Sign in to use this feature.

Years

Between: -

Subjects

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Journals

Article Types

Countries / Regions

Search Results (142)

Search Parameters:
Keywords = radiation carcinogenesis

Order results
Result details
Results per page
Select all
Export citation of selected articles as:
51 pages, 2918 KiB  
Review
Therapeutic Applications and Mechanisms of Superoxide Dismutase (SOD) in Different Pathogenesis
by Shehwaz Anwar, Tarique Sarwar, Amjad Ali Khan and Arshad Husain Rahmani
Biomolecules 2025, 15(8), 1130; https://doi.org/10.3390/biom15081130 - 5 Aug 2025
Abstract
An imbalance between the generation of reactive oxygen species (ROS) and antioxidant defenses is known as oxidative stress, and it is implicated in a number of diseases. The superoxide radical O2– is produced by numerous biochemically relevant redox processes and is thought [...] Read more.
An imbalance between the generation of reactive oxygen species (ROS) and antioxidant defenses is known as oxidative stress, and it is implicated in a number of diseases. The superoxide radical O2– is produced by numerous biochemically relevant redox processes and is thought to play role in diseases and pathological processes, such as aging, cancer, membrane or DNA damage, etc.; SOD, or superoxide dismutase, is essential for reducing oxidative stress. As a result, the elimination of ROS by SOD may be a useful disease prevention tactic. There have been reports of protective effects against neurodegeneration, apoptosis, carcinogenesis, and radiation. Exogenous SODs’ low bioavailability has drawn criticism. However, this restriction might be removed, and interest in SOD’s medicinal qualities increased with advancements in its formulation. This review discusses the findings of human and animal studies that support the benefits of SOD enzyme regulation in reducing oxidative stress in various ways. Additionally, this review summarizes contemporary understandings of the biology of Cu/Zn superoxide dismutase 1 (SOD1) from SOD1 genetics and its therapeutic potential. Full article
(This article belongs to the Topic Enzymes and Enzyme Inhibitors in Drug Research)
Show Figures

Figure 1

21 pages, 703 KiB  
Review
A Practical Narrative Review on the Role of Magnesium in Cancer Therapy
by Daniela Sambataro, Giuseppina Scandurra, Linda Scarpello, Vittorio Gebbia, Ligia J. Dominguez and Maria Rosaria Valerio
Nutrients 2025, 17(14), 2272; https://doi.org/10.3390/nu17142272 - 9 Jul 2025
Viewed by 852
Abstract
Magnesium (Mg2+) has gained oncologists’ attention due to its wide range of biological functions and frequent use as a complementary or integrative agent. This review outlines Mg’s actions, its complex role in carcinogenesis and tumor risk, and clinical issues. Mg2+ [...] Read more.
Magnesium (Mg2+) has gained oncologists’ attention due to its wide range of biological functions and frequent use as a complementary or integrative agent. This review outlines Mg’s actions, its complex role in carcinogenesis and tumor risk, and clinical issues. Mg2+ is essential in numerous biochemical processes, including adenosine triphosphate production, cellular signal transduction, DNA, RNA and protein synthesis, and bone formation. Pertinent full-text articles were thoroughly examined, and the most relevant ones were selected for inclusion in this review. There is conflicting scientific evidence about the relationship between Mg2+ changes and cancer risk, apart from colorectal cancer. Chronic Mg2+ deficiency leads to immune dysfunctions and enhanced baseline inflammation associated with oxidative stress related to various age-associated morbidities and cancer. On the other hand, Mg2+ deficiency is associated with drug or chemotherapy-related hypomagnesemia, postoperative pain, cachexia, opioid-induced constipation, normal tissue protection from radiation damage, and prevention of nephrotoxicity. A balanced diet usually provides sufficient Mg2+, but supplementation may be necessary in some clinical settings. Full article
(This article belongs to the Section Clinical Nutrition)
Show Figures

Figure 1

15 pages, 2646 KiB  
Article
Radiation Quality-Dependent Progressive Increase in Oxidative DNA Damage and Intestinal Tumorigenesis in Apc1638N/+ Mice
by Kamendra Kumar, Santosh Kumar, Jerry Angdisen, Kamal Datta, Albert J. Fornace and Shubhankar Suman
Curr. Oncol. 2025, 32(7), 382; https://doi.org/10.3390/curroncol32070382 - 1 Jul 2025
Viewed by 389
Abstract
Exposure to high-linear energy transfer (LET) heavy ions, such as 28Si, poses a significant cancer risk for astronauts. While previous studies have linked high-LET radiation exposure to persistent oxidative stress and dysregulated stress responses in intestinal crypt cells with an increased risk [...] Read more.
Exposure to high-linear energy transfer (LET) heavy ions, such as 28Si, poses a significant cancer risk for astronauts. While previous studies have linked high-LET radiation exposure to persistent oxidative stress and dysregulated stress responses in intestinal crypt cells with an increased risk of tumorigenesis, the relationship between IR-induced oxidative DNA damage and intestinal cancer risk remains incompletely understood. Here, we investigated the time-dependent effects of 28Si-ion radiation on intestinal tumorigenesis and oxidative DNA damage in Apc1638N/+ mice, a model for human intestinal cancer predisposition. Male Apc1638N/+ mice were exposed to 10 cGy of either γ-rays (low-LET) or 28Si-ions (high-LET), and intestinal tumor burden was assessed at 60 and 150 days post-irradiation. While both radiation groups showed modest, non-significant tumor increases at 60 days, 28Si-irradiated mice exhibited an approximately 2.5-fold increase in tumor incidence by 150 days, with a higher incidence of invasive carcinomas compared to γ and sham groups. Serum 8-OxodG levels, a marker of systemic oxidative stress, were significantly elevated in the 28Si-ion group, correlating with increased intestinal 8-OxodG staining. Additionally, assessment of the proliferation marker Cyclin D1 and metaplasia marker Guanylyl Cyclase C (GUCY2C) also revealed significant crypt cell hyperproliferation accompanied by increased metaplasia in 28Si-exposed mouse intestines. Positive correlations between serum 8-OxodG and tumor-associated endpoints provide compelling evidence that exposure to 28Si-ions induces progressive intestinal tumorigenesis through sustained oxidative DNA damage, crypt cell hyperproliferation, and metaplastic transformation. This study provides evidence in support of the radiation quality-dependent progressive increase in systemic and intestinal levels of 8-OxodG during intestinal carcinogenesis. Moreover, the progressive increase in oxidative DNA damage and simultaneous increase in oncogenic events after 28Si exposure also suggest that non-targeted effects might be a significant player in space radiation-induced intestinal cancer development. The correlation between serum 8-OxodG and oncogenic endpoints supports its potential utility as a predictive biomarker of high-LET IR-induced intestinal carcinogenesis, with implications for astronaut health risk monitoring during long-duration space missions. Full article
(This article belongs to the Section Gastrointestinal Oncology)
Show Figures

Graphical abstract

24 pages, 592 KiB  
Review
Caffeine as a Modulator in Oncology: Mechanisms of Action and Potential for Adjuvant Therapy
by Nina Rembiałkowska, Alina Demiy, Alicja Dąbrowska, Jakub Mastalerz and Wojciech Szlasa
Int. J. Mol. Sci. 2025, 26(13), 6252; https://doi.org/10.3390/ijms26136252 - 28 Jun 2025
Viewed by 1048
Abstract
Caffeine, one of the most widely consumed bioactive compounds worldwide, is gaining recognition for its potential anticancer properties beyond its well-known neurological and metabolic effects. Mechanistically, caffeine exerts anti-tumor activity by modulating key cellular pathways involved in carcinogenesis, including the inhibition of phosphodiesterases, [...] Read more.
Caffeine, one of the most widely consumed bioactive compounds worldwide, is gaining recognition for its potential anticancer properties beyond its well-known neurological and metabolic effects. Mechanistically, caffeine exerts anti-tumor activity by modulating key cellular pathways involved in carcinogenesis, including the inhibition of phosphodiesterases, antagonism of adenosine A2A receptors, and disruption of the DNA damage response through ATR-Chk1 pathway inhibition. These actions collectively promote apoptosis, suppress tumor cell proliferation, and impair metastatic spread. In vitro and in vivo studies have demonstrated that caffeine can enhance the cytotoxic effects of chemotherapeutic agents and radiation therapy, suggesting a synergistic role in conventional cancer treatments. Epidemiological data further supports an inverse association between habitual caffeine consumption and the incidence of several cancers, notably liver, colorectal, breast, and prostate cancers. Among these, the most consistent experimental and clinical evidence exists for liver and colorectal cancer, where caffeine’s modulatory effects on inflammation and cell proliferation have been repeatedly observed. Additionally, caffeine’s anti-oxidant and anti-inflammatory properties may contribute to a microenvironment less conducive to tumor initiation and progression. While promising, the anticancer effects of caffeine are influenced by factors such as dosage, individual genetic variability, and cancer type, underscoring the need for further clinical investigation. This review explores the emerging role of caffeine as a potential chemopreventive and adjuvant therapeutic agent in oncology. Full article
Show Figures

Figure 1

27 pages, 1266 KiB  
Systematic Review
Genotoxicity Induced by Carcinogenic Agents or Occupational Exposure with Sufficient Evidence for Bladder Cancer
by Edyta Kasperczyk, Kateryna Tarhonska and Ewa Jablonska
J. Clin. Med. 2025, 14(13), 4492; https://doi.org/10.3390/jcm14134492 - 25 Jun 2025
Viewed by 594
Abstract
Background: There is substantial evidence supporting the role of genetic alterations in chemically induced carcinogenesis. We analyzed the existing literature to gather data on genetic alterations linked to human carcinogens and their possible connection to genotoxic outcomes. The review emphasizes carcinogenic substances [...] Read more.
Background: There is substantial evidence supporting the role of genetic alterations in chemically induced carcinogenesis. We analyzed the existing literature to gather data on genetic alterations linked to human carcinogens and their possible connection to genotoxic outcomes. The review emphasizes carcinogenic substances and occupational exposures identified as “carcinogenic to humans”. In particular, we searched for studies describing genotoxic alterations linked to agents and occupational exposures for which the International Agency for Research on Cancer has found sufficient evidence of an association with bladder cancer. Methods: The review was carried out in compliance with the PRISMA standards. A comprehensive search of the PubMed database was conducted to identify studies published through March 2024. Results: We identified 60 studies that evaluated genetic alterations for 16 carcinogenic agents and occupations (such as aluminum production, 4-aminobiphenyl, auramine production, benzidine, chlornaphazine, cyclophosphamide, firefighters, magenta production, 2-naphthylamine, opium consumption, ortho-toluidine, painters, the rubber manufacturing industry, Schistosoma haematobium infection, X-radiation, gamma-radiation) in healthy humans. Conclusions: The genotoxic effects of chemical agents in healthy individuals have been well studied and characterized. Additionally, this review presents numerous studies concerning occupational exposure but not exclusively. Genotoxicity assessments have mainly been conducted on biological materials such as blood, peripheral blood lymphocytes, urine, and buccal epithelial cells. The most frequently examined genotoxic effects were DNA damage, chromosomal abnormalities, and micronuclei. Standardized data to clearly define a dose–response relationship for predicting delayed health effects are still lacking. Full article
(This article belongs to the Special Issue Clinical Management of Bladder Cancer)
Show Figures

Figure 1

22 pages, 12881 KiB  
Article
TOPK Drives IL19-Mediated Crosstalk Between Cancer Cells and Fibroblasts to Promote Solar UV-Induced Skin Damage and Carcinogenesis
by Asad U. Khan, Qiushi Wang, Eunmiri Roh, Sally E. Dickinson, Georg T. Wondrak, Clara Curiel-Lewandowski, Ann M. Bode and Tianshun Zhang
Cancers 2025, 17(13), 2067; https://doi.org/10.3390/cancers17132067 - 20 Jun 2025
Viewed by 569
Abstract
Background/Objectives: Non-melanoma skin cancer (NMSC) is among the most common cancers in the United States, with solar ultraviolet (UV) radiation being a primary etiological factor. T-LAK cell-originated protein kinase (TOPK), a serine/threonine kinase activated by solar UV, has been implicated in skin carcinogenesis. [...] Read more.
Background/Objectives: Non-melanoma skin cancer (NMSC) is among the most common cancers in the United States, with solar ultraviolet (UV) radiation being a primary etiological factor. T-LAK cell-originated protein kinase (TOPK), a serine/threonine kinase activated by solar UV, has been implicated in skin carcinogenesis. This study aimed to investigate the mechanistic role of TOPK in solar UV-induced skin damage and tumor development. Methods: RNA sequencing (RNA-seq) was performed on skin tissues from wild-type (WT) and TOPK knockout (KO) mice, with or without solar UV exposure, to identify TOPK-regulated genes and pathways. Follow-up experiments using Western blotting, immunofluorescence, and luciferase assays were conducted in vitro and in vivo. Functional assays included 3D spheroid and Transwell co-culture systems involving cutaneous squamous cell carcinoma (cSCC) and fibroblast cells. Results: TOPK deletion altered gene expression profiles and inhibited solar UV-induced activation of multiple signaling pathways, including cytokine–cytokine receptor interaction, PI3K/AKT, MAPKs, PKG, cAMP, and calcium signaling. RNA-seq and protein analyses identified interleukin-19 (IL19) as a key downstream effector suppressed by TOPK deletion. In cSCC and fibroblast cells, TOPK knockdown reduced IL19 expression and secretion. IL19 promoted cSCC growth and activated PI3K/AKT, ERK, and TOPK pathways. Additionally, chronic TGFβ exposure increased IL19 expression and activated fibroblasts, as indicated by elevated αSMA and FAPα levels. Conclusions: These findings establish TOPK as a central regulator of solar UV-induced skin carcinogenesis, partially via modulation of IL19 signaling and fibroblast activation. Targeting TOPK may offer a novel strategy for the prevention and treatment of NMSC. Full article
(This article belongs to the Special Issue The Advance of Biomarker-Driven Targeted Therapies in Cancer)
Show Figures

Figure 1

20 pages, 279 KiB  
Review
Radon Exposure and Cancer Risk: Assessing Genetic and Protein Markers in Affected Populations
by Yerlan Kashkinbayev, Baglan Kazhiyakhmetova, Nursulu Altaeva, Meirat Bakhtin, Pavel Tarlykov, Elena Saifulina, Moldir Aumalikova, Danara Ibrayeva and Aidos Bolatov
Biology 2025, 14(5), 506; https://doi.org/10.3390/biology14050506 - 6 May 2025
Viewed by 1125
Abstract
Radon is an inert gas produced by the radioactive decay of uranium-238, commonly found in the environment. Radon and its decay products are the main sources of human exposure to radiation from natural sources. When inhaled, radon’s alpha particles impact lung tissue, potentially [...] Read more.
Radon is an inert gas produced by the radioactive decay of uranium-238, commonly found in the environment. Radon and its decay products are the main sources of human exposure to radiation from natural sources. When inhaled, radon’s alpha particles impact lung tissue, potentially causing lung cancer by damaging DNA and altering oxidative processes. This review article addresses the need for a deeper understanding of the genetic and molecular changes associated with radon-induced lung cancer, aiming to clarify key genetic mutations and protein markers linked to carcinogenesis. Particular attention in recent studies has been given to mutations in tumor suppressor genes (RASSF1, TP53), oncogenes (KRAS, EGFR), and changes in the expression levels of protein biomarkers associated with inflammation, stress, and apoptosis. Identifying these markers is critical for developing effective screening methods for radon-induced lung cancer, enabling timely identification of high-risk patients and supporting effective preventive strategies. Summarizing current genetic and protein biomarkers, this review highlights the importance of a comprehensive approach to studying radon-induced carcinogenesis. Understanding these molecular mechanisms could ultimately improve early diagnostic methods and enhance therapy for cancers associated with radon exposure. Full article
17 pages, 11922 KiB  
Article
Assessing Skin Photoprotection in the Infrared Range: The Reflectance Profiles of Cold-Pressed Plant Oils
by Elżbieta Mickoś, Monika Michalak, Magdalena Hartman-Petrycka, Anna Banyś, Paula Babczyńska, Robert Koprowski and Sławomir Wilczyński
Cosmetics 2025, 12(2), 80; https://doi.org/10.3390/cosmetics12020080 - 14 Apr 2025
Viewed by 1076
Abstract
The harmful effects of solar radiation on the skin are known and scientifically proven, with recent studies indicating that not only ultraviolet (UV) radiation but also infrared (IR) radiation contributes to skin photoaging and increases the risk of carcinogenesis. Infrared radiation is also [...] Read more.
The harmful effects of solar radiation on the skin are known and scientifically proven, with recent studies indicating that not only ultraviolet (UV) radiation but also infrared (IR) radiation contributes to skin photoaging and increases the risk of carcinogenesis. Infrared radiation is also responsible for the degradation of protective carotenoids in the skin, the disruption of calcium homeostasis, and the activation of apoptosis pathways. The biological mechanisms underlying these effects include an increased level of reactive oxygen species and increased expression of metalloproteinases in the skin. The aim of this study was to evaluate the photoprotective properties of 10 cold-pressed plant oils in the infrared spectral range from 1000 nm to 2500 nm by assessing their impact on the directional–hemispherical reflectance (DHR) of human skin after their topical application. This study was conducted in vivo on the skin of 12 volunteers, with non-invasive DHR measurements taken before and directly after the application of the oil and 30 min later. Additionally, the correlation between the oil’s compounds (chlorophyll a, chlorophyll b, lycopene, and β-carotene) and antioxidant activity, expressed as the DPPH free radical scavenging capacity, was analyzed in relation to the differences in the skin’s DHR observed. An interesting result was obtained in the context of protecting the skin against IR radiation. A statistically significant increase in the skin’s reflectance after the penetration of the oil (p < 0.05) was observed in the 1700–2500 nm range for the chokeberry, fig, pomegranate, and perilla oils, suggesting their potential as photoprotective agents against IR. These findings indicate that chokeberry, fig, pomegranate, and perilla oils may serve as ingredients in cosmetic formulations designed for broad-spectrum skin photoprotection, complementing traditional UV filters with additional protection against infrared radiation. However, further research is needed to confirm these findings in a larger population. Full article
(This article belongs to the Section Cosmetic Dermatology)
Show Figures

Figure 1

14 pages, 1819 KiB  
Article
Ultraviolet B Exposure Does Not Influence the Expression of YAP mRNA in Human Epidermal Keratinocytes—Preliminary Study
by Igor Aleksander Bednarski, Izabela Dróżdż, Magdalena Ciążyńska, Karolina Wódz, Joanna Narbutt and Aleksandra Lesiak
Biomedicines 2025, 13(3), 596; https://doi.org/10.3390/biomedicines13030596 - 1 Mar 2025
Viewed by 732
Abstract
Background: The causal relationship between exposure to ultraviolet radiation and the development of skin cancers requires constant research for possible orchestrating mechanisms. In recent years, the Hippo pathway, along with its effector protein YAP, became implicated in cutaneous carcinogenesis; however, Hippo pathway regulation [...] Read more.
Background: The causal relationship between exposure to ultraviolet radiation and the development of skin cancers requires constant research for possible orchestrating mechanisms. In recent years, the Hippo pathway, along with its effector protein YAP, became implicated in cutaneous carcinogenesis; however, Hippo pathway regulation by ultraviolet radiation has not been described thoroughly. In order to address this issue, we focused on how different doses of ultraviolet B affect Hippo signaling pathway components and its upstream regulators, JNK1/2 and ABL1, in human keratinocytes. Additionally, we decided to determine how silencing of YAP influences Hippo pathway component expression. Methods: Primary epidermal keratinocytes were irradiated using UVB lamps with increasing doses of ultraviolet B radiation (including 311 nm UVB). Real-time PCR was used to determine the mRNA levels of each investigated gene. The experiment was then performed after YAP silencing using siRNA transfection. Additionally, we determined the mRNA expression of Hippo pathway components in an A431 cSCC cell line. Results: We observed that YAP mRNA expression in the A431 cell line was insignificant in comparison to control, while in the case of LATS1/2, a significant increase was noted. UVB irradiation did not change the levels of YAP mRNA expression in human epidermal keratinocytes. LATS1, LATS2, ABL1 and MAP4K4 mRNA expression was significantly upregulated after UVB irradiation in non-YAP-silenced keratinocytes in a dose-dependent manner, while after YAP silencing, only LATS2 and ABL1 showed significant mRNA upregulation. The 311 nm UVB irradiation resulted in significant, dose-dependent mRNA upregulation in non-YAP-silenced keratinocytes for LATS1, ABL1 and MAP4K4. After YAP silencing, a significant change in mRNA expression was present only in the case of ABL1. Conclusions: YAP mRNA expression does not significantly increase after exposure to UVB; however, it upregulates the expression of its proven (LATS1/2, JNK1/2) regulators, suggesting that in real-life settings, UV-induced dysregulation of the Hippo pathway may not be limited to YAP. Full article
Show Figures

Figure 1

13 pages, 5267 KiB  
Article
Identification of Thyroid Genes Whose Expression Is Altered by Neonatal Irradiation in Rats
by Nariaki Fujimoto, Mutsumi Matsuu-Matsuyama and Masahiro Nakashima
Int. J. Mol. Sci. 2025, 26(5), 1874; https://doi.org/10.3390/ijms26051874 - 21 Feb 2025
Viewed by 724
Abstract
Childhood radiation is a risk factor for thyroid cancer that became well known after the Chernobyl nuclear plant accident. Although these human cases have been extensively studied, the mechanisms underlying childhood susceptibility to radiation-induced thyroid cancer have yet to be explained. Our previous [...] Read more.
Childhood radiation is a risk factor for thyroid cancer that became well known after the Chernobyl nuclear plant accident. Although these human cases have been extensively studied, the mechanisms underlying childhood susceptibility to radiation-induced thyroid cancer have yet to be explained. Our previous study showed that neonatal X-irradiation resulted in long-term alterations in the mRNA expression of thyroid cancer-related marker genes, which may be a critical mechanism for understanding the higher radiation sensitivity in young patients. In this study, RNA sequencing (RNA-Seq)-based gene expression analysis was employed to identify thyroid genes whose mRNA expression was changed by neonatal irradiation. Male Wistar rats aged 1 week and 4 months were subjected to cervical X-irradiation at 4 Gy. After 8 weeks, total RNA was extracted from the thyroid and subjected to RNA-Seq analysis to identify differentially expressed genes following irradiation. We identified five upregulated genes (i.e., Adm2, Vnn1, Snph, Gria3, and Cpa4) and one downregulated gene (i.e., Crtac1) explicitly altered by neonatal radiation exposure. Western blotting confirmed the corresponding changes in CPA4 and CRTAC1 expression. The gene expressions identified were also altered in thyroid tumors induced by an iodine-deficient diet. These long-term changes in thyroid gene expression caused by neonatal irradiation may be involved in the increased risk of thyroid carcinogenesis. Full article
(This article belongs to the Section Molecular Toxicology)
Show Figures

Figure 1

12 pages, 561 KiB  
Review
Pharmacological Modulation of Mutant TP53 with Oncotargets Against Esophageal Cancer and Therapy Resistance
by Pei-I Lin, Yu-Cheng Lee, I-Hung Chen and Hsien-Hui Chung
Biomedicines 2025, 13(2), 450; https://doi.org/10.3390/biomedicines13020450 - 12 Feb 2025
Viewed by 1253
Abstract
The prevalence and deaths from esophageal cancer (EC) have recently increased. Although therapeutic strategies depend on the EC stage and recurrence, such as surgical intervention, chemotherapy, radiation therapy, chemoradiation therapy, targeted therapy, and immunotherapy, a more effective and novel treatment for EC is [...] Read more.
The prevalence and deaths from esophageal cancer (EC) have recently increased. Although therapeutic strategies depend on the EC stage and recurrence, such as surgical intervention, chemotherapy, radiation therapy, chemoradiation therapy, targeted therapy, and immunotherapy, a more effective and novel treatment for EC is still required. This review briefly describes and summarizes some insightful oncotargets involved in the metabolic modulation of EC, including (1) cancer stem cells (CSCs) for EC progression, poor prognosis, tumor recurrence, and therapy resistance; (2) retinoic acid receptors (RARs) for esophageal carcinogenesis and regeneration; (3) phosphofructokinase (PFK) for EC-reprogrammed glycolysis; (4) lactate dehydrogenase (LDH) as an EC peripheral blood biomarker; and (5) hypoxia-inducible factor-1 alpha (HIF-1α) for the tumor microenvironment under hypoxic conditions. Moreover, the aforementioned oncotargets can be modulated by mutant TP53 and have their own features in the carcinogenesis, differentiation, proliferation, and metastasis of EC. Thus, the clarification of pharmacological mechanisms regarding the interaction between mutant TP53 and the abovementioned oncotargets could provide precise and perspective opinions for minimizing prediction errors, reducing therapy resistance, and developing novel drugs against EC. Full article
Show Figures

Figure 1

26 pages, 2553 KiB  
Review
Illuminating the Connection: Cutaneous Vitamin D3 Synthesis and Its Role in Skin Cancer Prevention
by Nazlı Uçar and Michael F. Holick
Nutrients 2025, 17(3), 386; https://doi.org/10.3390/nu17030386 - 22 Jan 2025
Cited by 2 | Viewed by 7423
Abstract
Sunlight exposure plays an important role in human health, impacting processes such as mood, blood pressure regulation, and vitamin D3 production. Solar ultraviolet B radiation initiates vitamin D3 synthesis in the skin, which is subsequently metabolized into its biologically active form. [...] Read more.
Sunlight exposure plays an important role in human health, impacting processes such as mood, blood pressure regulation, and vitamin D3 production. Solar ultraviolet B radiation initiates vitamin D3 synthesis in the skin, which is subsequently metabolized into its biologically active form. UVB exposure plays a key role in enabling vitamin D3 synthesis, but it can also contribute to skin carcinogenesis, creating a complex interplay between its beneficial and harmful effects. Vitamin D deficiency, affecting over half the global population, is linked to a range of chronic diseases, including cancers, cardiovascular conditions, and autoimmune disorders. Simultaneously, excessive solar UVB exposure increases the risk of non-melanoma and melanoma skin cancers through mechanisms involving DNA damage and oxidative stress. This review examines the dual role of UVB radiation in health and disease, focusing on the mechanisms of cutaneous vitamin D3 synthesis, the epidemiology of skin cancer, and the protective roles of vitamin D3’s photoproducts and its active metabolite, 1,25-dihydroxyvitamin D3. Understanding these interconnections is critical for developing strategies that balance adequate sun-induced vitamin D3 production with skin cancer prevention. Full article
(This article belongs to the Section Micronutrients and Human Health)
Show Figures

Figure 1

13 pages, 2538 KiB  
Article
Integrative Analysis of Radiation-Induced Senescence-Associated Secretory Phenotype Factors in Kidney Cancer Progression
by Shubhankar Suman
Genes 2025, 16(1), 85; https://doi.org/10.3390/genes16010085 - 15 Jan 2025
Cited by 1 | Viewed by 1612
Abstract
Background: Ionizing radiation (IR) is a well-known inducer of cellular senescence and the senescence-associated secretory phenotype (SASP). SASP factors play dual roles in cancer, either promoting or inhibiting its development. This study investigates IR-induced SASP factors specifically secreted by renal cortical epithelial (RCE) [...] Read more.
Background: Ionizing radiation (IR) is a well-known inducer of cellular senescence and the senescence-associated secretory phenotype (SASP). SASP factors play dual roles in cancer, either promoting or inhibiting its development. This study investigates IR-induced SASP factors specifically secreted by renal cortical epithelial (RCE) cells and their role in promoting renal cell carcinoma (RCC) progression. Methods: Proteomic data from the SASP Atlas were analyzed to identify IR-induced factors unique to RCE cells, with subsequent evaluations performed at both the gene and protein levels. Thirty-seven proteins were identified as exclusively upregulated and secreted by senescent RCE cells. Gene expression analysis of these RCE-specific SASP factors was conducted using the Gene Expression database of Normal and Tumor tissues (GENT2) and The Cancer Genome Atlas (TCGA). To assess their prognostic relevance in RCC, the corresponding proteins were further analyzed using the Human Protein Atlas (HPA), emphasizing the relationship between SASP factor expression and RCC progression. Results: ALDH18A1 and ASPH emerged as key RCE-specific SASP factors with significant upregulation at both the gene and protein levels (Log2 ratio > 1.15, p < 0.05). These proteins are implicated in pro-cancer activities and are strongly associated with poor prognostic outcomes in RCC. Their critical roles in RCC progression underscore their potential as promising therapeutic targets for the prevention and treatment of the disease. Conclusions: This study provides novel insights into the role of IR-induced SASP in renal carcinogenesis, marking the first identification of ALDH18A1 and ASPH as specific secreted proteins associated with tumor progression in RCC. This study suggests that ALDH18A1 and ASPH hold promise as early biomarkers for RCC and as therapeutic targets for disease prevention and treatment. Full article
Show Figures

Figure 1

14 pages, 865 KiB  
Review
Radiotherapy for Rectal Cancer and Radiation-Induced Malignancies from Epidemiological and Dosimetric Data
by Stefanos Kachris and Michalis Mazonakis
Appl. Sci. 2024, 14(24), 12063; https://doi.org/10.3390/app142412063 - 23 Dec 2024
Viewed by 1208
Abstract
Preoperative or postoperative radiation therapy is broadly employed in patients with rectal carcinoma. Radiotherapy directs high-energy beams of ionizing radiation toward the tumor area to destroy cancer cells. High radiation doses are needed for cell killing. The radiation exposure of the healthy tissues/organs [...] Read more.
Preoperative or postoperative radiation therapy is broadly employed in patients with rectal carcinoma. Radiotherapy directs high-energy beams of ionizing radiation toward the tumor area to destroy cancer cells. High radiation doses are needed for cell killing. The radiation exposure of the healthy tissues/organs may lead to carcinogenesis. This study describes the evolving role of radiotherapy in rectal cancer management. The present report also reviews epidemiological and dosimetric studies related to the radiation-induced second malignancies from pelvic radiotherapy. Some epidemiological studies have concluded that the second-cancer risk in patients subjected to radiation therapy does not increase compared to unexposed rectal cancer patients. Other researchers found an elevated or a marginally increased probability for second-cancer induction. Dosimetric studies reported cancer risk estimates for critical organs or tissues in the near and far periphery of the treatment volume. Useful information about the effect of the treatment parameters such as the irradiation technique, photon beam energy, and fractionation schedule on the organ-specific second-cancer risk was derived from the dose data analysis. The knowledge of these effects is needed for the selection of the optimal treatment parameters enabling a reduction in the resultant risk of carcinogenesis. Full article
Show Figures

Figure 1

21 pages, 1422 KiB  
Review
Population Studies and Molecular Mechanisms of Human Radioadaptive Capabilities: Is It Time to Rethink Radiation Safety Standards?
by Dmitry Vitalievich Sosin, Denis S. Baranovskii, Denis Nikolaevich Nechaev, Mariya Aleksandrovna Sosina, Alexander Vladimirovich Shaposhnikov, Georgy Aleksandrovich Trusov, Anastasia Germanovna Titova, Boris Fedorovich Krasnikov, Alexey Nikolaevich Lomov, Valentin Vladimirovich Makarov, Vladimir Sergeevich Yudin, Anton Arturovich Keskinov, Sergey Mihailovich Yudin and Ilya Dmitrievich Klabukov
Int. J. Mol. Sci. 2024, 25(24), 13543; https://doi.org/10.3390/ijms252413543 - 18 Dec 2024
Viewed by 1579
Abstract
The evolution of man on Earth took place under conditions of constant exposure to background ionizing radiation (IR). From this point of view, it would be reasonable to hypothesize the existence of adaptive mechanisms that enable the human organism to safely interact with [...] Read more.
The evolution of man on Earth took place under conditions of constant exposure to background ionizing radiation (IR). From this point of view, it would be reasonable to hypothesize the existence of adaptive mechanisms that enable the human organism to safely interact with IR at levels approximating long-term natural background levels. In some situations, the successful operation of molecular mechanisms of protection against IR is observed at values significantly exceeding the natural background level, for example, in cancer cells. In 15–25% of cancer patients, cancer cells develop a phenotype that is resistant to high doses of IR. While further investigations are warranted, the current evidence suggests a strong probability of observing positive health effects, including an increased lifespan, a reduced cancer risk, and a decreased incidence of congenital pathologies, precisely at low doses of ionizing radiation. This review offers arguments primarily based on a phenomenological approach and critically reconsidering existing methodologies for assessing the biological risks of IR to human health. Currently, in the most economically developed countries, there are radiation safety rules that interpret low-dose radiation as a clearly negative environmental factor. Nowadays, this approach may pose significant challenges to the advancement of radiomedicine and introduce complexities in the regulation of IR sources. The review also examines molecular mechanisms that may play a key role in the formation of the positive effects of low-dose IR on human radioadaptive capabilities. Full article
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Show Figures

Figure 1

Back to TopTop