Evidence map›Paper›PMID 38045829›Full record

ReviewMedComm2023

Oncofetal reprogramming in tumor development and progression: novel insights into cancer therapy.

Jiangjun Cao, Zhe Zhang, Li Zhou, Maochao Luo, Lei Li, Bowen Li, Edouard C Nice, Weifeng He, Shaojiang Zheng, Canhua Huang

Abstract readReview
In one paragraph

Review in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Review
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  6. Review
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  10. Review
  11. A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.bioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
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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

10 authors.

Jiangjun CaoWest China School of Basic Medical Sciences and Forensic Medicine, and Department of Biotherapy Cancer Center and State Key Laboratory of Biotherapy, West China Hospital Sichuan University Chengdu China.
Zhe ZhangZhejiang Provincial Key Laboratory of Pancreatic Disease the First Affiliated Hospital School of Medicine Zhejiang University Zhejiang China.
Li ZhouKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education) Department of Infectious Diseases the Second Affiliated Hospital Institute for Viral Hepatitis, Chongqing Medical University Chongqing China.
Maochao LuoWest China School of Basic Medical Sciences and Forensic Medicine, and Department of Biotherapy Cancer Center and State Key Laboratory of Biotherapy, West China Hospital Sichuan University Chengdu China.
Lei LiDepartment of anorectal surgery Hospital of Chengdu University of Traditional Chinese Medicine and Chengdu University of Traditional Chinese Medicine Chengdu China.
Bowen LiWest China School of Basic Medical Sciences and Forensic Medicine, and Department of Biotherapy Cancer Center and State Key Laboratory of Biotherapy, West China Hospital Sichuan University Chengdu China.
Edouard C NiceDepartment of Biochemistry and Molecular Biology Monash University Clayton VIC Australia.
Weifeng HeState Key Laboratory of Trauma Burn and Combined Injury Institute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University) Chongqing China.
Shaojiang ZhengHainan Cancer Medical Center of The First Affiliated Hospital, the Hainan Branch of National Clinical Research Center for Cancer, Hainan Engineering Research Center for Biological Sample Resources of Major Diseases Hainan Medical University Haikou China.ORCID https://orcid.org/0000-0002-2323-0736
Canhua HuangWest China School of Basic Medical Sciences and Forensic Medicine, and Department of Biotherapy Cancer Center and State Key Laboratory of Biotherapy, West China Hospital Sichuan University Chengdu China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence indicates that cancer cells can mimic characteristics of embryonic development, promoting their development and progression. Cancer cells share features with embryonic development, characterized by robust proliferation and differentiation regulated by signaling pathways such as Wnt, Notch, hedgehog, and Hippo signaling. In certain phase, these cells also mimic embryonic diapause and fertilized egg implantation to evade treatments or immune elimination and promote metastasis. Additionally, the upregulation of ATP-binding cassette (ABC) transporters, including multidrug resistance protein 1 (MDR1), multidrug resistance-associated protein 1 (MRP1), and breast cancer-resistant protein (BCRP), in drug-resistant cancer cells, analogous to their role in placental development, may facilitate chemotherapy efflux, further resulting in treatment resistance. In this review, we concentrate on the underlying mechanisms that contribute to tumor development and progression from the perspective of embryonic development, encompassing the dysregulation of developmental signaling pathways, the emergence of dormant cancer cells, immune microenvironment remodeling, and the hyperactivation of ABC transporters. Furthermore, we synthesize and emphasize the connections between cancer hallmarks and embryonic development, offering novel insights for the development of innovative cancer treatment strategies.

Indexed as

cancer therapydrug resistanceembryonic developmenttumor development and progression

Identifiers

PMID38045829
PMCPMC10693315

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.