Effects of <i>Xeroderma pigmentosum group C</i> polymorphism on the likelihood of prostate cancer

Yan, Yi–Dan; Xu, Bin; Wen, Qiaxian; Zhou, Jing; Zhang, Lifeng; Zuo, Li; Lv, Guoqiang; Shi, Yunfeng

doi:10.1002/jcla.23403

Cited by 4 publications

(4 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…People with BER gene polymorphisms and deficiencies have been shown to have increased cancer susceptibility (2,25,(58)(59)(60)(61)(62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72)(73)(74) and show a link to degenerative diseases (75)(76)(77)(78). Similarly, reduced NER capacity is also associated with increased risk of cancer (33,(79)(80)(81)(82)(83)(84)(85)(86)(87)(88)(89)(90)(91). DNA double strand breaks (DSBs) are repaired primarily by NHEJ and HR.…”

Section: Introductionmentioning

confidence: 99%

CometChip enables parallel analysis of multiple DNA repair activities

Ngo

Kaushal

et al. 2021

DNA Repair

View full text Add to dashboard Cite

DNA damage can be cytotoxic and mutagenic, and it is directly linked to aging, cancer, and other diseases. To counteract the deleterious effects of DNA damage, cells have evolved highly conserved DNA repair pathways. Many commonly used DNA repair assays are relatively low throughput and are limited to analysis of one protein or one pathway. Here, we have explored the capacity of the CometChip platform for parallel analysis of multiple DNA repair activities. Taking advantage of the versatility of the traditional comet assay and leveraging micropatterning techniques, the CometChip platform offers increased throughput and sensitivity compared to the traditional comet assay. By exposing cells to DNA damaging agents that create substrates of Base Excision Repair, Nucleotide Excision Repair, and Non-Homologous End Joining, we show that the CometChip is an effective method for assessing repair deficiencies in all three pathways. With these applications of the CometChip platform, we expand the utility of the comet assay for precise, high-throughput, parallel analysis of multiple DNA repair activities.

show abstract

Section: Introductionmentioning

confidence: 99%

CometChip enables parallel analysis of multiple DNA repair activities

Ngo

Kaushal

et al. 2021

DNA Repair

View full text Add to dashboard Cite

show abstract

“…On the contrary, these results can help us predict whether a smoker or betel quid chewer has a higher risk for oral cancer. An increased risk has also been seen in several types of cancers, including breast (33,34), lung (35), bladder (11,36), colorectal (37), prostate (38), gastric cancer (39) in various populations. Notably, the role of XPC in oral cancer is still lacking, and we are the first to investigate its expression levels of mRNA and protein.…”

Section: Discussionmentioning

confidence: 99%

Interaction of DNA Repair Gene XPC With Smoking and Betel Quid Chewing Behaviors of Oral Cancer

Chang

Shih

et al. 2021

Cancer Genomics Proteomics

View full text Add to dashboard Cite

Background/Aim: Xeroderma pigmentosum complementation group C (XPC) is reported to play important roles in DNA integrity and genomic instability, however, the contribution of XPC to oral carcinogenesis is largely uncertain. Therefore, we aimed at examining the contribution of XPC genotypes to oral cancer. Materials and Methods: The genotypes of XPC rs2228001 and rs2228000 were examined among 958 oral cancer patients and 958 control subjects by polymerase chain reaction-restriction fragment length polymorphism methodology and corresponding DNA repair capacity was checked. Results: First, the percentages of XPC rs2228001 AC and CC were higher among oral cancer patients than controls. Second, no significant association was observed regarding XPC rs2228000. Third, there was a synergistic influence of smoking and betel quid chewing behaviors and XPC rs2228001 genotype on oral cancer risk. Last, functional experiments showed DNA repair capacity was lower for AC/CC carriers than AA carriers. Conclusion: XPC rs2228001 C allele, which was associated with decreased DNA repair capacity, may interact with smoking and betel quid chewing behaviors on oral cancer risk.Oral cancer is the tenth most common cancer worldwide, and Taiwan has one of the highest incidences (1). Based on the most updated annual statistics from the government, oral cancer is of the fourth death-causing cancers among Taiwanese males (2). Uniquely, betel quid chewing, in addition to cigarrete smoking and alcohol drinking, has been identified as an effective environmental factor to oral cancer risk in Taiwan (3). The Taiwan government has embarked in population screen searching for the oral cancer candidates for early cure and medication to lower its incidence, however, the death rate and incidence of oral cancer were still high. Therefore, novel predictors for oral cancer risk are still needed.There are five major DNA repair systems, consisting of more than 130 genes, and teaming up to maintain the stability and integrity of the human genome. Among them, the nucleotide excision repair (NER) system is in charge of removing DNA crosslinks, bulky adducts, alkylating DNA adducts, oxidative DNA adducts and thymidine dimers (4-6). In NER machinery, four major steps (adduct recognition, lesion DNA incision, gapped DNA fulfilling and ligation) and several core players, including xeroderma pigmentosum complementation group C (XPC)-RAD23B, play critical roles as key enzymes (4, 5) Theoretically, subtle genetic 441 This article is freely accessible online.

show abstract

“…[103][104][105][106] Patients with XP have a 12-fold increased risk for internal malignancy, such as nasopharyngeal carcinoma, squamous cell carcinoma of the oesophagus, carcinoma of the thyroid, adenocarcinoma of the lung, carcinoma of the breast, carcinoma of the pancreas, leiomyosarcoma of the kidney, cancer of the ovary and cancer of the prostate, suggesting that UVR might not be the only culprit causing malignancy in patients with XP. [107][108][109][110][111][112][113][114][115][116] Patients with XP are at higher risk of developing smoking-induced cancers. 13 Women with XP are at risk for premature menopause.…”

Section: Complicationsmentioning

confidence: 99%

Xeroderma pigmentosum: an updated review

Leung¹,

Barankin²,

Lam³

et al. 2022

DIC

View full text Add to dashboard Cite

Background: Early recognition of xeroderma pigmentosum is important to minimize the complications arising from the harmful effects of exposure to ultraviolet radiation. This narrative review aims to familiarize physicians with the clinical features, diagnosis and management of xeroderma pigmentosum. Methods:A search was conducted in December 2021 in PubMed Clinical Queries using the key term "xeroderma pigmentosum". The search strategy included all clinical trials, observational studies and reviews published within the past 10 years. The information retrieved from the search was used in the compilation of this article.Results: Xeroderma pigmentosum is a condition of abnormal DNA repair of ultraviolet radiation-induced and oxidative DNA damage, which leads to increased skin cancer susceptibility. Approximately 50% of patients with xeroderma pigmentosum have increased photosensitivity and certain types of xeroderma pigmentosum are more prone to ocular disease and progressive neurodegeneration depending on the causative mutation. The diagnosis should be suspected in patients with increased photosensitivity and characteristic cutaneous, ophthalmological and neurological findings. A definite diagnosis can be made by the identification of biallelic mutation in one of the causative genes. Strict and consistent sun avoidance and protection and early detection and treatment of premalignant and malignant skin lesions are the mainstays of management. Treatment options for actinic keratosis include cryotherapy, topical imiquimod, topical 5-fluorouracil, chemical peeling, excision, CO 2 laser resurfacing, fractional/pulsed laser therapy, and photodynamic therapy. Cutaneous malignancy can be treated by photodynamic therapy, curettage and electrodesiccation, or surgical excision. Oral isotretinoin, oral niacinamide, topical imiquimod and topical fluorouracil can be used for the prevention of skin malignancy. Treatment options for poikiloderma include chemical peeling, dermabrasion and laser resurfacing. Methylcellulose eyedrops and soft ultraviolet-protective contact lenses may be used to keep the cornea moist and protect against the harmful effects of keratitis sicca. Investigational therapies include the use of T4 endonuclease-V liposome lotion and oral nicotinamide to reduce the rate of actinic keratoses and non-melanoma skin cancers and gene therapy for radical cure of this condition. Conclusion:Although currently there is no cure for xeroderma pigmentosum, increased awareness and early diagnosis of the condition, followed by rigorous sun avoidance and protection and optimal management, can dramatically improve the quality of life and life expectancy.

show abstract

Effects of Xeroderma pigmentosum group C polymorphism on the likelihood of prostate cancer

Cited by 4 publications

References 32 publications

CometChip enables parallel analysis of multiple DNA repair activities

CometChip enables parallel analysis of multiple DNA repair activities

Interaction of DNA Repair Gene XPC With Smoking and Betel Quid Chewing Behaviors of Oral Cancer

Xeroderma pigmentosum: an updated review

Contact Info

Product

Resources

About