Signaling in Cancer Stem Cells
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Stem Cells".
Deadline for manuscript submissions: 30 January 2025 | Viewed by 223
Special Issue Editor
Special Issue Information
Dear Colleagues,
Cancer stem cells have made a significant contribution to cancer initiation and progression, metastasis, recurrence, and therapeutic resistance. Their ability to self-renew and the differential heterogeneity cause the reasons associated with multi-drug resistance and subsequent recurrence. This puts forward the necessity of unraveling the key oncogenic events that regulate cancer stemness, addressing chemotherapeutic resistance, underpinning tumor heterogeneity, finding novel targets for therapy, developing precision targeted therapy, and identifying diagnostic biomarkers.
This Special Issue will examine both original research articles and reviews that identify and investigate oncogenic events in cancer stem cells and associated drug resistance to cancer recurrence, contributing insights into the determination of new therapeutic targets to overcome resistance. The aim and scope of this Special Issue are also to focus on recent advances in targeting cancer stem cells, including both targeted therapies and immunopharmacological approaches.
Submissions to this Special Issue may consist of, but are not restricted to, the following potential areas of research:
(1) Oncogenic events and signaling pathways leading to cancer stemness;
(2) Targeting cancer stem cell pathways, targeted therapy, and precision medicine advancements;
(3) Drug resistance and CSCs;
(4) Biomarker study in CSCs;
(5) Heterogeneity and microenvironment of CSCs.
Dr. Upasana Ray
Guest Editor
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
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Keywords
- cancer stem cells (CSCs)
- stem cells signaling pathways
- cancer progression and metastasis
- therapeutic resistance
- targeting cancer stem cells signaling
- cancer heterogeneity
- targeted therapy for CSCs
- identifying biomarkers for CSCs
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Planned Papers
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Pharmacological inhibition of cFLIP targets breast cancer stem cells
Authors: Richard Clarkson
Affiliation: University of Cardiff https://www.cardiff.ac.uk/cancer-stem-cell/about-us/in-conversation/dr-richard-clarkson
Title: Cancer Stem Cell of Glioblastoma: The Role of mTOR Pathway
Authors: Meena Jhanwar-Uniyal, Monica C. Mureb, Mohan Das, Chirag D Gandhi
Affiliation: Department of Neurosurgery, New York Medical College/Westchester Medical Center, Valhalla, New York 10595, USA
Abstract: Glioblastoma (GBM), the most aggressive primary brain tumor, portends a poor prognosis despite current treatment modalities due to the recurrence of disease. The major cause of tumor recurrence, growth, and invasion is the presence of the unique population of cancer stem cells (CSCs). Resistance to conventional therapies is caused by both extensive genetic abnormalities and dysregulation of the transcription landscape. Consequently, CSCs have emerged as targets of interest in new treatment paradigms. The mechanistic target of rapamycin (mTOR) forms two multiprotein complexes, mTORC1 and mTORC2, which regulate proliferation and migration. The pathogenesis of GBM is largely due to the frequent loss of the tumor suppressor gene PTEN, leading to an aberrant activation of the mTOR pathway in GBM and its CSCs. Therefore, strategies to treat GBM may involve inhibition of the mTOR pathway to target CSCs. Here, we explore the role of mTOR and related signaling pathways in the regulation of GBM CSCs and define their roles as therapeutic targets in the treatment of GBM.
