Evidence map›Paper›PMID 38997794›Full record

ReviewCancer communications (London, England)2024

Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment.

Fusheng Zhang, Junchen Guo, Shengmiao Yu, Youwei Zheng, Meiqi Duan, Liang Zhao, Yihan Wang, Zhi Yang, Xiaofeng Jiang

Abstract readReview
In one paragraph

Review in Cancer communications (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing 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

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

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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.

Fusheng ZhangDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Junchen GuoDepartment of Radiology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Shengmiao YuOutpatient Department, The Fourth Affiliated Hospital, China Medical University, Shenyang, Liaoning, P. R. China.
Youwei ZhengDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Meiqi DuanDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Liang ZhaoDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Yihan WangDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Zhi YangDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Xiaofeng JiangDepartment of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, P. R. China.ORCID 0000-0002-5483-8111

Funding

Grants from the Liaoning Nature Science Foundation of China 2022JH2/101300042National Natural Science Foundation of China 81672877National Natural Science Foundation of China 82173194
6 · The paper itself

Abstract

The intrinsic oncogenic mechanisms and properties of the tumor microenvironment (TME) have been extensively investigated. Primary features of the TME include metabolic reprogramming, hypoxia, chronic inflammation, and tumor immunosuppression. Previous studies suggest that senescence-associated secretory phenotypes that mediate intercellular information exchange play a role in the dynamic evolution of the TME. Specifically, hypoxic adaptation, metabolic dysregulation, and phenotypic shifts in immune cells regulated by cellular senescence synergistically contribute to the development of an immunosuppressive microenvironment and chronic inflammation, thereby promoting the progression of tumor events. This review provides a comprehensive summary of the processes by which cellular senescence regulates the dynamic evolution of the tumor-adapted TME, with focus on the complex mechanisms underlying the relationship between senescence and changes in the biological functions of tumor cells. The available findings suggest that components of the TME collectively contribute to the progression of tumor events. The potential applications and challenges of targeted cellular senescence-based and combination therapies in clinical settings are further discussed within the context of advancing cellular senescence-related research.

Indexed as

Cellular SenescenceNeoplasmsTumor MicroenvironmentAnimalsHumansMetabolic Reprogrammingcellular senescencechronic inflammationhypoxiaimmunosuppressive tumor microenvironmentmetabolic reprogrammingtumor‐targeted therapy

Identifiers

PMID38997794
PMCPMC11492308

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.