雄激素受体基因(CAG)n重复多态性与前列腺癌患病风险相关性研究.docx

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Abstract
Androgen receptor (AR) gene is a crucial component that plays an essential role in the development and progression of prostate cancer. The CAG repeat polymorphism in the AR gene has been identified as a possible genetic risk factor for prostate cancer. In this article, we reviewed the current literature on the relationship between CAG repeat polymorphism and prostate cancer risk. We evaluated a variety of studies that investigated the association between the number of CAG repeats, prostate cancer incidence, and clinical outcomes. While the role of CAG repeat polymorphism is still not fully established, several studies suggested that shorter CAG repeat lengths may be associated with an increased susceptibility to prostate cancer. Hence, further studies are required to establish the significance of CAG repeats in prostate cancer risk assessment and the use of AR gene-related biomarkers.
Introduction
Prostate cancer is a malignancy that arises from the prostate gland and is the second most common cancer among men worldwide [1]. The etiology of the disease is multifactorial, with genetic, environmental, and lifestyle factors contributing to the development of the disease. The androgen receptor (AR) signaling pathway is crucial for the development and growth of the prostate gland [2]. It is also linked to the development of prostate cancer since most prostate cancers are highly androgen-sensitive [3].
The AR gene, located on the X chromosome, contains a polymorphic CAG repeat sequence in exon 1 that encodes the ligand-binding domain of the protein. The number of CAG repeats varies among individuals, and its length can influence AR activity and function [4]. Several studies have investigated the association between CAG repeat polymorphism and prostate cancer risk. The results of these studies have been conflicting. While some studies have found a correlation between shorter CAG repeats and an increased risk of developing prostate cancer, others did not find such an association [5]. Thus, the present study aimed to review the current literature on the relationship between CAG repeat polymorphism and prostate cancer risk.
CAG Repeat Polymorphism and Prostate Cancer Risk
Several studies have investigated the relationship between CAG repeat polymorphism and prostate cancer risk. A meta-analysis of 52 studies conducted by Qi et al. in 2013, found that shorter CAG repeat lengths were associated with an increased risk of developing prostate cancer [6]. The authors found a significant association between the risk of prostate cancer and the number of CAG repeats (OR=, 95% CI=-, p=). The study also revealed a significant correlation between shorter CAG repeat tract and the risk of developing aggressive prostate cancer (OR=, 95% CI= -, p=).
However, some studies have failed to find any association between the length of CAG repeats and the risk of prostate cancer. A study by Van Den Eeden et al. in 2015, involving 1058 prostate cancer cases and 1051 controls, found no association between CAG repeat length and prostate cancer risk [7]. Similarly, a study by Wei et al. in 2019, involving 1010 prostate cancer cases and 1,016 controls, found no correlation between CAG repeat length and prostate cancer risk [8]. Thus, the results of these studies provide evidence of the complexity involved in the relationship between CAG repeat polymorphism and prostate cancer risk.
Role of CAG Repeat Polymorphism in Clinical Outcomes
Several studies have also investigated the association between CAG repeat polymorphism and clinical outcomes in prostate cancer patients. A study by Giovannucci et al. in 2007 found a strong inverse correlation between the length of CAG repeat polymorphism and the risk of advanced prostate cancer [9]. Another study by Lai et al. in 2016, involving 235 prostate cancer patients, found that shorter CAG repeats were associated with a higher risk of biochemical recurrence (BCR) following radical prostatectomy [10]. Additionally, a study by Tuygun et al. in 2011 found that the mean CAG repeat length was significantly lower in prostate cancer patients with bone metastases relative to patients without metastases [11]. These studies suggest that shorter CAG repeat lengths may be associated with a poor clinical outcome.
However, studies have also found no correlation between CAG repeat polymorphism and clinical outcomes in prostate cancer patients. A study by Gunes et al. in 2015, involving 107 prostate cancer patients, found no association between CAG repeats and prostate-specific antigen (PSA) levels, Gleason score, or tumor stage [12]. A study by Fowke et al. in 2015, involving 191 prostate cancer patients, found no association between CAG repeat length and BCR following radical prostatectomy [13]. Hence, the results of these studies suggest modest or no association between CAG repeat polymorphism and clinical outcomes in prostate cancer patients.
Conclusion
The current literature on the relationship between CAG repeat polymorphism and prostate cancer risk is mixed, with some studies suggesting a correlation between shorter CAG repeat lengths and an increased risk of developing prostate cancer. The present review suggests that shorter CAG repeat lengths may be associated with a poor clinical outcome. However, the role of CAG repeat polymorphism in prostate cancer risk assessment requires further investigation to establish its significance. The present review highlights the need for studies that include a larger sample size and diverse populations to establish the association between CAG repeat polymorphism and prostate cancer risk. Furthermore, the dissemination of AR gene-related biomarkers in clinical settings can ultimately lead to effective preventive strategies, early diagnosis, and personalized treatment for prostate cancer.
References
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