Evidence map›Paper›PMID 39270064›Full record

ReviewClinical and translational medicine2024

Targeting senescence-associated secretory phenotypes to remodel the tumour microenvironment and modulate tumour outcomes.

Jiaqiang Xiong, Lu Dong, Qiongying Lv, Yutong Yin, Jiahui Zhao, Youning Ke, Shixuan Wang, Wei Zhang, Meng Wu

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
–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

34 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 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.

Jiaqiang XiongDepartment of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Lu DongThe Second Clinical College of Wuhan University, Wuhan, China.
Qiongying LvDepartment of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Yutong YinThe First Clinical College of Wuhan University, Wuhan, China.
Jiahui ZhaoDepartment of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Youning KeDepartment of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Shixuan WangDepartment of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0002-8610-952X
Wei ZhangDepartment of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Meng WuDepartment of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0001-8822-4700

Funding

Fund of Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology 2023A16Major Science and Technology Foundation of Hubei Province 2023BCA002National Key Research and Development Program of China 2021YFC2009105National Key Research and Development Program of China 2022YFC2704100National Natural Science Foundation of China 82001514Program of Excellent Doctor of Zhongnan Hospital of Wuhan University ZNYB2023005Technology Research Project Foundation of Hubei Province 2023BAA016
6 · The paper itself

Abstract

Tumour cell senescence can be induced by various factors, including DNA damage, inflammatory signals, genetic toxins, ionising radiation and nutrient metabolism. The senescence-associated secretory phenotype (SASP), secreted by senescent tumour cells, possesses the capacity to modulate various immune cells, including macrophages, T cells, natural killer cells and myeloid-derived suppressor cells, as well as vascular endothelial cells and fibroblasts within the tumour microenvironment (TME), and this modulation can result in either the promotion or suppression of tumorigenesis and progression. Exploring the impact of SASP on the TME could identify potential therapeutic targets, yet limited studies have dissected its functions. In this review, we delve into the causes and mechanisms of tumour cell senescence. We then concentrate on the influence of SASP on the tumour immune microenvironment, angiogenesis, extracellular matrix and the reprogramming of cancer stem cells, along with their associated tumour outcomes. Last, we present a comprehensive overview of the diverse array of senotherapeutics, highlighting their prospective advantages and challenge for the treatment of cancer patients. KEY POINTS: Senescence-associated secretory phenotype (SASP) secretion from senescent tumour cells significantly impacts cancer progression and biology. SASP is involved in regulating the remodelling of the tumour microenvironment, including immune microenvironment, vascular, extracellular matrix and cancer stem cells. Senotherapeutics, such as senolytic, senomorphic, nanotherapy and senolytic vaccines, hold promise for enhancing cancer treatment efficacy.

Indexed as

NeoplasmsSenescence-Associated Secretory PhenotypeTumor MicroenvironmentCellular SenescenceHumanscell senescenceSASPsenolytictumour microenvironment

Identifiers

PMID39270064
PMCPMC11398298

What OpenQuestion holds

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Registered trials

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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.