Genetic susceptibility to cutaneous radiation injury

Abstract

The use of ionizing radiation is critical to cancer treatment and fluoroscopic procedures. However, despite efforts to minimize total radiation dose, many patients experience toxic cutaneous side-effects of ionizing radiation, ranging from mild erythema to subcutaneous fibrosis, telangiectasia formation, and ulceration. Extent of injury is highly variable among patients. Studying the genetic determinants of radiation injury can help develop protocols to reduce radiation toxicity, as well as drive research into effective modulators of the genes and gene products associated with radiation injury. Many studies in the past two decades have identified single-nucleotide polymorphisms that may be associated with susceptibility to cutaneous radiation injury, such as those in genes related to the following cellular responses to ionizing radiation: inflammation, DNA repair, oxidation and stress response, and cell-cycle and apoptosis. This review summarizes the current literature on potential major genes and polymorphisms, in the previously described damage response pathways, that are involved in susceptibility to cutaneous radiation injury. Potential pitfalls of current research and further avenues of discovery will be explored.

The relationship between TNF-α gene promoter polymorphism (− 1211 T > C), the plasma concentration of TNF-α, and risk of oral mucositis and shortening of overall survival in patients subjected to intensity-modulated radiation therapy due to head and neck cancer

“…Classical risk factors for OM include C-RTH, poor oral hygiene, smoking, malnutrition or cachexia and lack of antibiotic use at the early stage of OM development [10]. However, even in the group of patients with the same characteristics, more severe OM develops only in some of them which suggests the important role of genetic predisposition [14]. The pathophysiology of OM is still not fully understood.…”

“…To date, many studies were trying to evaluate the correlation between genetic variants and radiosensitivity and the reaction of normal tissues to irradiation. However, most of the studies assessing the association of SNPs with OM are focused on the following processes: DNA repair, oxidation and stress response, apoptosis [14], embryogenesis [27], as well as inflammation [14], and only one (our previous paper) concerned TNF-α -TNFR axis [28].…”

What is new when it comes to acute and chronic radiation-induced dermatitis in head and neck cancer patients?

“…It secretes factors that increase the number of cells that divide both cancerous and healthy tissues [3]. Undoubtedly, the study conducted by Huang and Glick shows how many risk factors are associated with human genetic material and how many factors affect the development of radiodermatitis [10]. Kawamura et al present a new radiation dermatitis scoring system.…”

“…The secretion of TGF-β, which is a central mediator of fibrogenesis, increases following the exposure to ionizing radiation, and it is proportional to the radiation dose delivered [8,9]. Huang and Glick summarize the knowledge about major genes and polymorphisms, and delineate the role of TGF-β as a peptide protein gene associated with an immune response that plays an important role in both early and late dermatitis [10]. Studies using the rat and mice model show that those less equipped with this protein are not as sensitive to radiotherapy as wild rats [9,11].…”

Evidências científicas sobre os fatores associados à qualidade de vida de pacientes com radiodermatite

“…These cutaneous repercussions are present in 95% of patients undergoing radiotherapeutic treatment, and they usually develop after the second week of treatment, being limited to the radiation field, and ranging from benign erythema, dry or wet desquamation, dermis exposure and fluid leakage to necrosis, deep ulceration and local infection (1,(3)(4) .…”