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Targeting of Tumor Dormancy Pathway
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Targeting of Tumor Dormancy Pathway

A special issue of Onco (ISSN 2673-7523).

Deadline for manuscript submissions: 31 December 2025 | Viewed by 15165

Special Issue Editors

Dr. Athanassios Kotsinas

E-Mail Website
Guest Editor
Laboratory of Histology-Embryology, Faculty of Medicine, National & Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, 11527 Athens, Greece
Interests: DNA polymorphisms; RNA; miRNAs; carcinogenesis; bioinformatics; DNA damage; cell cycle; cancer
Dr. Constantin N. Baxevanis

E-Mail Website
Guest Editor
1. Cancer Immunology and Immunotherapy Center, Saint Savas Cancer Hospital, 171 Alexandras Avenue, 11522 Athens, Greece
2. Flow Cytometry Unit, Section of Animal and Human Physiology, Department of Biology, National and Kapodistrian University of Athens, Panepistimiopolis, Ilisia, 15784 Athens, Greece
Interests: cancer immunology; cancer immunotherapy; biomarkers; precision oncology; immune resistance; cancer vaccines; immune escape; immune checkpoint inhibitors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Dormant tumor cells, also known as minimal residual disease, represent a population of cancer cells that have entered a state of growth arrest, typically after primary tumor removal or during periods of remission. This dormant state allows them to evade conventional cancer therapies, such as chemotherapy or radiation, which primarily target actively dividing cells. It is generally thought that dormant tumor cells have the potential to reactivate and give rise to metastatic tumors years or even decades after initial treatment. However, from another perspective, keeping tumor cells silent for decades can be regarded as tantamount to cure. From both perspectives, it is important to understand the mechanisms underlying dormancy. Keeping tumor cells dormant for indefinite periods of time could form a new strategy of cancer treatment. This Special Issue will highlight the current state of the knowledge in tumor dormancy, targeting of tumor dormancy pathways, and future prospects for exploiting tumor dormancy for cancer therapies.

Dr. Athanassios Kotsinas
Dr. Constantin N. Baxevanis
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Onco is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). 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

  • dormant tumor cells
  • conventional cancer therapies
  • cancer therapies
  • chemotherapy
  • radiation
  • tumor dormancy
  • targeting of tumor dormancy pathways

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Published Papers (6 papers)

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Research

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7 pages, 231 KB  
Communication
Association of TP53 Arg72Pro (rs1042522) Polymorphism with Pancreatic Cancer Risk in a Patient Cohort
by Laura Antolino, Germana de Nucci, Stefania Scarpino, Giuseppe Bianco, Gianluca Lopez, Paolo Aurello, Niccolò Petrucciani, Roberto Santoro, Giuseppe Nigri, Salvatore Agnes, Gianpiero Manes and Francesco A. D’Angelo
Onco 2025, 5(4), 44; https://doi.org/10.3390/onco5040044 - 24 Sep 2025
Viewed by 293
Abstract
Pancreatic cancer is expected to become the second leading cause of death by 2030 in Western countries. There is a need to pinpoint high-risk populations since extensive screening would be economically impractical. Methods: This study, conducted on liquid biopsies of patients affected by [...] Read more.
Pancreatic cancer is expected to become the second leading cause of death by 2030 in Western countries. There is a need to pinpoint high-risk populations since extensive screening would be economically impractical. Methods: This study, conducted on liquid biopsies of patients affected by pancreatic ductal adenocarcinoma (PDAC), sequenced, by NGS, the main genes involved in pancreatic carcinogenesis. Results: The study was discontinued due to a low recruitment rate. NGS analysis, conducted on included patients, revealed the TP53 variant rs1042522 in 30 out of 35 patients, with a cytosine (C) replaced by a guanine (G), hence inserting an Arginine in the final protein instead of a Proline. The presence of the rs1042522 variant confers an odds ratio of 6.11 for PaC and an OR of 20 for homozygosity G/G when comparing our cohort of PaC patients to a healthy population from the 1000GenomeProject. Conclusion: These findings could identify a very-high-risk population deserving of being screened for PDAC, even though a wider validation of rs1042522 as a risk factor is needed. Impact: These preliminary data may open the way for identification of a population more prone to developing pancreatic cancer. Full article
(This article belongs to the Special Issue Targeting of Tumor Dormancy Pathway)
14 pages, 1718 KB  
Article
The Role of the Bone Marrow Microenvironment in Physical Function and Quality of Life in Patients with Multiple Myeloma After First-Line Treatment with Novel Agents and Autologous Transplantation
by Polyxeni Spiliopoulou, Pantelis Rousakis, Chrysanthi Panteli, Evangelos Eleutherakis-Papaiakovou, Magdalini Migkou, Nikolaos Kanellias, Ioannis Ntanasis-Stathopoulos, Panagiotis Malandrakis, Foteini Theodorakakou, Despina Fotiou, Evangelos Terpos, Vassilios Myrianthopoulos, Maria Gavriatopoulou, Ourania E. Tsitsilonis, Efstathios Kastritis, Meletios Athanasios Dimopoulos and Gerasimos Terzis
Onco 2025, 5(2), 21; https://doi.org/10.3390/onco5020021 - 1 May 2025
Viewed by 1148
Abstract
Background/Objectives: Multiple myeloma is a malignancy of plasma cells detected in the bone marrow, inducing symptoms like anemia, hypercalcemia, renal problems, and bone fractures in multiple myeloma patients, affecting their quality of life. The bone marrow microenvironment plays a crucial role in the [...] Read more.
Background/Objectives: Multiple myeloma is a malignancy of plasma cells detected in the bone marrow, inducing symptoms like anemia, hypercalcemia, renal problems, and bone fractures in multiple myeloma patients, affecting their quality of life. The bone marrow microenvironment plays a crucial role in the prognosis and progression of the disease. The purpose of this study was to examine the relationship between the percentages of the major cell populations of the bone marrow, including immune cells, and physical function/quality of life in multiple myeloma patients after first-line treatment. Methods: Twenty-one multiple myeloma patients (N = 14 men, N = 7 women) participated in the study after completing first-line treatment. Bone marrow and blood samples were taken one hundred days after transplantation, while physical function (6 min walking test, handgrip test, maximal aerobic power, and isometric strength), health-related quality of life (QLQ-C30), and body composition (DXA) were assessed 2–5 days later. Flow cytometry was used to assess the percentages of plasma cells, mast cells, B cells (total, precursors, naïve, and memory), T cells (total, CD27− and CD27+), NK/NKT cells (total, CD27− and CD27+), eosinophils, monocytes, neutrophils, myeloid progenitors, erythroblasts, and erythroid progenitors, expressed as percentages of total nucleated cells of the bone marrow. Results: The percentage of CD27+ NK/NKT cells was correlated with five parameters of the quality of life questionnaire: physical function (r = 0.78, p = 0.005), role functioning (r = 0.69, p = 0.020), fatigue (r = −0.86, p = 0.000), pain (r = 0.68, p = 0.021), and dyspnea (r = −0.80, p = 0.003). Conclusions: In conclusion, stronger immune surveillance in the bone marrow from CD27+ NK/NKT cells is correlated with better quality of life in multiple myeloma patients. Full article
(This article belongs to the Special Issue Targeting of Tumor Dormancy Pathway)
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Review

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26 pages, 2910 KB  
Review
Targeting Pathways and Mechanisms in Gynecological Cancer with Antioxidant and Anti-Inflammatory Phytochemical Drugs
by Sandhya Shukla, Arvind Kumar Shukla, Navin Ray, Adarsha Mahendra Upadhyay, Fowzul Islam Fahad, Sayan Deb Dutta, Arulkumar Nagappan and Raj Kumar Mongre
Onco 2025, 5(2), 24; https://doi.org/10.3390/onco5020024 - 9 May 2025
Cited by 1 | Viewed by 3166
Abstract
Globally, women’s cancer-related morbidity and death are still caused mainly by gynecologic cancer. Antioxidant and anti-inflammatory drugs have shown promise in treating gynecologic cancer because of the complex interactions among oxidative stress, inflammation, and the development of tumors. This review focuses on how [...] Read more.
Globally, women’s cancer-related morbidity and death are still caused mainly by gynecologic cancer. Antioxidant and anti-inflammatory drugs have shown promise in treating gynecologic cancer because of the complex interactions among oxidative stress, inflammation, and the development of tumors. This review focuses on how these drugs, which include polyphenols, terpenoids, and thiols-related phytochemical-derived compounds target different pathways associated with developing and progressing gynecologic cancer. We investigate what factors affect the tumor microenvironment, specifically how they affect immunological response and vasculogenesis. Through the review of recent studies, we have gained an extensive understanding of the molecular pathways that anti-inflammatory and antioxidant drugs use to achieve their therapeutic benefits. Gynecologic cancer is still a potent cause of cancer-related deaths and fatalities for women globally. Antioxidant and anti-inflammatory drugs have shown promise in treating gynecologic cancer because of the complex interactions among oxidative stress, inflammation, and the development of tumors. This review focuses on how these drugs target different pathways associated with developing and progressing gynecologic cancer. We investigate what factors affect the tumor microenvironment, specifically how they affect immunological response and vasculogenesis. Through the review of recent studies, we have gained an extensive understanding of the molecular pathways that anti-inflammatory and antioxidant drugs use to achieve their therapeutic benefits. Full article
(This article belongs to the Special Issue Targeting of Tumor Dormancy Pathway)
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21 pages, 769 KB  
Review
Dormant Tumor Cells: Current Opportunities and Challenges in Clinical Practice
by Emma Boydell, Maxime Borgeaud and Petros Tsantoulis
Onco 2025, 5(1), 3; https://doi.org/10.3390/onco5010003 - 10 Jan 2025
Cited by 1 | Viewed by 4062
Abstract
Tumor dormancy plays a pivotal role in cancer relapse. Dormant tumor cells have been identified in distant sites, even in early-stage tumors, and are associated with worse outcomes. This review explores the current understanding of the molecular and cellular mechanisms behind tumor dormancy, [...] Read more.
Tumor dormancy plays a pivotal role in cancer relapse. Dormant tumor cells have been identified in distant sites, even in early-stage tumors, and are associated with worse outcomes. This review explores the current understanding of the molecular and cellular mechanisms behind tumor dormancy, including the role of the immune system and the microenvironment. Targeting dormant tumor cells could be a therapeutic strategy to offer long-term remission and potentially cure cancer. Unfortunately, the translation of this knowledge in clinical practice is lacking. We assess the feasibility of detecting and measuring dormant tumor cells in clinical practice, and give an overview of potential therapeutic targets, both in terms of maintaining tumor cells in a dormant state, and in terms of eradicating this tumor population. Full article
(This article belongs to the Special Issue Targeting of Tumor Dormancy Pathway)
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Other

Jump to: Research, Review

23 pages, 507 KB  
Systematic Review
Metabolic Reprogramming as a Therapeutic Target in Cancer: A Qualitative Systematic Review (QualSR) of Natural Compounds Modulating Glucose and Glutamine Pathways
by Michael Enwere, Edward Irobi, Victoria Chime, Ada Ezeogu, Adamu Onu, Mohamed Toufic El Hussein, Gbadebo Ogungbade, Emmanuel Davies, Omowunmi Omoniwa, Charles Omale, Mercy Neufeld, Ojochide Akagwu, Terkaa Atim and Laurens Holmes, Jr.
Onco 2025, 5(3), 43; https://doi.org/10.3390/onco5030043 - 22 Sep 2025
Viewed by 1091
Abstract
Background: Despite advances in gene-targeted and immunotherapies, many aggressive cancers—including glioblastoma and triple-negative breast cancer—remain refractory to treatment. Mounting evidence implicates metabolic reprogramming, especially dysregulation of glucose and glutamine metabolism, as a core hallmark of tumor progression. Natural compounds with metabolic-modulatory effects have [...] Read more.
Background: Despite advances in gene-targeted and immunotherapies, many aggressive cancers—including glioblastoma and triple-negative breast cancer—remain refractory to treatment. Mounting evidence implicates metabolic reprogramming, especially dysregulation of glucose and glutamine metabolism, as a core hallmark of tumor progression. Natural compounds with metabolic-modulatory effects have emerged as promising adjuncts in oncology. Research Question and Objectives: This review investigates the following question: How can metabolic-targeted therapies—particularly those modulating the Warburg effect and glutamine metabolism—improve cancer treatment outcomes, and what role do natural compounds play in this strategy? The objectives were to (1) evaluate the therapeutic potential of metabolic interventions targeting glucose and glutamine metabolism, (2) assess natural compounds with metabolic regulatory activity, (3) examine integration of metabolic-targeted therapies with conventional treatments, and (4) identify metabolic vulnerabilities in resistant malignancies. Methods: A qualitative systematic review (QualSR) was conducted following PRISMA guidelines. A total of 87 peer-reviewed studies published between 2000 and 2024 were included. Inclusion criteria required clearly defined mechanistic or clinical endpoints and, for clinical trials, sample sizes ≥ 30. Data extraction focused on tumor response, survival, metabolic modulation, and safety profiles. Results: Curcumin significantly reduced serum TNF-α and IL-6 (both p = 0.001) and improved antioxidant capacity (p = 0.001). EGCG downregulated ERα (p = 0.002) and upregulated tumor suppressors p53 and p21 (p = 0.001, p = 0.02). High-dose intravenous vitamin C combined with chemoradiotherapy yielded a 44.4% pathologic complete response rate in rectal cancer. Berberine suppressed Akt/mTOR signaling and glutamine transporter SLC1A5 across tumor types (q < 10−10). However, poor bioavailability (e.g., EGCG t½ = 3.4 ± 0.3 h) and systemic toxicity limit their standalone clinical application. Conclusions: Metabolic-targeted therapies—particularly natural compounds acting on glucose and glutamine pathways—offer a viable adjunct to standard cancer therapies. Clinical translation will require biomarker-driven patient stratification, improved delivery systems, and combination trials to optimize the therapeutic impact in treatment-resistant cancers. Full article
(This article belongs to the Special Issue Targeting of Tumor Dormancy Pathway)
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9 pages, 1755 KB  
Commentary
When Therapy-Induced Cancer Cell Apoptosis Fuels Tumor Relapse
by Razmik Mirzayans
Onco 2024, 4(1), 37-45; https://doi.org/10.3390/onco4010003 - 4 Feb 2024
Cited by 3 | Viewed by 4084
Abstract
Most therapeutic strategies for solid tumor malignancies are designed based on the hypothesis that cancer cells evade apoptosis to exhibit therapy resistance. This is somewhat surprising given that clinical studies published since the 1990s have demonstrated that increased apoptosis in solid tumors is [...] Read more.
Most therapeutic strategies for solid tumor malignancies are designed based on the hypothesis that cancer cells evade apoptosis to exhibit therapy resistance. This is somewhat surprising given that clinical studies published since the 1990s have demonstrated that increased apoptosis in solid tumors is associated with cancer aggressiveness and poor clinical outcome. This is consistent with more recent reports demonstrating non-canonical (pro-survival) roles for apoptotic caspases, including caspase 3, as well as the ability of cancer cells to recover from late stages of apoptosis via a process called anastasis. These activities are essential for the normal development and maintenance of a healthy organism, but they also enable malignant cells (including cancer stem cells) to resist anticancer treatment and potentially contribute to clinical dormancy (minimal residual disease). Like apoptosis, therapy-induced cancer cell dormancy (durable proliferation arrest reflecting various manifestations of genome chaos) is also not obligatorily a permanent cell fate. However, as briefly discussed herein, compelling pre-clinical studies suggest that (reversible) dormancy might be the “lesser evil” compared to treacherous apoptosis. Full article
(This article belongs to the Special Issue Targeting of Tumor Dormancy Pathway)
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