Evidence map›Paper›PMID 42861166›Full record

ArticleImmuno-oncology technology2026

Age-related tumor mutational burden and inflammaging: a pan-cancer multi-omics study of treatment-naïve patients.

S Yajima, Y Tsukada, Y Sota, S J-Y Ohtani-Kim, R Yamashita, T Fujisawa, T Kuwata, G Ishii, N Gabelia, H Juhl and 6 more

Abstract read
In one paragraph

Article in Immuno-oncology technology, 2026. 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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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

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

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

16 authors.

S YajimaDepartment of Urology, National Cancer Center Hospital East, Kashiwa, Japan.
Y TsukadaDepartment of Colorectal Surgery, National Cancer Center Hospital East, Kashiwa, Japan.
Y SotaDepartment of Colorectal Surgery, National Cancer Center Hospital East, Kashiwa, Japan.
S J-Y Ohtani-KimDepartment of Thoracic Surgery, National Cancer Center Hospital East, Kashiwa, Japan.
R YamashitaDivision of Translational Informatics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan.
T FujisawaTranslational Research Support Office, National Cancer Center Hospital East, Kashiwa, Japan.
T KuwataDepartment of Genetic Medicine and Services, National Cancer Center Hospital East, Kashiwa, Japan.
G IshiiDepartment of Pathology and Clinical Laboratories, National Cancer Center Hospital East, Kashiwa, Japan.
N GabeliaDepartment of Indivumed GmbH, Hamburg, Germany.
H JuhlDepartment of Indivumed GmbH, Hamburg, Germany.
S TakasuLocal Support Office/Clinical Research Coordinator Office, National Cancer Center Hospital East, Kashiwa, Japan.
M TakahashiTranslational Research Sample Management Office, National Cancer Center Hospital East, Kashiwa, Japan.
H BandoTranslational Research Support Office, National Cancer Center Hospital East, Kashiwa, Japan.
T YoshinoDepartment of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.
M ItoDepartment of Colorectal Surgery, National Cancer Center Hospital East, Kashiwa, Japan.
H MasudaDepartment of Urology, National Cancer Center Hospital East, Kashiwa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Aging is a major nonmodifiable risk factor for cancer, yet age-associated genomic instability, inflammatory activation, and tumor microenvironment interactions remain poorly characterized. Patients and methods: The primary genomic cohort comprised 153 treatment-naïve patients with six cancer types, stratified at age 60 years; four additional patients without genomic profiling contributed to nongenomic analyses. Tumor mutational burden (TMB) and fraction genome altered were derived from whole-genome sequencing, and inflammatory pathway activity was determined from single-sample gene set enrichment analysis of RNA sequencing and proteomics in paired tumor and normal tissue. Because cancer type distribution differed between age groups, all principal associations were re-examined in multivariable models. Results: TMB was higher in older patients (median 4.55 compared with 2.84 mutations per megabase; Conclusions: Most age-associated molecular differences were substantially explained by cancer type. Only the age-related increase in normal-tissue inflammation at the protein level and the greater inflammation amplification of MSI-H tumors persisted. The correlation between normal-tissue inflammation and tumor TMB is not evidence that systemic inflammaging drives genomic instability.

Indexed as

aginginflammagingmulti-omicspan-cancer analysistumor microenvironmenttumor mutational burden

Identifiers

PMID42861166
PMCPMC13654048

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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.