Evidence map›Paper›PMID 40001013›Full record

ArticleBMC cancer2025

Association of phenotypic age acceleration with all-cause and cause-specific mortality among U.S. cancer survivors: a retrospective cohort study.

Xiaoqiang Liu, Yubin Wang, Yingxuan Huang, Chanchan Lin, Boming Xu, Yilin Zeng, Peizhong Chen, Xiaobo Liu, Yisen Huang

Abstract read
In one paragraph

Article in BMC cancer, 2025. 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
–field-weighted citation impact
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.

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  4. Association of the waist-to-weight index with low back pain: a mediation analysis involving accelerated biological ageing.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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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

9 authors.

Xiaoqiang Liu *Department of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Yubin Wang *Department of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Yingxuan HuangDepartment of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Chanchan LinDepartment of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Boming XuDepartment of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Yilin ZengDepartment of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Peizhong ChenDepartment of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China.
Xiaobo LiuMcConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
Yisen HuangDepartment of Gastroenterology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, Fujian, China. 18159503331@163.com.

Funding

China Scholarship Council 201906070289Fujian Medical University 2022QH1268
6 · The paper itself

Abstract

backgroundCancer survivors may experience accelerated biological aging, increasing their risk of mortality. However, the association between phenotypic age acceleration (PAA) and mortality among cancer survivors remains unclear. This study aimed to evaluate the relationship between PAA and all-cause mortality, cancer-specific mortality, and non-cancer mortality among adult cancer survivors in the United States.

methodsWe utilized data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018, including 2,643 (unweighted) cancer patients aged ≥ 20 years. Phenotypic age was calculated using ten physiological biomarkers, and the residuals from regressing phenotypic age on chronological age (age acceleration residuals, AAR) were used to determine PAA status. Participants were divided into PAA and without PAA groups based on the sign of the residuals. Weighted Cox proportional hazards regression models were used to assess the association between PAA and mortality, adjusting for demographic characteristics, lifestyle factors, and comorbidities. Restricted cubic spline (RCS) models were employed to explore the dose-response relationship between AAR and mortality.

resultsOver a median follow-up of 9.16 years, 991 (unweighted) participants died. After adjusting for multiple covariates, PAA was significantly associated with increased risks of all-cause mortality (HR = 2.07; 95% CI: 1.69-2.54), cancer-specific mortality (HR = 2.15; 95% CI: 1.52-3.04), and non-cancer mortality (HR = 2.06; 95% CI: 1.66-2.57). Each one-unit increase in AAR was associated with a 4% increase in the risk of all-cause, cancer-specific, and non-cancer mortality (HR = 1.04; 95% CI: 1.03-1.05). RCS models indicated a linear dose-response relationship between AAR and mortality.

conclusionsAmong U.S. adult cancer survivors, PAA is significantly associated with all-cause, cancer-specific, and non-cancer mortality. PAA may serve as an important biomarker for predicting prognosis in cancer survivors.

Indexed as

AgingCancer SurvivorsNeoplasmsAdultAgedAge FactorsCause of DeathFemaleHumansMaleMiddle AgedNutrition SurveysPhenotypeRetrospective StudiesUnited StatesYoung AdultAll-cause mortalityBiological agingCancer survivorsNHANESPhenotypic age acceleration (PAA)

Identifiers

PMID40001013
PMCPMC11853897

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LicenceCC BY-NC-ND
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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.