Association of GSTP1 and ERCC1 polymorphisms with toxicity in locally advanced head and neck cancer platinum‐based chemoradiotherapy treatment

Duran, Goretti; Aguín, Santiago; Cruz, Raquel; Barros, Francisco; Giráldez, José María; Bernárdez, Beatriz; López‐López, Rafael; Carracedo, Ángel; Lamas, María Jesús

doi:10.1002/hed.25754

Cited by 13 publications

(9 citation statements)

References 38 publications

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“…In the literature, there have been several ERCC1 SNPs examined for their cancer risk and s11615 and rs3212986 have been the most frequently studied. For example, identifying the ERCC1 rs11615 genotype may help in predicting a positive or poor outcome of platinum-based chemotherapy for patients with colorectal (29), advanced gastric (30-32) and breast cancer (33) as well as testicular germ cell tumors (34), ovarian (35,36), esophageal (37), and most importantly, non-small cell lung cancer (17)(18)(19)(20). Molecular studies consistently provided evidence showing that ERCC1 rs11615 T allele is associated with relatively lower expression of ERCC1 at both the mRNA and protein levels; however, its role as a predictive marker for cancer therapy is controversial (38-42).…”

Section: Discussionmentioning

confidence: 99%

The Significant Interaction of Excision Repair Cross-complementing Group 1 Genotypes and Smoking to Lung Cancer Risk

Chen

Shen

et al. 2020

Cancer Genomics Proteomics

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Background: The study aims to evaluate the contribution of excision repair cross-complementing group 1 (ERCC1), which plays an important role in genome integrity maintenance, to lung cancer risk. Materials and Methods: ERCC1 rs11615 and rs3212986 genotypes were identified by polymerase chain reaction-restriction fragment length polymorphism analysis and their association with lung cancer risk was examined among 358 lung cancer patients and 716 controls. Results: The proportions of CC, CT and TT for the rs11615 genotype were 43.6%, 41.6% and 14.8% in the case group and 50.0%, 41.1% and 8.9% in the control group, respectively (p for trend=0.0082). Allelic analysis showed that ERCC1 rs11615 T-allele carriers have a 1.32-fold higher risk of lung cancer than wild-type C-allele carriers [95%confidence interval (CI)=1.09-1.60, p=0.0039]. In addition, a significant interaction between the rs11615 genotype and smoking status was observed. Conclusion: The T allele of ERCC1 rs11615 jointly with smoking habits may contribute to a higher lung cancer risk in Taiwan. According to the most recent report on cancer incidence and mortality by the International Agency for Research on Cancer, lung cancer has remained as the leading cause of cancer deaths all over the world (1). An estimated 2.1 million new lung cancer cases and 1.8 million cancer-related deaths occurred worldwide in 2018 (1). The rapidly increasing cases and the high death rate have urged us to look for effective marker(s) for the prediction of the risk of lung cancer, the outcome of the prognosis and the responsiveness of patient drug treatment. The initiation and development of lung cancer is related to multiple exogenous and endogenous factors including behavioral, environmental and genetic discrepancies, among which the consumption of cigarettes is the most significant factor to be associated with lung cancer risk (2). On the other hand, the fact that about 10% to 25% of lung cancer patients are non-smokers worldwide indicates that the individual genomic influences also play a critical part for personal lung cancer etiology (3). In Taiwan, the incidence and mortality of lung cancer has been ranked on the third and first place, respectively, among different types of cancer, for several years (4). Although several biomarkers for the early detection of lung cancer are being examined during recent years (5-11), the continuous search for effective clinically practical markers and the undermining mechanisms is still largely ongoing. Our genome is regularly and frequently damaged by various kinds of endogenous and exogenous mutagens and the DNA repair systems play a vital role in protecting it from irreversible mutations that can lead to carcinogenesis (12, 13). Concerning non-small cell lung cancer, genomic instability was 571 This article is freely accessible online.

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Section: Discussionmentioning

confidence: 99%

The Significant Interaction of Excision Repair Cross-complementing Group 1 Genotypes and Smoking to Lung Cancer Risk

Chen

Shen

et al. 2020

Cancer Genomics Proteomics

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“…Ionizing radiation-induced DNA damage leads to cellular responses including DNA damage response, apoptosis, immune response, inflammation, and cell-cycle arrest. Consequently, genetic variability in these signalling pathways could influence radiosensitivity, and in turn could be associated with acute and late toxicity [ 29 – 32 ]. As a central element in these pathways, it is plausible that NF- κ B activation is associated with radiation-induced toxicity.…”

Section: Discussionmentioning

confidence: 99%

Association between NF-κB Activation in Peripheral Blood Mononuclear Cells and Late Skin and Subcutaneous Fibrosis following Radiotherapy

Zhang

Sun

et al. 2020

BioMed Research International

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Background. This study aimed at evaluating the association between the speed of nuclear factor-kappa B (NF-κB) activation in peripheral blood mononuclear cells (PBMCs) and late skin and subcutaneous fibrosis in patients with head and neck squamous cell carcinoma (HNSCC) after radiotherapy. Methods. The speed of NF-κB activation was represented by the nuclear p65 expression ratio before and after irradiation. The optimal time point to measure the ratio was determined by Western blot in the PBMCs from healthy outpatients ranging from 0 to 12 hours after ex vivo irradiation. We recruited patients with HNSCC who had received ratiotherapy and who were under regular follow-up care. We assessed the association between the risk of developing ≥grade 2 late fibrosis and the nuclear p65 expression ratio in the PBMCs after ex vivo irradiation in these patients. Results. The maximum nuclear p65 ratio was observed at 1 hour after ex vivo irradiation in the PBMCs from the healthy outpatients. The speed of NF-κB activation was then represented by the nuclear p65 ratio in the PBMCs before and 1 hour after ex vivo irradiation. A total of 200 patients with HNSCC were recruited, 32.50% (n=65) of which presented with ≥grade 2 late fibrosis. There was a significant association between the speed of NF-κB activation in the PBMCs and an increased risk of developing ≥grade 2 late fibrosis in these patients (P=0.004). Subgroup analysis suggested that this finding was independent of the known clinical characteristics. Conclusions. The speed of NF-κB activation might be a potential predictor of late toxicity in cancer patients after radiotherapy. Prospective studies are needed for validation.

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“…Soares et al [26] studied the relationship between ERCC1 rs3212986 polymorphism and clinical side effects of chemotherapy and radiation for cervical cancer and reported a link between this gene and the late gastrointestinal toxicity onset. In addition, previous studies have shown the correlation between the ERCC1 status and toxicity and patient-reported quality of life [27].…”

Section: Effects Of Ccl4 and Art On Testicular Histologymentioning

confidence: 96%

Artemisa herba-alba ameliorates CCI 4 -induced spermatozoa toxicity through the downregulation of ERCC1 expression

Domiaty¹

2022

Pharmacophore

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Testicular toxicity has been implicated as a remote cause of infertility in men. In this study, we aimed at investigating the ameliorative potentials of Artemisa herba-alba against calcium tetrachloride (CCl4) induced toxicity in rats and its influence on ERCC1 gene expression. Four groups of twenty male Wistar rats (n =5) were created at random. Group I was the untreated control group. Group II was given a dose of 0.4 ml/200g CCl4 orally every other day for 3 weeks. Group III was given a dose (500 mg/ kg b.w) of Artemisia herba-alba (ART) extract orally every other day for 3 weeks. Group IV, received an oral dose of an extract of Artemisia herba-alba at a dose level of (500 mg/ kg b.w) alternated every other day with 0.4 ml/200g of CCl4 at a dose for 3 weeks. Bodyweight, relative kidney weight, serum testosterone, tissue oxidative stress, the expression of the ERCC1 gene, and testis histology were accessed. Our results showed that the administration of CCl4 to rats led to a decrease in body weight, tissue GSH, serum testosterone, increase in lipid peroxidation, an upregulation of ERCC1 gene expression, and modification of testicular histology. However, Artemisa herba-alba treatment following CCl4 administration to rats resulted in the restoration of testicular histology and the downregulation of ERCC1 gene expression in addition to modestly maintaining the body weight of rats and serum testosterone level. More studies with a prolonged treatment duration are, therefore, required to establish ART as a potential therapeutic for its use in testicular toxicity.

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Association of GSTP1 and ERCC1 polymorphisms with toxicity in locally advanced head and neck cancer platinum‐based chemoradiotherapy treatment

Cited by 13 publications

References 38 publications

The Significant Interaction of Excision Repair Cross-complementing Group 1 Genotypes and Smoking to Lung Cancer Risk

The Significant Interaction of Excision Repair Cross-complementing Group 1 Genotypes and Smoking to Lung Cancer Risk

Association between NF-κB Activation in Peripheral Blood Mononuclear Cells and Late Skin and Subcutaneous Fibrosis following Radiotherapy

Artemisa herba-alba ameliorates CCI 4 -induced spermatozoa toxicity through the downregulation of ERCC1 expression

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