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结直肠癌合并肥胖预示着更好的生存预后——相关机制的研究。

Colon cancer combined with obesity indicates improved survival- research on relevant mechanism.

机构信息

Department of General Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai 201399, China.

Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, Jiangsu, China.

出版信息

Aging (Albany NY). 2020 Nov 10;12(23):23778-23794. doi: 10.18632/aging.103972.

DOI:10.18632/aging.103972
PMID:33197880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7762486/
Abstract

Obesity contributes to the incidence of various tumors, including colon cancer. However, the impact of obesity on patients' survival and related mechanisms remains unclear. Multi-omics data of 227 cases of colon cancer patients combined with clinical characteristics data were acquired from The Cancer Genome Atlas (TCGA) database. We confirmed obesity as an independent prognostic factor for improved overall survival of colon cancer patients. We demonstrated that hypoxia pathways were repressed in obese patients by regulating miR-210. Immune checkpoints PD-1 and LAG3 were also downregulated in obese patients, which indicated enhanced immune surveillance. The frequency of PIK3CA and KRAS mutations was decreased in obese patients. The sites and types of TP53 mutation were alternated in obesity patients. In conclusion, our research demonstrated the potential mechanisms of prolonged survival in colon cancer patients combined with obesity, which may provide potential value for improving the prognosis of colon cancer.

摘要

肥胖会导致多种肿瘤的发生，包括结肠癌。然而，肥胖对患者生存的影响及其相关机制尚不清楚。我们从癌症基因组图谱（TCGA）数据库中获取了 227 例结肠癌患者的多组学数据，并结合临床特征数据。我们证实肥胖是改善结肠癌患者总体生存的独立预后因素。我们通过调节 miR-210 证实肥胖患者的低氧途径受到抑制。肥胖患者的免疫检查点 PD-1 和 LAG3 也下调，这表明免疫监视增强。肥胖患者中 PIK3CA 和 KRAS 突变的频率降低。TP53 突变的部位和类型在肥胖患者中发生了改变。总之，我们的研究表明肥胖与结肠癌患者生存延长的潜在机制，这可能为改善结肠癌的预后提供潜在价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/8412192b5026/aging-12-103972-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/948e09b66b73/aging-12-103972-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/07565f2aa539/aging-12-103972-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/67ab550ba03a/aging-12-103972-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/8084957f1d03/aging-12-103972-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/8412192b5026/aging-12-103972-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/948e09b66b73/aging-12-103972-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/07565f2aa539/aging-12-103972-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/67ab550ba03a/aging-12-103972-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/8084957f1d03/aging-12-103972-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34a7/7762486/8412192b5026/aging-12-103972-g005.jpg

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本文引用的文献

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A dominant-negative effect drives selection of missense mutations in myeloid malignancies.显性负效应驱动髓系恶性肿瘤中错义突变的选择。
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