Yahyapour Yousef, Sadeghi Farzin, Alizadeh Ahad, Rajabnia Ramazan, Siadati Sepideh
Infectious Diseases & Tropical Medicine Research Center, Babol University of Medical Sciences, Babol, Iran.
Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Pathol Oncol Res. 2016 Oct;22(4):667-72. doi: 10.1007/s12253-016-0048-7. Epub 2016 Feb 15.
Human papillomavirus (HPV) infection is one of the hypothesized causes of esophageal squamous cell carcinoma (ESCC), but the etiological association remains uncertain. It was postulated that other infectious agents together with HPV may increase the risk of ESCC. The current investigation aimed to explore the presence of a new human tumor virus, Merkel cell polyomavirus (MCPyV), together with HPV in ESCC tumors and non-cancerous esophageal samples in northern Iran. In total, 96 esophageal samples (51 with ESCC, and 45 without esophageal malignancy) were examined. HPV DNA was detected in esophageal specimens of 16 out of the 51 ESCC cases (31.4 %) and 20 out of the 45 non-cancerous samples (44.4 %). Untypable HPV genotypes were recognized in high rates in cancerous (75.0 %) and non-cancerous (55.0 %) esophageal specimens. MCPyV DNA was detected in esophageal specimens of 23 out of the 51 ESCC cases (45.1 %) and 16 out of the 45 non-cancerous samples (35.6 %). The mean MCPyV DNA copy number was 1.0 × 10(-5) ± 2.4 × 10(-5) and 6.0 × 10(-6) ± 1.3 × 10(-5) per cell in ESCC cases and non-cancerous samples, respectively. There was no statistically significant difference between cancerous and non-cancerous samples regarding mean MCPyV DNA load (P = 0.353). A bayesian logistic regression model adjusted to the location of esophageal specimen and MCPyV infection, revealed a significant association between HPV and odds of ESCC (OR, 2.45; 95 % CI: 1.01-6.16). This study provides the evidence of the detection of the MCPyV DNA at a low viral copy number in cancerous and non- cancerous esophageal samples.
人乳头瘤病毒(HPV)感染是食管鳞状细胞癌(ESCC)的假设病因之一,但病因关联仍不确定。据推测,其他感染因子与HPV共同作用可能会增加ESCC的发病风险。当前的研究旨在探究伊朗北部ESCC肿瘤及非癌性食管样本中新型人类肿瘤病毒——默克尔细胞多瘤病毒(MCPyV)与HPV的共存情况。总共检测了96份食管样本(51份为ESCC样本,45份为无食管恶性病变的样本)。在51例ESCC病例的食管标本中,有16例(31.4%)检测到HPV DNA;在45份非癌性样本中,有20例(44.4%)检测到HPV DNA。在癌性(75.0%)和非癌性(55.0%)食管标本中,不可分型的HPV基因型检出率较高。在51例ESCC病例的食管标本中,有23例(45.1%)检测到MCPyV DNA;在45份非癌性样本中,有16例(35.6%)检测到MCPyV DNA。ESCC病例和非癌性样本中,MCPyV DNA的平均拷贝数分别为每细胞1.0×10⁻⁵±2.4×10⁻⁵和6.0×10⁻⁶±1.3×10⁻⁵。癌性样本和非癌性样本在平均MCPyV DNA载量方面无统计学显著差异(P = 0.353)。经食管标本位置和MCPyV感染校正的贝叶斯逻辑回归模型显示,HPV与ESCC发病几率之间存在显著关联(比值比,2.45;95%置信区间:1.01 - 6.16)。本研究提供了在癌性和非癌性食管样本中检测到低病毒拷贝数MCPyV DNA的证据。