to distinguish patients with different survival outcomes. This may enhance our understanding of the immune microenvironment of RTK and could use to design individualized treatments for RTK patients.

摘要

背景

肾横纹肌样瘤(RTK)是一种罕见且高度侵袭性的儿科恶性肿瘤。免疫系统功能障碍与肿瘤的发生和进展显著相关。

方法

我们基于治疗性应用研究以产生有效治疗(TARGET)数据库,整合并分析了 65 例 RTK 患者的免疫相关基因(IRGs)表达谱。基于单变量和多变量分析,对 RTK 患者的预后相关 IRGs 进行分析,在此基础上构建了一个基于 IRGs 的预后模型。还研究了我们模型的风险评分与肿瘤浸润细胞之间的相关性。

结果

22 个 IRGs 与 RTK 患者的临床结局显著相关。基因本体(GO)分析表明,炎症途径最常涉及 RTK。使用 7 个 IRGs()构建了一个预后模型,这些 IRGs 是独立的预后指标,可以根据患者的生存结局进行区分。此外,我们预后模型的风险评分与癌症相关成纤维细胞(CAFs)呈正相关。

结论

我们筛选了 7 个具有临床意义的 IRGs,以区分具有不同生存结局的患者。这可能有助于我们了解 RTK 的免疫微环境,并可用于为 RTK 患者设计个体化治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/0313ce3e967a/aging-13-202475-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/934043418c00/aging-13-202475-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/ac95f63b5a3c/aging-13-202475-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/b6f2b05f2296/aging-13-202475-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/cd6512bb8468/aging-13-202475-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/20c61abcb979/aging-13-202475-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/0313ce3e967a/aging-13-202475-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/934043418c00/aging-13-202475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/680b5452c0cb/aging-13-202475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/d8fc5d14e3a3/aging-13-202475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/ce06fed69916/aging-13-202475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/ac95f63b5a3c/aging-13-202475-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/b6f2b05f2296/aging-13-202475-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/cd6512bb8468/aging-13-202475-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/20c61abcb979/aging-13-202475-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6fb/7950296/0313ce3e967a/aging-13-202475-g009.jpg

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