Evidence map›Paper›PMID 36105485›Full record

ArticleOxidative medicine and cellular longevity2022

Identification of Warning Transition Points from Hepatitis B to Hepatocellular Carcinoma Based on Mutation Accumulation for the Early Diagnosis and Potential Drug Treatment of HBV-HCC.

Fei Xu, Qingkang Meng, Feng Wu, Yakun Wang, Wenjun Yang, Yun Tong, Lei Liu, Xiujie Chen

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 48% 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

3 citing papers in PubMed, 3 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

8 authors at 1 institution in 1 country.

Fei XuDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Qingkang MengDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Feng WuDepartment of Orthopedic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150001, China.
Yakun WangDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Wenjun YangDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Yun TongDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Lei LiuDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.ORCID https://orcid.org/0000-0003-4512-8203
Xiujie ChenDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.ORCID https://orcid.org/0000-0003-2423-8569
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of multiple genetic mutations is essential during the occurrence and development of hepatocellular carcinoma induced by hepatitis B (HBV-HCC), but understanding their cooperative effects and identifying the warning transition point from hepatitis B to HCC are challenges. In the genomic analysis of somatic mutations of the patient with HBV-HCC in a patient-specific protein-protein interaction (ps-PPI) network, we find mutation influence can propagate along the ps-PPI network. Therefore, in the article, we got the mutation cluster as a new research unit using the Random Walks with Restarts algorithm that is used to describe the efficient boundary of mutation influences. The connection of mutation cluster leads to dysregulation of signaling pathways corresponding to HCC, while dysregulated signaling pathways accumulate gradually and experience a process from quantitative to qualitative changes including a critical mutation cluster called transition point (TP) from hepatitis B to HCC. Moreover, two subtypes of HCC patients with different prognosis and their corresponding biological and clinical characteristics were identified according to TP. The poor prognosis HCC subtype was associated with significant metabolic pathway dysregulation and lower immune cell infiltration, while we also identified several preventive drugs to block the transformation of hepatitis B to hepatocellular carcinoma. The network-level study integrated multiomics data not only showed the sequence of multiple somatic mutations and their cooperative effect but also identified the warning transition point in HCC tumorigenesis for each patient. Our study provides new insight into exploring the cooperative molecular mechanism of chronic inflammatory malignancy in the liver and lays the foundation for the development of new approaches for early prediction and diagnosis of hepatocellular carcinoma and personalized targeted therapy.

Indexed as

Carcinoma, HepatocellularHepatitis BLiver NeoplasmsEarly DiagnosisHepatitis B virusHumansMutation Accumulation

Identifiers

PMID36105485
PMCPMC9467738
OpenAlexW4295898361

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.