GYPC methylation performance in detecting cervical (pre)cancer in high-risk HPV-positive women using liquid-based cervical scrapes.

IF 2.8 2区医学 Q3 IMMUNOLOGY

Infectious Agents and Cancer Pub Date : 2025-10-09 DOI:10.1186/s13027-025-00699-3

Xing Fan, Zhengjiao Tong, Saiping Mao, Fang Yu, Rong Wang

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引用次数: 0

Abstract

Background: Methylation of host genes is promising for the triage of women with high-risk human papillomavirus (HR-HPV) infections. This study aimed to validate the potential value of Glycophorin C (GYPC) methylation (GYPC^m) in the early detection of cervical cancer.

Methods: We recruited HR-HPV-positive women at the hospital outpatient clinic between August and December 2023, using cytology triage. The remaining exfoliated cervical cells were subjected to GYPC^m testing. A total of 549 cases were finally included for analysis: 156 cervicitis, 303 cervical intraepithelial neoplasia (CIN)1, 49 CIN2, 37 CIN3, and 4 CC.

Results: The difference of GYPC^m ΔCp values between CIN1 and CIN2 was statistically significant in the pathology results of 549 participants (P < 0.001). The optimal threshold value of GYPC^m for detecting CIN2 + was 6.35. The GYPC^m adjusted ORs for CIN2 + and CIN3 + were 31.23 (95%CI: 16.53-58.99) and 34.68 (95%CI: 11.90-101.11), respectively. In all individuals, the sensitivity of GYPC^m for CIN2 + and CIN3 + was consistent with that of cytology (CIN2 + 83.3%; CIN3 + 90.2%), with higher specificity than that of cytology (CIN2 + 85.8 vs. 29.4%; CIN3 + 79.7 vs. 28.7%, all P < 0.001). The sensitivity and negative predictive value (NPV) of HPV16/18 combined GYPC^m for CIN3 + were not statistically different from those of HPV combined with cytology (sensitivity 95.1 vs. 97.6%, P = 0.317; NPV 99.4 vs. 99.0%, P = 0.613). The net reclassification improvement for HPV16/18 combined GYPC^m and its combined cytology to classify CIN2 + vs. < CIN2 was 48.8% (95%CI: 39.7-57.9%, P < 0.001), with a relative colposcopy referral rate of 50.1% (95%CI: 45.5-54.7%).

Conclusion: GYPC^m has a higher CIN2 + OR and higher specificity and positive predictive value than cytology in HR-HPV-positive women and is a potential molecular biomarker for triaging HR-HPV (+) to detect cervical (pre)cancer.

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GYPC甲基化在高危hpv阳性妇女宫颈（前）癌检测中的应用

背景：宿主基因甲基化对高危人乳头瘤病毒（HR-HPV）感染妇女的分类很有希望。本研究旨在验证Glycophorin C （GYPC）甲基化（GYPCm）在宫颈癌早期检测中的潜在价值。方法：我们于2023年8月至12月在医院门诊招募hr - hpv阳性妇女，采用细胞学分诊。剩余脱落的宫颈细胞进行GYPCm检测。最终纳入549例进行分析：宫颈炎156例，宫颈上皮内瘤变（CIN）1 303例，CIN2 49例，CIN3 37例，cc 4例。结果：549例患者病理结果中，CIN1与CIN2的GYPCm ΔCp值差异有统计学意义（检测CIN2 +的P m为6.35）。CIN2 +和CIN3 +的GYPCm校正or分别为31.23 （95%CI: 16.53-58.99）和34.68 （95%CI: 11.90-101.11）。在所有个体中，GYPCm对CIN2 +和CIN3 +的敏感性与细胞学（CIN2 + 83.3%; CIN3 + 90.2%）一致，特异性高于细胞学（CIN2 + 85.8 vs. 29.4%; CIN3 + 79.7 vs. 28.7%）， CIN3 +的所有P m与HPV合并细胞学的P m无统计学差异（敏感性95.1 vs. 97.6%, P = 0.317; NPV 99.4 vs. 99.0%, P = 0.613）。HPV16/18联合GYPCm的净重分类改善及其联合细胞学对CIN2 + vs的分类。< CIN2为48.8% (95%CI: 39.7-57.9%) P结论：与细胞学相比，GYPCm在HR-HPV阳性妇女中具有更高的CIN2 + OR和更高的特异性和阳性预测值，是鉴别HR-HPV（+）检测宫颈癌（前）的潜在分子生物标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Infectious Agents and Cancer ONCOLOGY-IMMUNOLOGY

CiteScore

5.80

自引率

2.70%

发文量

期刊介绍： Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer. The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular: • HPV and anogenital cancers, as well as head and neck cancers; • EBV and Burkitt lymphoma; • HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases; • HHV8 and Kaposi sarcoma; • HTLV and leukemia; • Cancers in Low- and Middle-income countries. The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries. Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.