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Cancers
Special Issues
Radiation Exposure, Inflammation and Cancers
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Radiation Exposure, Inflammation and Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 10 January 2025 | Viewed by 1524

Special Issue Editor

Dr. Santosh Kumar

E-Mail Website
Guest Editor
Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA
Interests: radiation; aging; cancer; stem cells; immunology

Special Issue Information

Dear Colleagues,

Radiation therapy stands as a crucial pillar in the realm of cancer treatment, employing targeted approaches to obliterate cancerous cells. The efficacy of this treatment is undeniable; nevertheless, it comes with challenges. Exposure to ionizing radiation, encompassing gamma and X-rays, and the utilization of sophisticated particle beams in therapy, while instrumental in battling cancer, can concurrently result in damage to normal tissues and elevate the risk of developing subsequent cancers. As the scope extends beyond the confines of terrestrial cancer treatment, our attention pivots toward the cosmos, unraveling the potential implications of radiation exposure on the health of astronauts during future space missions. Prolonged exposure to cosmic radiation presents a multifaceted challenge to the health and well-being of astronauts, necessitating a comprehensive exploration of preventative strategies and effective mitigation techniques to safeguard their physical integrity.

This Special Issue aims to unravel the complexities surrounding the effectiveness and potential adverse effects of various radiation types in biological systems. By examining the mechanisms and consequences of radiation exposure, the issue seeks to enhance our collective knowledge, inform strategies that advance cancer treatment and address the unique challenges posed by cosmic radiation in the extraterrestrial realm.

You are invited to contribute a research or review article to this Special Issue. As an expert, your insights will undoubtedly enrich the discourse, providing a more comprehensive understanding of how radiation exposure affects cancer growth, and your contribution will have a crucial role in advancing our knowledge and developing innovative solutions.

Dr. Santosh Kumar
Guest Editor

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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • radiation
  • DNA damage response
  • inflammation
  • oxidative stress
  • senescence and cancer

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Published Papers (2 papers)

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Research

17 pages, 4481 KiB  
Article
Simulated Galactic Cosmic Radiation Exposure-Induced Mammary Tumorigenesis in ApcMin/+ Mice Coincides with Activation of ERα-ERRα-SPP1 Signaling Axis
by Kamendra Kumar, Jerry Angdisen, Jinwenrui Ma, Kamal Datta, Albert J. Fornace, Jr. and Shubhankar Suman
Cancers 2024, 16(23), 3954; https://doi.org/10.3390/cancers16233954 - 26 Nov 2024
Viewed by 145
Abstract
Background: Exposure to galactic cosmic radiation (GCR) is a breast cancer risk factor for female astronauts on deep-space missions. However, the specific signaling mechanisms driving GCR-induced breast cancer have not yet been determined. Methods: This study aimed to investigate the role of the [...] Read more.
Background: Exposure to galactic cosmic radiation (GCR) is a breast cancer risk factor for female astronauts on deep-space missions. However, the specific signaling mechanisms driving GCR-induced breast cancer have not yet been determined. Methods: This study aimed to investigate the role of the estrogen-induced ERα-ERRα-SPP1 signaling axis in relation to mammary tumorigenesis in female ApcMin/+ mice exposed to simulated GCR (GCRsim) at 100–110 days post-exposure. Results: In GCRsim-exposed mice, we observed marked elevations in serum estradiol, increased ductal overgrowth, ERα activation, and upregulation of ERα target genes with pro-tumorigenic functions in mammary tissues that was coupled with a higher mammary tumorigenesis, relative to control. Additionally, the ERα target gene Esrra, which encodes ERRα, was also upregulated along with its oncogenic target gene Spp1, indicating the activation of the ERα-ERRα-SPP1 axis in mouse mammary tissues after GCRsim exposure. Using a human tissue microarray and human breast cancer gene expression analysis, we also highlighted the conserved nature of the ERα-ERRα-SPP1 signaling in human breast cancer development. Conclusions: We identified the ERα-ERRα-SPP1 signaling axis as a potential key mediator in GCR-induced breast cancer with conserved activation in human breast cancer. These findings suggest that targeting this pathway could serve as a potential target for therapeutic intervention to safeguard female astronauts during and after a prolonged outer space mission. Full article
(This article belongs to the Special Issue Radiation Exposure, Inflammation and Cancers)
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17 pages, 6815 KiB  
Article
Effects of High-Linear-Energy-Transfer Heavy Ion Radiation on Intestinal Stem Cells: Implications for Gut Health and Tumorigenesis
by Santosh Kumar, Shubhankar Suman, Jerry Angdisen, Bo-Hyun Moon, Bhaskar V. S. Kallakury, Kamal Datta and Albert J. Fornace, Jr.
Cancers 2024, 16(19), 3392; https://doi.org/10.3390/cancers16193392 - 4 Oct 2024
Viewed by 965
Abstract
Heavy ion radiation, prevalent in outer space and relevant for radiotherapy, is densely ionizing and poses a risk to intestinal stem cells (ISCs), which are vital for maintaining intestinal homeostasis. Earlier studies have shown that heavy-ion radiation can cause chronic oxidative stress, persistent [...] Read more.
Heavy ion radiation, prevalent in outer space and relevant for radiotherapy, is densely ionizing and poses a risk to intestinal stem cells (ISCs), which are vital for maintaining intestinal homeostasis. Earlier studies have shown that heavy-ion radiation can cause chronic oxidative stress, persistent DNA damage, cellular senescence, and the development of a senescence-associated secretory phenotype (SASP) in mouse intestinal mucosa. However, the specific impact on different cell types, particularly Lgr5+ intestinal stem cells (ISCs), which are crucial for maintaining cellular homeostasis, GI function, and tumor initiation under genomic stress, remains understudied. Using an ISCs-relevant mouse model (Lgr5+ mice) and its GI tumor surrogate (Lgr5+Apc1638N/+ mice), we investigated ISCs-specific molecular alterations after high-LET radiation exposure. Tissue sections were assessed for senescence and SASP signaling at 2, 5 and 12 months post-exposure. Lgr5+ cells exhibited significantly greater oxidative stress following 28Si irradiation compared to γ-ray or controls. Both Lgr5+ cells and Paneth cells showed signs of senescence and developed a senescence-associated secretory phenotype (SASP) after 28Si exposure. Moreover, gene expression of pro-inflammatory and pro-growth SASP factors remained persistently elevated for up to a year post-28Si irradiation. Additionally, p38 MAPK and NF-κB signaling pathways, which are critical for stress responses and inflammation, were also upregulated after 28Si radiation. Transcripts involved in nutrient absorption and barrier function were also altered following irradiation. In Lgr5+Apc1638N/+ mice, tumor incidence was significantly higher in those exposed to 28Si radiation compared to the spontaneous tumorigenesis observed in control mice. Our results indicate that high-LET 28Si exposure induces persistent DNA damage, oxidative stress, senescence, and SASP in Lgr5+ ISCs, potentially predisposing astronauts to altered nutrient absorption, barrier function, and GI carcinogenesis during and after a long-duration outer space mission. Full article
(This article belongs to the Special Issue Radiation Exposure, Inflammation and Cancers)
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