Abstract | BACKGROUND:
Intrahepatic cholangiocarcinoma (ICC) is the second most common primary hepatic malignancy with poor prognosis. Intrahepatic bile duct stone (IBDS) is one of the key causes to ICC occurrence and can increase morbidity rate of ICC about forty times. However, the specific carcinogenesis of IBDS is still far from clarified. Insight into the metabolic phenotype difference between IBDS and ICC can provide potential mechanisms and therapeutic targets, which is expected to inhibit the carcinogenesis of IBDS and improve the prognosis of ICC. METHODS: A total of 34 participants including 25 ICC patients and 9 IBDS patients were recruited. Baseline information inclusive of liver function indicators, tumor biomarkers, surgery condition and constitution parameters etc. from patients were recorded. ICC and IBDS pathological tissues, as well as ICC para- carcinoma tissues, were collected for GC-MS based metabolomics experiments. Multivariate analysis was performed to find differentially expressed metabolites and differentially enriched metabolic pathways. Spearman correlation analysis was then used to construct correlation network between key metabolite and baseline information of patients. RESULTS: CONCLUSION: Long-term monitoring of metabolites from linoleic acid metabolism pathway and protein indicators of liver function in IBDS patients has important guiding significance for the monitoring of IBDS carcinogenesis. Meanwhile, further insight into the causal relationship between linoleic acid pathway disturbance and changes in liver function can provide important therapeutic targets for both IBDS and ICC.
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Authors | Jun Li, Jiongjiong Lu, Shaodong Lv, Shujun Sun, Caifeng Liu, Feng Xu, Haiying Sun, Jiamei Yang, Xinjun Wang, Xingyang Zhong, Junhua Lu |
Journal | BMC gastroenterology
(BMC Gastroenterol)
Vol. 22
Issue 1
Pg. 269
(May 30 2022)
ISSN: 1471-230X [Electronic] England |
PMID | 35637430
(Publication Type: Journal Article)
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Copyright | © 2022. The Author(s). |
Chemical References |
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Topics |
- Bile Duct Neoplasms
(genetics)
- Bile Ducts, Intrahepatic
(pathology)
- Carcinogenesis
(metabolism, pathology)
- Cholangiocarcinoma
(etiology)
- Humans
- Linoleic Acid
(metabolism)
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