Evidence map›Paper›PMID 40999125›Full record

ReviewMedical oncology (Northwood, London, England)2025

Targeting the crosstalk of metabolism reprogramming and replication stress: novel strategy to combat cancer.

Wenbo Liu, Xiangyan Jiang, Yong Ma, Huiguo Qing, Yingcun Bao, Zuoyi Jiao

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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

6 authors.

Wenbo LiuDepartment of General Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China.
Xiangyan JiangDepartment of General Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China.
Yong MaDepartment of General Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China.
Huiguo QingDepartment of General Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China.
Yingcun BaoDepartment of Rehabilitation Medicine, Lanzhou University Second Hospital, Lanzhou, 730030, China.
Zuoyi JiaoDepartment of General Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China. jiaozy@lzu.edu.cn.

Funding

"Cuiying Science and Technology Innovation" Programme of Lanzhou University Second Hospital, Applied Basic Research - General Program CY2021-MS-B12Gansu Province Joint Scientific Research Fund 24JRRA920Gansu Province Traditional Chinese Medicine Science and Technology Tackling Key Projects GZKZ-2024-23Gansu Provincial Health Industry Science and Technology Innovation Major Scientific Research Project GSWSZD2024-14Gansu Provincial Science and Technology Program Projects (Major Science and Technology Special Projects Program) 25ZDFA002Lanzhou Science and Technology Plan Project 2023-1-29National Natural Science Foundation of China 82473377National Natural Science Foundation of China 824B2080
6 · The paper itself

Abstract

The induction of replication stress has emerged as a potent strategy for cancer therapy, with alkylating agents, nucleoside analogs, and inhibitors of cyclin and cyclin-dependent kinase remaining prominent drugs. As mechanistic insights into responses to replication stress are evolving, novel therapeutic agents targeting replication stress response pathways have been progressively developed. Despite the demonstrated pharmacological and clinical efficacy of certain agents, the therapeutic landscape remains characterized by suboptimal patient prognoses. Mounting evidence implicates cancer cell metabolic reprogramming as a critical determinant in both modulating replication stress and attenuating genotoxic drug efficacy. In addition, some metabolic enzymes demonstrate non-canonical functions that potentiate DNA damage response, while some metabolic pathways contribute vulnerability to replication stress in malignant cells. Therefore, this review seeks to elucidate the mechanisms by which metabolic reprogramming modulates replication stress in cancer cells and to provide an overview of the latest advancements in therapeutic regimens development.

Indexed as

Antineoplastic AgentsCellular ReprogrammingDNA ReplicationNeoplasmsAnimalsDNA DamageHumansMetabolic ReprogrammingAntineoplastic AgentsCancer therapyDrug combinationMetabolic reprogrammingReplication stress

Identifiers

What OpenQuestion holds

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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 OpenQuestion graph.