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Biomedicines
Special Issues
Radiation-Induced Carcinogenesis and Radiotherapy
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Radiation-Induced Carcinogenesis and Radiotherapy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 3664

Special Issue Editors

Dr. Wentao Hu

E-Mail Website
Guest Editor
School of Radiation Medicine and Protection, Soochow University, Suzhou, China
Interests: radiation-induced carcinogenesis; radiobiology in particle radiotherapy; epigenetic modifications of radiation response; space radiobiology
Dr. Cong Liu

E-Mail Website
Guest Editor
Department of Radiation Medicine, Naval Medical University, Shanghai, China
Interests: radiation science and biology; novel radio-protective targets and drugs; radiation-induced carcinogenesis; radiation-induced thymic lymphoma; secondary malignancies after radiotherapy

Special Issue Information

Dear Colleagues,

As one of the major cancer treatment modalities, radiotherapy is currently used to treat more than half of patients diagnosed with cancer alone or in combination with other modalities. Many new technologies have been developed over the past few years with the aim of killing tumor cells effectively with ionizing radiation while minimizing normal tissue injury, including 3D-CRT, IMRT, SBRT, as well as particle radiotherapy, etc., which have improved both the efficacy and safety of radiotherapy. However, acute and chronic normal tissue toxicities, even secondary carcinogenesis, seriously impair the quality of patients’ life due to inevitable radiation dose deposition in normal tissues. In addition to patients experiencing radiotherapy, people inevitably exposed to radiation such as uranium miners, operators in nuclear power plants, as well as astronauts are also at risk of radiation-induced injuries or carcinogenesis. Based on several epidemiological studies, a strong positive correlation has been observed between exposure to ionizing radiation and carcinogenesis, but the mechanism is poorly understood. Determining how to kill tumor cells and protect normal tissues more efficiently is key in the fields of radiotherapy and radioprotection. Answers to these questions lie in our better understanding of the related radiobiological processes, such as trafficking and signaling pathways in cellular responses to radiation, intercellular interactions, as well as cell fate determination upon radiation. We sincerely invite investigators to submit their original research and review articles regarding the above-mentioned topics to Biomedicines.

Dr. Wentao Hu
Dr. Cong Liu
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • signaling pathways in radiation response
  • combination of radiotherapy and immune treatment
  • carcinogenesis in astronauts and radiation workers
  • secondary carcinogenesis after radiotherapy
  • epigenetic modifications of radiation response
  • radiation-induced non-targeted effect and adaptive response
  • radioprotection and radiation preparedness
  • radiation-induced thymic lymphoma
  • novel radio-protective targets and drugs
  • immunomodulation of radiobiology

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Published Papers (2 papers)

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Research

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15 pages, 7638 KiB  
Article
6-n-Butoxy-10-nitro-12,13-dioxa-11-azatricyclo[7.3.1.02,7]trideca-2,4,6,10-tetraene Improves the X-ray Sensitivity on Inhibiting Proliferation and Promoting Oxidative Stress and Apoptosis of Oral Cancer Cells
by Kun-Han Yang, Ching-Yu Yen, Sheng-Chieh Wang, Fang-Rong Chang, Meng-Yang Chang, Chieh-Kai Chan, Jiiang-Huei Jeng, Jen-Yang Tang and Hsueh-Wei Chang
Biomedicines 2024, 12(2), 458; https://doi.org/10.3390/biomedicines12020458 - 19 Feb 2024
Viewed by 1365
Abstract
This in vitro study examines the anti-oral cancer effects and mechanisms of a combined X-ray/SK2 treatment, i.e., X-ray and 6-n-butoxy-10-nitro-12,13-dioxa-11-azatricyclo[7.3.1.02,7]trideca-2,4,6,10-tetraene (SK2). ATP cell viability and flow cytometry-based cell cycle, apoptosis, oxidative stress, and DNA damage assessments were conducted. The [...] Read more.
This in vitro study examines the anti-oral cancer effects and mechanisms of a combined X-ray/SK2 treatment, i.e., X-ray and 6-n-butoxy-10-nitro-12,13-dioxa-11-azatricyclo[7.3.1.02,7]trideca-2,4,6,10-tetraene (SK2). ATP cell viability and flow cytometry-based cell cycle, apoptosis, oxidative stress, and DNA damage assessments were conducted. The X-ray/SK2 treatment exhibited lower viability in oral cancer (Ca9-22 and CAL 27) cells than in normal (Smulow–Glickman, S-G) cells, i.e., 32.0%, 46.1% vs. 59.0%, which showed more antiproliferative changes than with X-ray or SK2 treatment. Oral cancer cells under X-ray/SK2 treatment showed slight subG1 and G2/M increments and induced high annexin V-monitored apoptosis compared to X-ray or SK2 treatment. The X-ray/SK2 treatment showed higher caspase 3 and 8 levels for oral cancer cells than other treatments. X-ray/SK2 showed a higher caspase 9 level in CAL 27 cells than other treatments, while Ca9-22 cells showed similar levels under X-ray and/or SK2. The X-ray/SK2 treatment showed higher reactive oxygen species (ROS) generation and mitochondrial membrane potential (MMP) depletion than other treatments. Meanwhile, the mitochondrial superoxide (MitoSOX) and glutathione levels in X-ray/SK2 treatment did not exhibit the highest rank compared to others. Moreover, oral cancer cells had higher γH2AX and/or 8-hydroxy-2-deoxyguanosine levels from X-ray/SK2 treatment than others. All these measurements for X-ray/SK2 in oral cancer cells were higher than in normal cells and attenuated by N-acetylcysteine. In conclusion, X-ray/SK2 treatment showed ROS-dependent enhanced antiproliferative, apoptotic, and DNA damage effects in oral cancer cells with a lower cytotoxic influence on normal cells. Full article
(This article belongs to the Special Issue Radiation-Induced Carcinogenesis and Radiotherapy)
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Review

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24 pages, 1455 KiB  
Review
The Mechanism of Ubiquitination or Deubiquitination Modifications in Regulating Solid Tumor Radiosensitivity
by Mengyun Zhang, Yingjie Shao and Wendong Gu
Biomedicines 2023, 11(12), 3240; https://doi.org/10.3390/biomedicines11123240 - 7 Dec 2023
Cited by 3 | Viewed by 1388
Abstract
Radiotherapy, a treatment method employing radiation to eradicate tumor cells and subsequently reduce or eliminate tumor masses, is widely applied in the management of numerous patients with tumors. However, its therapeutic effectiveness is somewhat constrained by various drug-resistant factors. Recent studies have highlighted [...] Read more.
Radiotherapy, a treatment method employing radiation to eradicate tumor cells and subsequently reduce or eliminate tumor masses, is widely applied in the management of numerous patients with tumors. However, its therapeutic effectiveness is somewhat constrained by various drug-resistant factors. Recent studies have highlighted the ubiquitination/deubiquitination system, a reversible molecular modification pathway, for its dual role in influencing tumor behaviors. It can either promote or inhibit tumor progression, impacting tumor proliferation, migration, invasion, and associated therapeutic resistance. Consequently, delving into the potential mechanisms through which ubiquitination and deubiquitination systems modulate the response to radiotherapy in malignant tumors holds paramount significance in augmenting its efficacy. In this paper, we comprehensively examine the strides made in research and the pertinent mechanisms of ubiquitination and deubiquitination systems in governing radiotherapy resistance in tumors. This underscores the potential for developing diverse radiosensitizers targeting distinct mechanisms, with the aim of enhancing the effectiveness of radiotherapy. Full article
(This article belongs to the Special Issue Radiation-Induced Carcinogenesis and Radiotherapy)
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