Evidence map›Paper›PMID 34482364›Full record

ReviewCell death & disease2021

The metabolic flexibility of quiescent CSC: implications for chemotherapy resistance.

Kangchen Chen, Chenzhi Zhang, Sunbin Ling, Rongli Wei, Jianguo Wang, Xiao Xu

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.6field-weighted citation impact, top 2% of its field
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

81 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  13. The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026
    Review
  14. Article
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  16. Review
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  18. Article
  19. The authors respond to feedback onFrontiers in oncology · 2026
    Article
  20. Review

21 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

Kangchen Chen *Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Chenzhi Zhang *NHC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou, China.
Sunbin LingDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Rongli WeiDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jianguo WangDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiao XuDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. zjxu@zju.edu.cn.ORCID 0000-0002-2761-2811
Hangzhou First People's Hospital · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

China National Funds for Distinguished Young Scientists 81625003National Natural Science Foundation of China (National Science Foundation of China) 81902407Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) 2019C03050
6 · The paper itself

Abstract

Quiescence has been observed in stem cells (SCs), including adult SCs and cancer SCs (CSCs). Conventional chemotherapies mostly target proliferating cancer cells, while the quiescent state favors CSCs escape to chemotherapeutic drugs, leaving risks for tumor recurrence or metastasis. The tumor microenvironment (TME) provides various signals that maintain resident quiescent CSCs, protect them from immune surveillance, and facilitates their recurrence potential. Since the TME has the potential to support and initiate stem cell-like programs in cancer cells, targeting the TME components may prove to be a powerful modality for the treatment of chemotherapy resistance. In addition, an increasing number of studies have discovered that CSCs exhibit the potential of metabolic flexibility when metabolic substrates are limited, and display increased robustness in response to stress. Accompanied by chemotherapy that targets proliferative cancer cells, treatments that modulate CSC quiescence through the regulation of metabolic pathways also show promise. In this review, we focus on the roles of metabolic flexibility and the TME on CSCs quiescence and further discuss potential treatments of targeting CSCs and the TME to limit chemotherapy resistance.

Indexed as

Cell CycleDrug Resistance, NeoplasmAnimalsAntineoplastic AgentsEpigenesis, GeneticHumansNeoplastic Stem CellsTumor MicroenvironmentAntineoplastic Agents

Identifiers

PMID34482364
PMCPMC8418609
OpenAlexW3196442466

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.