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Radiobiology and Radiotherapy in Tumour
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Radiobiology and Radiotherapy in Tumour

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (10 June 2024) | Viewed by 7019

Special Issue Editors

Prof. Dr. Loredana Marcu

E-Mail Website
Guest Editor
1. Faculty of Informatics & Science, University of Oradea, 410087 Oradea, Romania
2. UniSA Allied Health and Human Performance, University of South Australia, Adelaide 5000, Australia
Interests: modelling of tumour growth and development; risk of second cancer; personalised radiotherapy; treatment resistance; radiobiology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Eva Bezak

E-Mail Website
Guest Editor
1. UniSA Allied Health and Human Performance, University of South Australia, Adelaide, Australia
2. School of Physical Sciences, University of Adelaide, Adelaide, Australia
Interests: cancer; pet imaging

Special Issue Information

Dear Colleagues,

In 2023, the research community is still trying to elucidate the complex mechanisms behind one of the main causes of treatment failure in radiation oncology—tumour repopulation during treatment. There have been 35 years since the landmark publication by R. Withers et al. on The hazard of accelerated tumor clonogen repopulation during radiotherapy (Acta Oncol. 27:131), a paper that discusses accelerated tumour regrowth in head and neck carcinomas and presents quantitative parameters for the clonogen-doubling rate and the onset of tumour repopulation during radiotherapy.

Today, there is evidence towards the existence of cancer stem cells that are responsible for tumour repopulation, dissemination, and distant metastases in most solid cancers. Formerly known as clonogenic cells, cancer stem cells are closely investigated by the research community to understand their role in various biological processes that lead to tumour aggressiveness and, eventually, treatment failure. Repopulation during treatment is not limited to radiotherapy, as there is clinical proof for activating repopulation mechanisms through other conventional treatment techniques as well.

Whether in vivo, in vitro or in silico, all research aspects that explain diverse cellular properties responsible for tumour repopulation during treatment are welcome additions to current knowledge and to this Special Issue. We also encourage research on the cellular and molecular mechanisms involved in the response of tumour and normal tissues to ionizing radiation, as well as new insights into the molecular biological effects of radiation on tumour metabolism, cancer stem cells, the tumour microenvironment and novel environments.

Prof. Dr. Loredana Marcu
Prof. Dr. Eva Bezak
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • accelerated repopulation
  • radiotherapy
  • chemotherapy
  • cancer stem cells
  • tumor microenvironment
  • cancer therapy
  • tumor metabolism
  • molecular mechanisms

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Published Papers (3 papers)

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Research

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14 pages, 712 KiB  
Article
Replacing 2 Gy Per Fraction Equivalent Dose with Fractionation-Specific Biological Equivalent Dose for Normal Tissues
by Wei Luo and William St Clair
Int. J. Mol. Sci. 2024, 25(23), 12891; https://doi.org/10.3390/ijms252312891 - 30 Nov 2024
Cited by 2 | Viewed by 1162
Abstract
The 2 Gy per fraction equivalent dose (EQD2) is an important quantity used in determining equivalent prescription doses for different fractionation regimens and evaluating different fractionation regimens, but it does not match its definition when it is used for normal tissues. [...] Read more.
The 2 Gy per fraction equivalent dose (EQD2) is an important quantity used in determining equivalent prescription doses for different fractionation regimens and evaluating different fractionation regimens, but it does not match its definition when it is used for normal tissues. We propose to use the fractionation-specific biological equivalent dose to determine normal tissue dose constraints for different fractionation regimens. The concept of the biological equivalent dose is defined based on the linear-quadratic equation. The EQD2 is derived based on the biological effective dose (BED), mimicking the prescription dose of a standard fractionation regimen with a fractional dose of 2 Gy and a fixed number of fractions. The FEQD(n) is also defined based on the BED as a function of the number of fractions, n, which is determined by the dose prescription. The FEQD(n) mimics any fractionation regimens with any fractional doses and numbers of fractionations. A given dose constraint can have different BED values and EQD2 values for different fractionation regimens. The number of fractions for a given 2 Gy per fraction regimen derived from the EQD2 for the target dose is different from that for the normal tissues. The value of the EQD2 derived for the target represents the total dose for the target for the 2 Gy fractional dose regimen, but the EQD2 value derived for the normal tissues does not represent the total dose for the normal tissue for the same fractionation regimen. The fractionation-specific biological equivalent dose (FEQD(n)) for both target and normal tissues has the same number of fractions for any fractionation regimen, and represents the total dose for either the target or the normal tissue. Based on the clinical outcomes, the FEQD(n) curves for the brainstem, spinal cord, rectum, and lung were derived and can be directly used as dose constraints for various fractionation regimens in clinical practice. The EQD2 does not match its definition and is not realistic when describing the biological equivalent dose for normal tissues. It is also not practical when used in determining tolerance doses or dose constraints. Instead, the FEQD(n) can be used to determine or convert the normal tissue dose constraints for any fractionation regimens in a realistic and practical manner. Using the FEQD(n), the dose constraints as a function of the number of fractions for the brainstem, spinal cord, rectum, and lung, which correspond to the given toxicity rates, were derived and can be directly used in clinical practice. Full article
(This article belongs to the Special Issue Radiobiology and Radiotherapy in Tumour)
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Review

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16 pages, 943 KiB  
Review
Opportunities in Cancer Therapies: Deciphering the Role of Cancer Stem Cells in Tumour Repopulation
by Loredana G. Marcu, Mikaela Dell’Oro and Eva Bezak
Int. J. Mol. Sci. 2023, 24(24), 17258; https://doi.org/10.3390/ijms242417258 - 8 Dec 2023
Cited by 4 | Viewed by 1676
Abstract
Tumour repopulation during treatment is a well acknowledged yet still challenging aspect of cancer management. The latest research results show clear evidence towards the existence of cancer stem cells (CSCs) that are responsible for tumour repopulation, dissemination, and distant metastases in most solid [...] Read more.
Tumour repopulation during treatment is a well acknowledged yet still challenging aspect of cancer management. The latest research results show clear evidence towards the existence of cancer stem cells (CSCs) that are responsible for tumour repopulation, dissemination, and distant metastases in most solid cancers. Cancer stem cell quiescence and the loss of asymmetrical division are two powerful mechanisms behind repopulation. Another important aspect in the context of cancer stem cells is cell plasticity, which was shown to be triggered during fractionated radiotherapy, leading to cell dedifferentiation and thus reactivation of stem-like properties. Repopulation during treatment is not limited to radiotherapy, as there is clinical proof for repopulation mechanisms to be activated through other conventional treatment techniques, such as chemotherapy. The dynamic nature of stem-like cancer cells often elicits resistance to treatment by escaping drug-induced cell death. The aims of this scoping review are (1) to describe the main mechanisms used by cancer stem cells to initiate tumour repopulation during therapy; (2) to present clinical evidence for tumour repopulation during radio- and chemotherapy; (3) to illustrate current trends in the identification of CSCs using specific imaging techniques; and (4) to highlight novel technologies that show potential in the eradication of CSCs. Full article
(This article belongs to the Special Issue Radiobiology and Radiotherapy in Tumour)
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17 pages, 1525 KiB  
Review
Parp Inhibitors and Radiotherapy: A New Combination for Prostate Cancer (Systematic Review)
by Inés Rivero Belenchón, Carmen Belen Congregado Ruiz, Carmen Saez, Ignacio Osman García and Rafael Antonio Medina López
Int. J. Mol. Sci. 2023, 24(16), 12978; https://doi.org/10.3390/ijms241612978 - 19 Aug 2023
Cited by 11 | Viewed by 3155
Abstract
PARPi, in combination with ionizing radiation, has demonstrated the ability to enhance cellular radiosensitivity in different tumors. The rationale is that the exposure to radiation leads to both physical and biochemical damage to DNA, prompting cells to initiate three primary mechanisms for DNA [...] Read more.
PARPi, in combination with ionizing radiation, has demonstrated the ability to enhance cellular radiosensitivity in different tumors. The rationale is that the exposure to radiation leads to both physical and biochemical damage to DNA, prompting cells to initiate three primary mechanisms for DNA repair. Two double-stranded DNA breaks (DSB) repair pathways: (1) non-homologous end-joining (NHEJ) and (2) homologous recombination (HR); and (3) a single-stranded DNA break (SSB) repair pathway (base excision repair, BER). In this scenario, PARPi can serve as radiosensitizers by leveraging the BER pathway. This mechanism heightens the likelihood of replication forks collapsing, consequently leading to the formation of persistent DSBs. Together, the combination of PARPi and radiotherapy is a potent oncological strategy. This combination has proven its efficacy in different tumors. However, in prostate cancer, there are only preclinical studies to support it and, recently, an ongoing clinical trial. The objective of this paper is to perform a review of the current evidence regarding the use of PARPi and radiotherapy (RT) in PCa and to give future insight on this topic. Full article
(This article belongs to the Special Issue Radiobiology and Radiotherapy in Tumour)
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