Evidence map›Paper›PMID 37368186›Full record

ArticleHepatology international2023

Hepatitis B virus-related intrahepatic cholangiocarcinoma originates from hepatocytes.

Zimin Song, Shuirong Lin, Xiwen Wu, Xiaoxue Ren, Yifan Wu, Haoxiang Wen, Baifeng Qian, Haozhong Lin, Yihao Huang, Chenfeng Zhao and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 1 country.

Zimin Song *Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Shuirong Lin *Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Xiwen Wu *Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Xiaoxue RenDepartment of Oncology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Yifan WuDepartment of Oncology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Haoxiang WenCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Baifeng QianCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Haozhong LinCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Yihao HuangCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Chenfeng ZhaoDepartment of Laboratory Medicine, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Nian WangZhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, 510030, China.
Yan HuangZhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, 510030, China.
Baogang PengCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China.
Xiaoxing LiInstitute of Precision Medicine, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China. lixiaox23@mail.sysu.edu.cn.
Hong PengCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China. pengh25@mail.sysu.edu.cn.
Shunli ShenCenter of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510030, China. shenshli@mail.sysu.edu.cn.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China 8197110372National Science Fund for Distinguished Young Scholars 81900546Natural Science Foundation of Guangdong Province 2021A1515010757Natural Science Foundation of Guangdong Province 2022A1515010862
6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) infection is one of the most common risk factors for intrahepatic cholangiocarcinoma (ICC). However, there is no direct evidence of a causal relationship between HBV infection and ICC. In this study, we attempted to prove that ICC may originate from hepatocytes through a pathological study involving ICC tissue-derived organoids.

methodThe medical records and tumor tissue samples of 182 patients with ICC after hepatectomy were collected. The medical records of 182 patients with ICC were retrospectively analyzed to explore the prognostic factors. A microarray of 182 cases of ICC tumor tissue and 6 cases of normal liver tissue was made, and HBsAg was stained by immunohistochemistry (IHC) to explore the factors closely related to HBV infection. Fresh ICC tissues and corresponding adjacent tissues were collected to make paraffin sections and organoids. Immunofluorescence (IF) staining of factors including HBsAg, CK19, CK7, Hep-Par1 and Albumin (ALB) was performed on both fresh tissues and organoids. In addition, we collected adjacent nontumor tissues of 6 patients with HBV (+) ICC, from which biliary duct tissue and normal liver tissue were isolated and RNA was extracted respectively for quantitative PCR assay. In addition, the expression of HBV-DNA in organoid culture medium was detected by quantitative PCR and PCR electrophoresis.

resultsA total of 74 of 182 ICC patients were HBsAg positive (40.66%, 74/182). The disease-free survival (DFS) rate of HBsAg (+) ICC patients was significantly lower than that of HBsAg (-) ICC patients (p = 0.0137). IF and IHC showed that HBsAg staining was only visible in HBV (+) ICC fresh tissues and organoids, HBsAg expression was negative in bile duct cells in the portal area. Quantitative PCR assay has shown that the expression of HBs antigen and HBx in normal hepatocytes were significantly higher than that in bile duct epithelial cells. Combined with the IF and IHC staining, it was confirmed that HBV does not infect normal bile duct epithelial cells. In addition, IF also showed that the staining of bile duct markers CK19 and CK7 were only visible in ICC fresh tissue and organoids, and the staining of hepatocyte markers Hep-Par1 and ALB was only visible in normal liver tissue fresh tissue. Real-time PCR and WB had the same results. High levels of HBV-DNA were detected in the culture medium of HBV (+) organoids but not in the culture medium of HBV (-) organoids.

conclusionHBV-related ICC might be derived from hepatocytes. HBV (+) ICC patients had shorter DFS than HBV (-) ICC patients.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaHepatitis BBile Ducts, IntrahepaticDNA, ViralHepatitis B Surface AntigensHepatitis B virusHepatocytesHumansReceptor, PAR-1Retrospective StudiesDNA, ViralHepatitis B Surface AntigensReceptor, PAR-1HBVHepatocytesIntrahepatic cholangiocarcinoma (ICC)Organoids

Identifiers

PMID37368186
PMCPMC10522522
OpenAlexW4382181234

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.