Evidence map›Paper›PMID 36675306›Full record

ReviewInternational journal of molecular sciences2023

Targeting Cancer Stem Cells as the Key Driver of Carcinogenesis and Therapeutic Resistance.

Refaat A Eid, Muhammad Alaa Edeen, Eslam M Shedid, Al Shaimaa S Kamal, Mona M Warda, Farag Mamdouh, Sohila A Khedr, Mohamed A Soltan, Hee Won Jeon, Mohamed Samir A Zaki and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

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  10. Targeting WEE1 Kinase for Breast Cancer Therapeutics: An Update.International journal of molecular sciences · 2025
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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

11 authors at 6 institutions in 3 countries.

Refaat A EidPathology Department, College of Medicine, King Khalid University, Abha P.O. Box 62529, Saudi Arabia.ORCID 0000-0001-5633-9562
Muhammad Alaa EdeenCell Biology, Histology & Genetics Division, Biology Department, Faculty of Science, Zagazig University, Zagazig 44519, Egypt.ORCID 0000-0001-5280-7736
Eslam M ShedidBiotechnology Division, Zoology Department, Faculty of Science, Benha University, Al Qalyubia Governorate, Banha 13511, Egypt.
Al Shaimaa S KamalBiotechnology Department, Faculty of Agriculture, Benha University, Al Qalyubia Governorate, Banha 13511, Egypt.
Mona M WardaBiotechnology Division, Zoology Department, Faculty of Science, Benha University, Al Qalyubia Governorate, Banha 13511, Egypt.
Farag MamdouhBiotechnology Division, Zoology Department, Faculty of Science, Benha University, Al Qalyubia Governorate, Banha 13511, Egypt.ORCID 0000-0001-6479-3861
Sohila A KhedrIndustrial Biotechnology Department, Faculty of Science, Tanta University, Tanta 31733, Egypt.
Mohamed A SoltanDepartment of Microbiology and Immunology, Faculty of Pharmacy, Sinai University, Ismailia 41611, Egypt.ORCID 0000-0003-3030-1659
Hee Won JeonDepartment of Pathology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea.
Mohamed Samir A ZakiAnatomy Department, College of Medicine, King Khalid University, Abha P.O. Box 62529, Saudi Arabia.ORCID 0000-0003-0010-0506
Bonglee KimDepartment of Pathology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea.ORCID 0000-0002-8678-156X
Benha University · EGKyung Hee University · KRZagazig University · EGKing Khalid University · SASinai University · EGTanta University · EG

Funding

King Khalid University The Deanship of Scientific Research of King Khalid University in Abha, Saudi Arabia, entirely supported this research (Grant No. G.R.P.1-23-43)Korea government (MSIT) No. 2020R1A5A2019413Korea Health Industry Development Institute HF20C0038Korea Health Industry Development Institute HF20C0116National Research Foundation of Korea NRF-2020R1I1A2066868
6 · The paper itself

Abstract

The emerging concept of cancer stem cells (CSCs) as the key driver behind carcinogenesis, progression, and diversity has displaced the prior model of a tumor composed of cells with similar subsequently acquired mutations and an equivalent capacity for renewal, invasion, and metastasis. This significant change has shifted the research focus toward targeting CSCs to eradicate cancer. CSCs may be characterized using cell surface markers. They are defined by their capacity to self-renew and differentiate, resist conventional therapies, and generate new tumors following repeated transplantation in xenografted mice. CSCs' functional capabilities are governed by various intracellular and extracellular variables such as pluripotency-related transcription factors, internal signaling pathways, and external stimuli. Numerous natural compounds and synthetic chemicals have been investigated for their ability to disrupt these regulatory components and inhibit stemness and terminal differentiation in CSCs, hence achieving clinical implications. However, no cancer treatment focuses on the biological consequences of these drugs on CSCs, and their functions have been established. This article provides a biomedical discussion of cancer at the time along with an overview of CSCs and their origin, features, characterization, isolation techniques, signaling pathways, and novel targeted therapeutic approaches. Additionally, we highlighted the factors endorsed as controlling or helping to promote stemness in CSCs. Our objective was to encourage future studies on these prospective treatments to develop a framework for their application as single or combined therapeutics to eradicate various forms of cancer.

Indexed as

Drug Resistance, NeoplasmNeoplasmsAnimalsCarcinogenesisMiceNeoplastic Stem CellsSignal Transductioncancercancer stem cellscarcinogenesisresistancetherapeutic

Identifiers

PMID36675306
PMCPMC9861138
OpenAlexW4316672829

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.