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Cell aging after cancer treatment may help or hurt tumour growth

A summary of earlier studies · Cancers · Oct 16, 2026

What this means

This paper is a review of earlier research on aged cells and cancer. It says these cells may either slow or speed up tumour growth.

Plain-English summary written by an AI model from the abstract. The original is below.

Tested inSummary of earlier studies
Who it was tested in
A review of earlier studies
Kind of research
A summary of earlier studies

The science

Original title
The Molecular Landscape of the Senescence-EMT Interplay: Deciphering Tumour Plasticity Through Molecular Signatures and Multi-Omic Profiling.
Authors
Verdugo-Sivianes EM, Campos-Silva C, García-Márquez JL et al.
Journal
Cancers
Published
Oct 16, 2026
Study type
Review

Abstract

Therapy-induced senescence (TIS) is a common response to anticancer treatments, characterised by stable cell cycle arrest and the acquisition of a complex senescence-associated secretory phenotype (SASP). Initially regarded as a beneficial mechanism that limits tumour growth, growing evidence indicates that TIS is a highly dynamic and heterogeneous process with context-dependent effects that can either suppress or promote tumour progression. The SASP is a central mediator of tumour plasticity, linking TIS to epithelial-to-mesenchymal transition (EMT), cancer stemness, microenvironmental remodelling, therapeutic resistance, and metastatic dissemination. These findings highlight the therapeutic potential of senotherapeutic approaches, including senolytic and senomorphic agents, as key components of one-two-punch therapeutic strategies to selectively eliminate or modulate persistent senescent cells and improve treatment outcomes. Recent advances in multi-omics technologies, artificial intelligence, and liquid biopsy are further transforming the study of senescence by enabling comprehensive molecular characterisation, biomarker discovery, patient stratification, and real-time monitoring of tumour evolution. Collectively, current evidence supports a paradigm shift in which senescence should be considered a dynamic regulator of tumour plasticity and a promising target for precision oncology strategies.

Read it on PubMed ↗

Verdugo-Sivianes EM, Campos-Silva C, García-Márquez JL et al. The Molecular Landscape of the Senescence-EMT Interplay: Deciphering Tumour Plasticity Through Molecular Signatures and Multi-Omic Profiling. Cancers. 2026. doi:10.3390/cancers18193204. PMID: 42882898. https://pubmed.ncbi.nlm.nih.gov/42882898/

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