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Biological age & clocks
Research brief

Epigenetic cell-division and ageing markers and 5-year breast cancer survival

In 1992 breast tumours, higher DNA-methylation markers of cell division were weakly linked to poorer 5-year overall survival, while higher chronological-age markers were linked to better survival; biological-age markers varied. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The study measured DNA-methylation-based epigenetic markers in 1992 breast tumours from the Melbourne Collaborative Cohort Study and publicly available datasets. [1]

  2. After age adjustment and stratification by study, higher cell-division markers were associated with poorer 5-year overall survival, for example epiTOC2 with a hazard ratio of 1.14. [1]

  3. Higher chronological-age markers were linked to better prognosis, for example Horvath age with a hazard ratio of 0.70, and the authors describe the associations as quite weak. [1]

The source at a glance

Study type / format
Prognostic biomarker analysis using cohort tumour methylation data (abstract)
Population / context
1992 breast cancer tumours from the Melbourne Collaborative Cohort Study and publicly available datasets
Summary based on
Study abstract
Original publication
June 27, 2026

Methylation markers measured in 1992 breast tumours

The study measured epigenetic markers based on DNA methylation in breast tumours, using genome-wide methylation data from 1992 tumours in the Melbourne Collaborative Cohort Study and publicly available datasets. It calculated four cell-division markers (epiTOC2, stemTOC, MiAge, CellDRIFT), two chronological-age markers (Horvath age, BTEC) and four biological-age markers (PhenoAge, GrimAge, MRscore, DunedinPACE). The aim was to assess their prognostic value for breast cancer survival.

Supporting source [1]

Weak survival links that varied by tumour subtype

Cox regression models assessed age-adjusted markers in relation to 5-year overall survival, adjusting for clinical variables. After adjustment for age and stratification by study, higher cell-division markers were associated with poorer survival (epiTOC2: per one-standard-deviation increase, hazard ratio 1.14, 95% CI 1.03–1.27), whereas higher chronological-age markers were linked to better prognosis (Horvath age: hazard ratio 0.70, 95% CI 0.61–0.82). Biological-age markers showed variable associations. These associations were partly explained by main clinicopathological variables at diagnosis and varied across subtypes. The authors describe the associations as quite weak.

Supporting source [1]

Abstract-only scope and limited prognostic value

The authors conclude that several epigenetic markers were associated with breast cancer survival, but the associations were quite weak, suggesting limited prognostic value. They note that varying associations among subtypes may reflect underlying biological differences that should be further investigated. These are associations, not evidence of cause. This explainer is based on the abstract only; the full text was not reviewed, so details of the models, follow-up and publicly available datasets are not assessed here.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. Design details, follow-up and the publicly available datasets are not assessed here. Associations are not causal, and the authors themselves describe them as quite weak.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

[1]
Epigenetic Markers of Cell Division and Ageing in Relation to Breast Cancer Survival.

Li L, Zarean E, Li DL, Zhu Y, Li S, Makalic E, McLean C, Giles GG, Milne RL, Southey MC, Dugué PA. · europepmc.org · June 27, 2026

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    measured in 1992 breast cancer tumours
  2. Finding 2 ↑

    epiTOC2: per one-standard-deviation increase, hazard ratio [HR]
  3. Finding 3 ↑

    Horvath age: HR = 0.70

AI-assisted summary with linked source passages. No independent editorial or clinical review.

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