Evidence map›Paper›PMID 38974956›Full record

ArticleJournal of clinical and translational hepatology2024

Association of Mosaic Chromosomal Alterations and Genetic Factors with the Risk of Cirrhosis.

Xinyuan Ge, Lu Zhang, Maojie Liu, Xiao Wang, Xin Xu, Yuqian Yan, Chan Tian, Juan Yang, Yang Ding, Chengxiao Yu and 5 more

Abstract read
In one paragraph

Article in Journal of clinical and translational hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Xinyuan GeDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Lu ZhangDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Maojie LiuDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiao WangDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Xin XuDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Yuqian YanDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Chan TianDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Juan YangDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Yang DingDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Chengxiao YuDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Jing LuDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Longfeng JiangDepartment of Infectious Disease, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Qiang WangDepartment of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden.
Qun ZhangDepartment of Health Promotion Center, Jiangsu Province Hospital and Nanjing Medical University First Affiliated Hospital, Nanjing, Jiangsu, China.ORCID https://orcid.org/0000-0003-2208-7998
Ci SongDepartment of Epidemiology, China International Cooperation Center on Environment and Human Health, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.ORCID https://orcid.org/0000-0001-6483-9372

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Age-related mosaic chromosomal alterations (mCAs) detected from genotyping of blood-derived DNA are structural somatic variants that indicate clonal hematopoiesis. This study aimed to investigate whether mCAs contribute to the risk of cirrhosis and modify the effect of a polygenic risk score (PRS) on cirrhosis risk prediction. Methods: mCA call sets of individuals with European ancestry were obtained from the UK Biobank. The PRS was constructed based on 12 susceptible single-nucleotide polymorphisms for cirrhosis. Cox proportional hazard models were applied to evaluate the associations between mCAs and cirrhosis risk. Results: Among 448,645 individuals with a median follow-up of 12.5 years, we identified 2,681 cases of cirrhosis, 1,775 cases of compensated cirrhosis, and 1,706 cases of decompensated cirrhosis. Compared to non-carriers, individuals with copy-neutral loss of heterozygosity mCAs had a significantly increased risk of cirrhosis (hazard ratio (HR) 1.42, 95% confidence interval (CI) 1.12-1.81). This risk was higher in patients with expanded cell fractions of mCAs (cell fractions ≥10% vs. cell fractions <10%), especially for the risk of decompensated cirrhosis (HR 2.03 [95% CI 1.09-3.78] vs. 1.14 [0.80-1.64]). In comparison to non-carriers of mCAs with low genetic risk, individuals with expanded copy-neutral loss of heterozygosity and high genetic risk showed the highest cirrhosis risk (HR 5.39 [95% CI 2.41-12.07]). Conclusions: The presence of mCAs is associated with increased susceptibility to cirrhosis risk and could be combined with PRS for personalized cirrhosis risk stratification.

Indexed as

CirrhosisGenetic susceptibilityInteraction effectMosaic chromosomal alterationsPolygenic risk scoreUK Biobank

Identifiers

PMID38974956
PMCPMC11224905

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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.