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Advanced Research on Cancer Stem Cells
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Advanced Research on Cancer Stem Cells

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 November 2026 | Viewed by 3583

Special Issue Editors

Prof. Dr. Ilze Štrumfa

E-Mail Website
Guest Editor
Department of Pathology, Riga Stradins University, 16 Dzirciema Street, LV-1007 Riga, Latvia
Interests: tumour pathology; molecular pathology; cancer stem cells; tumour microenvironment; digital pathology
Special Issues, Collections and Topics in MDPI journals
Dr. Inta Liepniece-Karele

E-Mail Website
Guest Editor
Department of Pathology, Riga Stradins University, LV-1007 Riga, Latvia
Interests: cancer risk; tumors cell

Special Issue Information

Dear Colleagues,

Cancer research represents a wide and active field of science, yielding tremendous progress in the treatment and diagnostics of malignant tumours. Nevertheless, the proportion of malignant tumours in death statistics is increasing. Cancer currently ranks as the first or second leading cause of premature death in 112 out of 183 countries (Sung et al., 2021) and the dominant cause in 57 countries (Bray et al., 2021). The growing contribution of oncological diseases to the global mortality rate is partially attributable to the decreasing death rate from cardiovascular pathologies. However, the global cancer burden remains high, and failures of treatment significantly contribute to cancer mortality.

Tumour recurrence and treatment resistance are features classically associated with cancer stem cells (CSCs)—a minor population of quiescent, self-renewing, pluripotent malignant cells. CSCs have a low proliferation rate, but, when dividing, they are able to restore the population of stem cells and give rise to malignant daughter cells constituting the main tumour mass. Thus, when implanted in an experimental animal, CSCs can recapitulate the whole heterogeneity of the initial tumour. This feature of stem cells is reflected in the synonymous designation “tumour-initiating cells”. However, the ability to re-establish tumour diversity in an experimental animal model should not be equalized with the capacity to induce the malignant tumour in the patient. Indeed, four possible sources of CSCs are proposed, including normal stem cells, mature cells, cancer cells, and fusion cells. Currently, cancer stem cells are considered to be a status rather than an entity, likely being in dynamic balance with the general malignant population. The underlying molecular mechanisms of stemness represent an important driver of cancer pathogenesis, as well as an attractive treatment target.

We are pleased to invite you to submit your manuscript to this Special Issue, “Advanced Research on Cancer Stem Cells”, devoted to the molecular features of cancer stem cells in malignant human tumours, as well as innovative treatment options capable of showing efficacy against stem cells.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • The molecular characteristics of cancer stem cells, including genetic and epigenetic events, metabolic changes, and the expression of different proteins.
  • The interactions between cancer stem cells and tumour microenvironments, including the relevant molecular mechanisms.
  • The role of cancer stem cells in different solid and hematological tumours, e.g., breast cancer, pancreatic cancer, lung cancer, glioblastoma, renal carcinoma, liver cancer, gastric carcinoma, colorectal carcinoma, melanoma, leukemias and lymphomas, and others. Pathogenetic, prognostic, and other aspects of stemness can be discussed.
  • Innovative treatment approaches in order to eradicate stem cells.
  • Technological approaches, methods, and innovations in stem cell research.

I look forward to receiving your contributions.

Prof. Dr. Ilze Štrumfa
Dr. Inta Liepniece-Karele
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer stem cells
  • tumour microenvironment
  • pancreatic cancer
  • glioblastoma
  • gastric cancer
  • breast cancer
  • lung cancer
  • colorectal cancer
  • renal cancer
  • liver cancer
  • melanoma
  • leukemia
  • lymphoma

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Published Papers (3 papers)

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Research

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17 pages, 2447 KB  
Article
miR-136-5p Preferentially Suppresses Cancer Stem-like Cells in Pancreatic Cancer
by Hiroyuki Yamamoto, Yuhki Yokoyama, Shihori Kouda, Ruijia Yang, Yingjue Zhang, Jiaqi Wang, Yoshihiro Morimoto, Tsuyoshi Hata, Akira Inoue, Daisuke Okuzaki, Naotsugu Haraguchi, Hidekazu Takahashi, Satoshi Shibata, Hirofumi Yamamoto and Masaki Mori
Int. J. Mol. Sci. 2026, 27(8), 3686; https://doi.org/10.3390/ijms27083686 - 21 Apr 2026
Viewed by 399
Abstract
In pancreatic cancer, cancer stem-like cells (CSCs) contribute to tumor initiation, reduced drug sensitivity, and recurrence. Limited strategies are currently available to target this cell population. Here we used a proteasome-low CSC enrichment system to identify microRNAs that negatively regulate CSC-like properties. From [...] Read more.
In pancreatic cancer, cancer stem-like cells (CSCs) contribute to tumor initiation, reduced drug sensitivity, and recurrence. Limited strategies are currently available to target this cell population. Here we used a proteasome-low CSC enrichment system to identify microRNAs that negatively regulate CSC-like properties. From PANC-1 cells expressing a ZsGreen–ODC degron reporter, a proteasome-low population was isolated through sequential fluorescence-activated cell sorting of ZsGreen-positive cells. Molecular and functional analyses confirmed the CSC-like phenotype of this cell population. Integrated in silico analysis was used to select 31 microRNAs predicted to target CSC-related molecules, which were then evaluated by in vitro viability-based screening to identify candidates that selectively suppressed the viability of CSC-like cells, relative to non-CSCs. Moreover, comprehensive miRNA expression profiling revealed that miR-136-5p was downregulated in the CSC-like population and was therefore selected for further analysis. Mechanistically, miR-136-5p directly targets the 3′ untranslated region of DCLK1 and reduces its expression, with a greater reduction in the short isoform. Finally, in a CSC-derived xenograft mouse model, systemic delivery of miR-136-5p using super carbonate apatite nanoparticles significantly suppressed tumor growth. Taken together, these findings suggest that miR-136-5p restoration may provide a therapeutic approach for targeting CSC-driven tumor growth in pancreatic cancer. Full article
(This article belongs to the Special Issue Advanced Research on Cancer Stem Cells)
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14 pages, 1813 KB  
Article
Elevated Antigen-Presenting-Cell Signature Genes Predict Stemness and Metabolic Reprogramming States in Glioblastoma
by Ji-Yong Sung and Kihwan Hwang
Int. J. Mol. Sci. 2025, 26(15), 7411; https://doi.org/10.3390/ijms26157411 - 1 Aug 2025
Cited by 3 | Viewed by 1715
Abstract
Glioblastoma (GBM) is a highly aggressive and heterogeneous brain tumor. Glioma stem-like cells (GSCs) play a central role in tumor progression, therapeutic resistance, and recurrence. Although immune cells are known to shape the GBM microenvironment, the impact of antigen-presenting-cell (APC) signature genes on [...] Read more.
Glioblastoma (GBM) is a highly aggressive and heterogeneous brain tumor. Glioma stem-like cells (GSCs) play a central role in tumor progression, therapeutic resistance, and recurrence. Although immune cells are known to shape the GBM microenvironment, the impact of antigen-presenting-cell (APC) signature genes on tumor-intrinsic phenotypes remains underexplored. We analyzed both bulk- and single-cell RNA sequencing datasets of GBM to investigate the association between APC gene expression and tumor-cell states, including stemness and metabolic reprogramming. Signature scores were computed using curated gene sets related to APC activity, KEGG metabolic pathways, and cancer hallmark pathways. Protein–protein interaction (PPI) networks were constructed to examine the links between immune regulators and metabolic programs. The high expression of APC-related genes, such as HLA-DRA, CD74, CD80, CD86, and CIITA, was associated with lower stemness signatures and enhanced inflammatory signaling. These APC-high states (mean difference = –0.43, adjusted p < 0.001) also showed a shift in metabolic activity, with decreased oxidative phosphorylation and increased lipid and steroid metabolism. This pattern suggests coordinated changes in immune activity and metabolic status. Furthermore, TNF-α and other inflammatory markers were more highly expressed in the less stem-like tumor cells, indicating a possible role of inflammation in promoting differentiation. Our findings revealed that elevated APC gene signatures are associated with more differentiated and metabolically specialized GBM cell states. These transcriptional features may also reflect greater immunogenicity and inflammation sensitivity. The APC metabolic signature may serve as a useful biomarker to identify GBM subpopulations with reduced stemness and increased immune engagement, offering potential therapeutic implications. Full article
(This article belongs to the Special Issue Advanced Research on Cancer Stem Cells)
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Review

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16 pages, 665 KB  
Review
Glioblastoma Stem Cells and Tumour Microenvironment: Interactions Across Hypoxia, Vasculature and Immune Modulation
by Karina Biserova and Ilze Strumfa
Int. J. Mol. Sci. 2026, 27(6), 2557; https://doi.org/10.3390/ijms27062557 - 11 Mar 2026
Cited by 1 | Viewed by 692
Abstract
Glioblastoma (GBM) is an aggressive brain tumour known for its ability to resist the current treatment protocols. A major reason for this resistance is a minor group of cells within the tumour called glioblastoma stem cells (GSCs). These cells drive tumour growth, invasion, [...] Read more.
Glioblastoma (GBM) is an aggressive brain tumour known for its ability to resist the current treatment protocols. A major reason for this resistance is a minor group of cells within the tumour called glioblastoma stem cells (GSCs). These cells drive tumour growth, invasion, and recurrence after therapy. GSCs survive and expand within a specific microenvironment that protects and supports them. Three of the most important niches are: hypoxic (low oxygen) regions, which trigger survival pathways and make GSCs more resistant to treatment; perivascular areas near blood vessels, which provide nutrients and signals that maintain stem-like properties; and immune-related zones, where inflammatory and suppressive signals help GSCs escape the body’s defences. Together, these environments allow GSCs to thrive and contribute to the tumour’s persistence. This review highlights how hypoxia, blood vessel niches, and immune interactions work together to sustain GSCs and promote GBM progression. A clearer understanding of these supportive environments may lead to new treatment approaches aimed at disrupting GSC survival and improving patient outcomes. Full article
(This article belongs to the Special Issue Advanced Research on Cancer Stem Cells)
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