PDF(Pubmed)
Abstract：
UNASSIGNED: Gut microbiota (GM) influences the occurrence and development of pancreatic cancer (PC), potentially through the involvement of inflammatory cytokines (IC) and immune cells (IM). We aimed to investigate the causal impact of the gut microbiota (GM) on pancreatic cancer (PC) and identify potential IC and IM mediators.
UNASSIGNED: The summary statistics data from whole-genome association studies of gut microbiota, immune cells, inflammatory cytokines, and four types of pancreatic tumors (MNP: Malignant neoplasm of pancreas; BNP: Benign neoplasm of pancreas; ADCP: Adenocarcinoma and ductal carcinoma of pancreas; NTCP: Neuroendocrine tumor and carcinoma of pancreas). Two-sample univariable Mendelian randomization (UVMR), multivariable Mendelian randomization (MVMR), and mediation analysis were employed to assess the causal relationship between gut microbiota (GM) and pancreatic cancer (PC), as well as potential IC and IM mediators.
UNASSIGNED: The two-sample UVMR analysis showed causal relationships between 20 gut microbiota species and pancreatic cancer, with pancreatic cancer affecting the abundance of 37 gut microbiota species. Mediation analysis revealed that Interleukin-6 (IL-6), \"CD4 on naive CD4+ T cell\" and \"SSC-A on HLA DR+ Natural Killer\" mediated the causal effects of gut microbiota on pancreatic cancer.
UNASSIGNED: This Mendelian randomization study demonstrates causal relationships between several specific gut microbiota and pancreatic cancer, as well as potential mediators (IC, IM).
UNASSIGNED: The summary statistics data from whole-genome association studies of gut microbiota, immune cells, inflammatory cytokines, and four types of pancreatic tumors (MNP: Malignant neoplasm of pancreas; BNP: Benign neoplasm of pancreas; ADCP: Adenocarcinoma and ductal carcinoma of pancreas; NTCP: Neuroendocrine tumor and carcinoma of pancreas). Two-sample univariable Mendelian randomization (UVMR), multivariable Mendelian randomization (MVMR), and mediation analysis were employed to assess the causal relationship between gut microbiota (GM) and pancreatic cancer (PC), as well as potential IC and IM mediators.
UNASSIGNED: The two-sample UVMR analysis showed causal relationships between 20 gut microbiota species and pancreatic cancer, with pancreatic cancer affecting the abundance of 37 gut microbiota species. Mediation analysis revealed that Interleukin-6 (IL-6), \"CD4 on naive CD4+ T cell\" and \"SSC-A on HLA DR+ Natural Killer\" mediated the causal effects of gut microbiota on pancreatic cancer.
UNASSIGNED: This Mendelian randomization study demonstrates causal relationships between several specific gut microbiota and pancreatic cancer, as well as potential mediators (IC, IM).
摘要：
■肠道菌群（GM）影响胰腺癌（PC）的发生和发展，可能通过炎性细胞因子（IC）和免疫细胞（IM）的参与。我们旨在调查肠道微生物群（GM）对胰腺癌（PC）的因果影响，并确定潜在的IC和IM介质。
■来自肠道微生物群的全基因组关联研究的汇总统计数据，免疫细胞，炎性细胞因子，和四种类型的胰腺肿瘤（MNP：胰腺恶性肿瘤；BNP：胰腺良性肿瘤；ADCP：胰腺腺癌和导管癌；NTCP：神经内分泌肿瘤和胰腺癌）。双样本单变量孟德尔随机化(UVMR)，多变量孟德尔随机化(MVMR)，和中介分析用于评估肠道微生物群(GM)和胰腺癌(PC)之间的因果关系，以及潜在的IC和IM中介。
■双样本UVMR分析显示了20种肠道菌群与胰腺癌之间的因果关系，胰腺癌影响了37种肠道菌群的丰度。中介分析显示，白细胞介素-6(IL-6)，“CD4对幼稚CD4T细胞”和“SSC-A对HLADR自然杀伤”介导了肠道微生物对胰腺癌的因果作用。
■这项孟德尔随机研究证明了几种特定的肠道菌群与胰腺癌之间的因果关系。以及潜在的中介(IC，IM）。
■来自肠道微生物群的全基因组关联研究的汇总统计数据，免疫细胞，炎性细胞因子，和四种类型的胰腺肿瘤（MNP：胰腺恶性肿瘤；BNP：胰腺良性肿瘤；ADCP：胰腺腺癌和导管癌；NTCP：神经内分泌肿瘤和胰腺癌）。双样本单变量孟德尔随机化(UVMR)，多变量孟德尔随机化(MVMR)，和中介分析用于评估肠道微生物群(GM)和胰腺癌(PC)之间的因果关系，以及潜在的IC和IM中介。
■双样本UVMR分析显示了20种肠道菌群与胰腺癌之间的因果关系，胰腺癌影响了37种肠道菌群的丰度。中介分析显示，白细胞介素-6(IL-6)，“CD4对幼稚CD4T细胞”和“SSC-A对HLADR自然杀伤”介导了肠道微生物对胰腺癌的因果作用。
■这项孟德尔随机研究证明了几种特定的肠道菌群与胰腺癌之间的因果关系。以及潜在的中介(IC，IM）。
