Infectious Agents and Cancer最新文献

Objectives: The COVID-19 pandemic, while putting pressure on the global healthcare system, has had a significant impact on the prevention, diagnosis, and treatment of cervical cancer. The aim of this study is to provide an overview of the challenges and opportunities presented to cervical cancer during the COVID-19 pandemic and to provide lessons for better coping with cervical cancer in future pandemics.

Methods: The search terms included the following: SARS-CoV-2 and/or COVID-19 with cervical cancer and HPV. The initial literature search began on June 1, 2022 and ended on March 1, 2023.

Outcome: COVID-19 has hindered the cervical cancer screening, delayed the diagnosis and treatment of cervical cancer, increased the public's anxiety, and negatively affected the management of cervical cancer. However, the occurrence of COVID-19 pandemic has promoted the development of new human papillomavirus (HPV) tests and improved the rates of HPV self-sampling, offering a small window of opportunity to eliminate cervical cancer.

Conclusions: In the next few years, the COVID-19 pandemic will come to an end, and the eradication of cervical cancer should always be carried out. We should draw lessons and experience from this global pandemic, and make efforts for the subsequent eradication of cervical cancer.

Hepatitis C virus (HCV) chronically infects approximately 170 million people worldwide and is a known etiological agent of hepatocellular carcinoma (HCC). The molecular mechanisms of HCV-mediated carcinogenesis are not fully understood. This review article focuses on the oncogenic potential of NS3, a viral protein with transformative effects on cells, although the precise mechanisms remain elusive. Unlike the more extensively studied Core and NS5A proteins, NS3's roles in cancer development are less defined but critical. Research indicates that NS3 is implicated in several carcinogenic processes such as proliferative signaling, cell death resistance, genomic instability and mutations, invasion and metastasis, tumor-related inflammation, immune evasion, and replicative immortality. Understanding the direct impact of viral proteins such as NS3 on cellular transformation is crucial for elucidating HCV's role in HCC development. Overall, this review sheds light on the molecular mechanisms used by NS3 to contribute to hepatocarcinogenesis, and highlights its significance in the context of HCV-associated HCC, underscoring the need for further investigation into its specific molecular and cellular actions.

During the past two decades evidence has been developed that indicates a handful of viruses with known oncogenic capacity, have potential roles in breast cancer. These viruses are mouse mammary tumour virus (MMTV - the cause of breast cancer in mice), high-risk human papilloma viruses (HPV-the cause of cervical cancer), Epstein Barr virus (EBV-the cause of lymphomas and naso-pharyngeal cancer) and bovine leukemia virus (BLV - the cause of cancers in cattle). These viruses may act alone or in combination. Each of these viruses are significantly more prevalent in breast cancers than in normal and benign breast tissue controls. The odds ratios for the prevalence of these viruses in breast cancer compared to normal and benign breast controls, are based on case control studies - MMTV 13·40, HPV 5.56, EBV 4·43 and BLV 2·57. The odds ratios for MMTV are much greater compared to the other three viruses. The evidence for a causal role for mouse mammary tumour virus and high risk for cancer human papilloma viruses in human breast cancer is increasingly comprehensive. The evidence for Epstein Barr virus and bovine leukemia virus is more limited. Overall the evidence is substantial in support of a viral cause of breast cancer.

Background: The genetic susceptibility association between viral infection and the risk of colorectal cancer (CRC) has not been established.

Methods: We conducted two-sample Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data. In addition to traditional MR methods, we employed several other approaches, including cML, ConMix, MR-RAPS, and dIVW, to comprehensively assess causal effects. Sensitivity analyses were also performed to ensure the robustness of the results.

Results: After sensitivity analysis, presence of SNPs linked to increased susceptibility to cold sores infection was found to decrease the risk of CRC (OR: 0.73, 95% CI: 0.57-0.93, P = 0.01). In subgroup analysis, presence of SNPs linked to increased susceptibility to viral hepatitis (OR: 0.89, 95% CI: 0.81-0.98, P = 0.02) and infectious mononucleosis (OR: 0.91, 95% CI: 0.84-0.98, P = 0.02) were associated with a decreased risk of colon cancer, while measles virus (OR: 1.41, 95% CI: 1.07-1.85, P = 0.01) was associated with an increased risk of colon cancer. Presence of SNPs linked to increased susceptibility to herpes zoster (OR: 1.26, 95% CI: 1.05-1.52, P = 0.01) was associated with an increased risk of rectal cancer, while infectious mononucleosis (OR: 0.809, 95% CI: 0.80-0.98, P = 0.02) was associated with a decreased risk.

Conclusion: The study provides the first evidence of the genetic susceptibility associations between different viral infections and CRC, enhancing our understanding of the etiology of CRC.

Background: This study aimed to investigate whether persistent human papillomavirus integration at the same loci (PHISL) before and after treatment can predict recurrent/residual disease in women with CIN2-3.

Methods: A total of 151 CIN2-3 women treated with conization between August 2020 and September 2021 were included. To investigate the precision of HPV integration, we further analyzed HPV integration-positive patients. Sensitivity, specificity, positive and negative predictive values (PPV and NPV, respectively), and the Youden index for predicting recurrence/residual disease were calculated.

Results: Among the 151 enrolled CIN2-3 women, 56 were HPV integration-positive and 95 had HPV integration-negative results. Six (10.7%) experienced recurrence among 56 HPV integration-positive patients, which was more than those in HPV integration-negative patients (one patient, 1.1%). In the 56 HPV integration-positive patients, 12 had positive HPV results after treatment, seven had PHISL, and two had positive cone margin. Among the seven patients who tested with PHISL, six (85.7%) had residual/recurrent disease. PHISL was a prominent predictor of persistent/recurrent disease. The HPV test, the HPV integration test, and PHISL all had a sensitivity of 100% and a NPV of 100% for residual/recurrent disease. PHISL showed better specificity (98.0% vs. 82.0%, p = 0.005) and PPV (85.7% vs. 40.0%, p = 0.001) than the HPV test for predicting recurrence.

Conclusions: The HPV-integration-positive CIN2-3 women had much higher relapse rates than HPV-integration-negative CIN2-3 women. The findings indicate that PHISL derived from preoperative and postoperative HPV integration tests may be a precise biomarker for the identification of residual/recurrent CIN 2/3.

Background: High-risk human papillomavirus (hrHPV) infection causes almost all cervical cancer. Women living with human immunodeficiency virus (Women living with HIV: WLWHIV) are at a six-fold increased risk of developing cervical cancer. This study assessed hrHPV types in cervical cancer by HIV status and histologic subtypes at Muhimbili National Hospital (MNH) in Tanzania.

Methods: This cross-sectional study used formalin-fixed paraffin-embedded (FFPE) archived tissue blocks of cervical carcinomas diagnosed in the Department of Anatomical Pathology at MNH from January to December 2020. Tissue sections were tested for 15 HPV genotypes (16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, and 68) using the Ampfire assay. The distribution of HPV genotypes was assessed and compared by HIV status and histologic subtypes.

Results: The mean age ± standard deviation (N = 227, with valid HPV results) was 55 ± 12.9 years, 28.6% (n = 65) were WLWHIV, and squamous cell carcinoma (SCC) was the most common histologic subtype (91.2%). Most cervical carcinomas (81.1%, n = 184) tested positive for hrHPV with HPV16 (44.1%), HPV18 (15.9%), HPV35 (8.4%) and HPV45 (5.7%) being the most common HPV types. hrHPV was higher among older women with 64.5%, 85.1% and 81.3% among 30-40, 41-60 and ≥ 61-year-old women, respectively (p = 0.033). HPV16 was more commonly detected in SCC (47.8%) than in adenocarcinomas (5%) (p < 0.0001). There was no difference in hrHPV positivity by HIV status.

Conclusions: We found a high proportion of hrHPV among cervical carcinomas diagnosed in Tanzania. Rolling out HPV vaccines that target more hrHPV types than HPV16/18, especially HPV35 and HPV45, could optimize protection against cervical cancer in Tanzania.