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Impact of Single‑Nucleotide Polymorphisms on Radiation Pneumonitis in Cancer Patients (Review)

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Impact of Single‑Nucleotide Polymorphisms on Radiation Pneumonitis in Cancer Patients (Review) MOLECULAR AND CLINICAL ONCOLOGY 4: 3-10, 2016 Impact of single‑nucleotide polymorphisms on radiation pneumonitis in cancer patients (Review) CHENG-XIAN GUO1*, JING WANG2,3*, LI-HUA HUANG4, JIN-GAO LI3 and XIANG CHEN5 1Center of Clinical Pharmacology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013; 2Medical College of Nanchang University, Nanchang, Jiangxi 330006; 3Department of Radiation Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029; 4Center for Experimental Medical Research, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013; 5Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China Received March 27, 2015; Accepted July 6, 2015 DOI: 10.3892/mco.2015.666 Abstract. Radiation pneumonitis (RP) is one of the most Contents important dose-limiting toxicities in the radiotherapy of thoracic tumors, which reduces the rate of local tumor 1. Introduction control and overall survival and severely affects the patients' 2. Inflammation‑related genes quality of life. Single-nucleotide polymorphisms (SNPs) 3. DNA repair-related genes have recently attracted increasing attention as biomarkers 4. Stress response-related genes for predicting the development of RP. SNPs in inflamma- 5. Angiogenesis-related genes tion-related, DNA repair-related, stress response-related and 6. Summary and radiogenomics angiogenesis-related genes were proved to be associated with 7. Conclusion RP, with different underlying mechanisms. Radiogenomics focuses on the differences in radiosensitivity caused by gene sequence variation, which may prove helpful in investigating 1. Introduction the abovementioned associations. In this review, we aimed to investigate the associations between RP and SNPs reported in Radiation pneumonitis (RP) is the inflammation of the normal recent studies and highlight the main content and prospects of lung tissue within the radiation field following radiation radiogenomics. therapy. RP is one of the most common complications and one of the most important dose-limiting toxicities in the treatment of thoracic tumors by radiotherapy (1). Although significant progress has been made in the treatment technologies, a consid- erable number of patients experience RP following thoracic irradiation. Studies have demonstrated that ~10-20% of lung cancer patients develop severe RP (grade ≥3) following radio- Correspondence to: Professor Xiang Chen, Department therapy, of whom 50% succumb to this complication (2). The of Dermatology, Xiangya Hospital, Central South University, main risk factors of RP include patient-related factors, such as 87 Xiang Ya Road, Changsha, Hunan 410078, P.R. China gender, smoking and pulmonary function, and treatment-related E-mail: [email protected] factors, such as radiation dose, irradiated lung volume, Professor Jin-Gao Li, Department of Radiation Oncology, Jiangxi surgery and chemotherapy (3-7). However, it remains difficult Cancer Hospital, 519 East Beijing Road, Nanchang, Jiangxi 330029, to predict the occurrence of RP for any individual patient. P. R. Ch i na Based on the development of the human genome project and E-mail: [email protected] pharmacogenomics, it is reported that single-nucleotide poly- * morphisms (SNPs) in inflammation‑related, DNA repair‑related, Contributed equally stress response-related and angiogenesis-related genes, may be used as biomarkers to predict the development of R P. Abbreviations: RP, radiation pneumonitis; SNPs, single-nucleotide polymorphisms; BER, base excision repair; DSBR, DNA double-strand break repair; HR, homologous recombination; NHEJ, 2. Inflammation‑related genes non-homologous end-joining; NSCLC, non-small-cell lung cancer Inflammation is a defensive reaction that results from tissue Key words: radiation pneumonitis, single-nucleotide polymorphisms, damage or cellular injury, and is also a key process under- genetic markers lying radiation-induced toxicity (8,9). Several studies have been conducted to evaluate inflammation‑related biomarkers, focusing mostly on genes as described below. 4 GUO et al: SINGLE-NUCLEOTIDE POLYMORPHISMS AND RADIATION PNEUMONITIS Transforming growth factor‑β1 (TGF‑β1). TGF-β1 is a type Pro‑ and anti‑inflammatory genes. There are numerous pro- of cytokine that has been widely investigated and plays an and anti‑inflammatory cytokines in the human body. Whether important role in the processes of cell proliferation and differ- the inflammation occurs and to what severity, depends on the entiation, tissue fibrosis and inflammation (10‑12). Early in balance between the two types of cytokines. Thus, damage 1998, Anscher et al (13) found that patients who developed caused by radiotherapy, such as RP, likely results from the RP following radiotherapy had higher plasma TGF-β1 levels interaction between pro‑ and anti‑inflammatory cytokines. compared with those prior to radiotherapy, unlike patients who Hildebrandt et al (23) investigated 59 SNPs in 37 inflamma- did not develop RP. As a result, the plasma TGF-β1 levels may tion-related genes and found that 12 SNPs were associated with be used as a prediction index of RP. RP, including 7 SNPs in pro‑inflammatory genes and 5 SNPs In recent years, with the advances in molecular biology and in anti‑inflammatory genes (Table I). These SNPs were all genetics, the association between RP and individual differ- associated with an increased risk of RP, with the exception ences caused by gene polymorphisms has become a research of nitric oxide synthase 3 (NOS3) rs1799983. The study also focus. Yuan et al (14) analyzed the correlation between demonstrated a dose-related effect in inflammation‑related genetic variants of TGF-β1 in 164 cases of lung cancer SNPs. The higher the number of risk genotypes a patient patients (77.4% Caucasian) who developed RP following carries, the higher the risk for RP. Another study also identi- radiotherapy, and found that the TC̸CC genotypes in TGF-β1 fied the association between inflammation‑related SNPs and rs1982073 (T>C) were associated with a decreased risk of toxicity following radiotherapy in NSCLC patients (24) by grade ≥3 RP (HR=0.390, 95% CI: 0.197‑0.774, P=0.007) evaluating 11,930 SNPs in 904 inflammation‑related genes. and grade ≥2 RP (HR=0.489, 95% CI: 0.227‑0.861, P=0.013) Following double screening of the discovery and validation compared with the TT genotype. However, in 2010, Wang phases and polygenic risk score analysis, they observed that and Bi (15) found no association between TGF-β1 rs1982073 DEAD box polypeptide 58 rs11795343 affected the risk of RP. and grade ≥2 RP in Chinese patients (P=0.84) and the plasma However, the specific mechanisms underlying the association TGF-β1 levels were not dependent on this gene polymor- between inflammation‑related SNPs and RP remain unclear. phism. Subsequently, a study by Niu et al (16) validated and supported Wang's view and discovered that the AG/GG geno- 3. DNA repair‑related genes types of TGF-β1 rs11466345 (A>G) were associated with an increased risk of grade ≥3 RP in Chinese lung cancer patients Ionizing radiation may cause DNA damage, including DNA (HR=2.264, 95% CI: 1.126‑4.552, P=0.022). These studies strand breaks, base change, ribose destruction and dimer forma- suggested the presence of significant interethnic differences in tion. Radiotherapy-induced DNA damage mainly consists the SNPs of TGF-β1. of strand breaks and base alterations; therefore, the repair pathways involved in DNA damage are DNA double-strand Abnormal cell lineage protein 28 (Lin28) B. Lin28 (including break repair (DSBR) and base excision repair (BER) (25). The Lin28A and Lin28B) is a type of protein that binds RNA and genetic variants of DNA repair-related genes may affect the is involved in the processes of cell growth, tumorigenesis and capacity of the DNA repair pathways. Insufficient DNA repair tissue inflammation (17‑19). Lin28 binds with miRNA precur- capacity leads to increased DNA damage and high tissue sors and regulates the biosynthesis of miRNA, particularly the radiosensitivity, resulting in severe radiation-related complica- let-7 family miRNAs; therefore, Lin28 is the post-transcrip- tions (26,27). tional inhibitor of let-7 (20). It was previously demonstrated that, inhibiting the expression of Lin28 may increase the DNA DSBR genes. The ataxia telangiectasia mutated (ATM) synthesis of let-7 and reduce the expression of K-Ras, leading gene is located on chromosome 11q22-23 and its mutations to high radiosensitivity of lung cancer cells (21). Therefore, lead to ataxia-telangiectasia. The ATM protein is the main Lin28-let-7 may be a regulatory site of overcoming the low receptor for radiation-induced DNA injury that may detect and tumor radiosentivity caused by activated Ras signaling. In repair DNA DSBs and plays an important role in the DSBR addition, Iliopoulos et al (19) found that nuclear factor (NF)-κB pathway (28,29). Furthermore, the ATM protein is a type of may directly stimulate the transcription of Lin28 and decrease serine/threonine kinase, which may phosphorylate several let-7 miRNA levels, leading to high interleukin (IL)-6 levels. intermediates involved in cellular stress responses, modulation Although the mechanisms underlying the association between of cell cycle regulation point and apoptosis (30). Lin28 and inflammatory response are not clear, we may infer Studies in vivo and in vitro demonstrated that ATM that Lin28 plays an important role in inflammatory response heterozygosity or decreased expression may cause high based on the regulation of IL-6 expression. radiosensitivity among individuals or cells (31,32); thus, A previous study evaluated the association between Lin28 ATM may be a key checkpoint of radiosensitivity. In polymorphisms and the risk of grade ≥3 RP in 362 cases 2009, Zhang et al (33) found that ATM rs189037 (G>A) of non-small-cell lung cancer (NSCLC) patients receiving and rs373759 (G>A) exhibited a significant correlation definitive radiotherapy (22). Lin28B rs314280 (G>A) AG/AA with grade ≥2 RP in Chinese patients (n=253) and the (HR=2.23, 95% CI: 1.01‑4.94, P=0.048) and rs314276 (C>A) two SNPs are in linkage disequilibrium.
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