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Molecular Insights into Radiation Oncology

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 3176

Special Issue Editor


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Guest Editor
Department of Radiation Oncology, University of California, Irvine, CA 92868, USA
Interests: radiation; head and neck cancers; HPV; re-irradiation techniques; oncology

Special Issue Information

Dear Colleagues,

Radiation therapy or radiotherapy is a treatment using ionizing radiation that is generally provided as part of cancer therapy to either kill or control the growth of malignant cells. Radiation therapy works by damaging the DNA of cancer cells and can cause them to undergo mitotic catastrophe. However, radiation affects normal cells as well as cancerous cells, causing side effects in the treatment area.

In this Special Issue, we aim to comprehensively dissect the molecular mechanisms by which radiation therapy influences the initiation and progression of tumors. In addition, we would like to advance the development of cancer treatments that target the mechanisms of radiation therapy and reduce the side effects of radiation. We invite submissions of original research articles and comprehensive reviews that can help to advance our molecular understanding of radiation oncology. Subtopics may include, but are not limited to, the following:

  • Molecular mechanisms in radiation oncology;
  • Developing new drugs that target the mechanisms by which radiation affects tumor initiation and progression;
  • Reducing side effects from radiation and the mechanisms behind them;

• Exploring personalized treatment options related to radiation oncology.

Prof. Dr. Allen M. Chen
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 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

  • molecular and cellular radiobiology
  • radiation physics
  • DNA damage and repair
  • radiation response
  • cancers

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Published Papers (3 papers)

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Research

11 pages, 756 KiB  
Article
Investigating LATS1 and NF-κB as Predictors of Radiotherapy Response in Cervical Cancer
by Andi Darma Putra, Andrijono, Hariyono Winarto, Ani Retno Prijanti, Lisnawati, Trevino Aristarkus Pakasi, Supriadi Gandamihardja, Jourdan Wirasugianto, Amelia and Lasmini Syariatin
Curr. Issues Mol. Biol. 2025, 47(5), 365; https://doi.org/10.3390/cimb47050365 - 16 May 2025
Abstract
Cervical cancer is the fourth most prevalent cancer among women globally. Protein concentrations of Large Tumor Suppressor Kinase-1 (LATS1) and Nuclear Factor Kappa-B (NF-κB) have been identified as prospective biomarkers of radioresistance in cervical cancer. This preliminary study aimed to investigate the effectiveness [...] Read more.
Cervical cancer is the fourth most prevalent cancer among women globally. Protein concentrations of Large Tumor Suppressor Kinase-1 (LATS1) and Nuclear Factor Kappa-B (NF-κB) have been identified as prospective biomarkers of radioresistance in cervical cancer. This preliminary study aimed to investigate the effectiveness of LATS1 and NF-κB levels as a biomarker for radioresistance and evaluate their response to radiation in cervical cancer patients. A comprehensive cross-sectional study was conducted involving 114 subjects diagnosed with advanced stages cervical cancer (stage IIIB and IVA) who underwent definitive radiotherapy. The concentrations of LATS1 and NF-κB were measured using ELISA from biopsy samples taken prior to the initiation of radiotherapy. This study’s finding included 114 subjects, with a median age of 53 years. A total of 85 (74.5%) subjects had stage IIIB, while 29 (25.4%) subjects had stage IVA. The cut-offs for LATS1 and NF-κB were 0.02765 ng/mg and 192.42 pg/mg, respectively. Subjects with a higher expression of LATS1 were found to be unresponsive to radiation therapy (p ≤ 0.001; AUC = 32.7%), and subjects with a lower expression of NF-κB were found to be unresponsive to radiation therapy (p = 0.009; AUC = 61%). This study suggests that elevated LATS1 expression may inversely predict radioresistance, while NF-κB expression shows a weak correlation with resistance to radiation therapy. Full article
(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)
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21 pages, 3935 KiB  
Article
The Dose Rate of Corpuscular Ionizing Radiation Strongly Influences the Severity of DNA Damage, Cell Cycle Progression and Cellular Senescence in Human Epidermoid Carcinoma Cells
by Sergey S. Soroko, Dmitry V. Skamnitskiy, Ekaterina N. Gorshkova, Olga M. Kutova, Ismail R. Seriev, Anna V. Maslennikova, Evgeniy L. Guryev, Sergey V. Gudkov, Vladimir A. Vodeneev, Irina V. Balalaeva and Natalia Yu Shilyagina
Curr. Issues Mol. Biol. 2024, 46(12), 13860-13880; https://doi.org/10.3390/cimb46120828 - 6 Dec 2024
Viewed by 1689
Abstract
Modern radiotherapy utilizes a broad range of sources of ionizing radiation, both low-dose-rate (LDR) and high-dose-rate (HDR). However, the mechanisms underlying specific dose-rate effects remain unclear, especially for corpuscular radiation. To address this issue, we have irradiated human epidermoid carcinoma A431 cells under [...] Read more.
Modern radiotherapy utilizes a broad range of sources of ionizing radiation, both low-dose-rate (LDR) and high-dose-rate (HDR). However, the mechanisms underlying specific dose-rate effects remain unclear, especially for corpuscular radiation. To address this issue, we have irradiated human epidermoid carcinoma A431 cells under LDR and HDR regimes. Reducing the dose rate has lower lethality at equal doses with HDR irradiation. The half-lethal dose after HDR irradiation was three times less than after LDR irradiation. The study of mechanisms showed that under HDR irradiation, the radiation-induced halt of mitosis with the accompanying emergence of giant cells was recorded. No such changes were recorded after LDR irradiation. The level of DNA damage is significantly greater after HDR irradiation, which may be the main reason for the different mechanisms of action of HDR and LDR irradiations. Comparing the mechanisms of cell response to LDR and HDR irradiations may shed light on the mechanisms of tumor cell response to ionizing radiation and answer the question of whether different dose rates within the same dose range can cause different clinical effects. Full article
(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)
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16 pages, 1940 KiB  
Article
Preliminary Study on Lutetium-177 and Gold Nanoparticles: Apoptosis and Radiation Enhancement in Hepatic Cancer Cell Line
by Maria Anthi Kouri, Anastasios Georgopoulos, George E. Manios, Eirini Maratou, Aris Spathis, Sofia Chatziioannou, Kalliopi Platoni and Efstathios P. Efstathopoulos
Curr. Issues Mol. Biol. 2024, 46(11), 12244-12259; https://doi.org/10.3390/cimb46110727 - 30 Oct 2024
Viewed by 1096
Abstract
This study investigates a novel approach toward enhancing the efficacy of Lutetium-177 (Lu-177) radiopharmaceutical therapy by combining it with gold nanoparticles (AuNPs) in the HepG2 hepatic cancer cell line. Lu-177, known for its effective β radiation, also emits gamma rays at energies (113 [...] Read more.
This study investigates a novel approach toward enhancing the efficacy of Lutetium-177 (Lu-177) radiopharmaceutical therapy by combining it with gold nanoparticles (AuNPs) in the HepG2 hepatic cancer cell line. Lu-177, known for its effective β radiation, also emits gamma rays at energies (113 keV and 208 keV) near the photoelectric absorption range, suggesting potential for targeted and localized radiation enhancement when used in conjunction with AuNPs. Thus, HepG2 cells were treated at two different activity levels (74 MBq and 148 MBq), with Lu-177 alone, with a combination of Lu-177 and AuNPs in two sizes (10 nm and 50 nm), while some received no treatment. Treatment efficacy was assessed by quantifying the radiation enhancement ratio (RER) and the apoptosis levels. The results reveal that combining Lu-177 with AuNPs significantly increases cell death and apoptosis compared to Lu-177 alone, with 10 nm AuNPs demonstrating superior effectiveness. Additionally, varying Lu-177 activity levels influenced the treatment outcomes, with higher activity levels further augmenting the therapeutic impact of combined therapy. These findings underscore the potential of utilizing Lu-177’s beta, but also gamma, emissions, traditionally considered non-therapeutic, for localized radiation enhancement when combined with AuNPs. This novel strategy leverages Lu-177 as an internal irradiator to exploit gamma radiation for a targeted therapeutic advantage without requiring nanoparticle functionalization. The study provides a promising approach to improving radionuclide therapy and sets the stage for future research aimed at optimizing cancer treatments through the combined use of Lu-177 and AuNPs. Full article
(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)
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