The role of Epstein‐Barr virus‐expressed genes in breast cancer development

Mostafaei, Shayan; Manesh, Pegah Vahidi; Nahand, Javid Sadri; Nesaei, Abolfazl; Sorayyayi, Saba; Abasabadi, Fatemeh; Mirzaei, Hamed; Etemadi, Ashkan; Neill, Andrew O’; Donnelly, Seamas C; Doroudian, Mohammad; Armstrong, Michelle E.; Moghoofei, Mohsen

doi:10.1111/tbj.14021

Cited by 9 publications

(5 citation statements)

References 5 publications

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“…Chronic inflammation and infection may be associated with the development of cancer in various organs, including the thyroid, breast, stomach, liver, cervix, and colon. According to previous studies, inflammation is very common in the adult prostate [3][4][5][6][7]. Factors, such as dietary factors, hormonal changes, cell damage, and infection (especially sexually transmitted infections), are some of the etiological factors that contribute to the initiation of prostatic inflammation.…”

Section: Introductionmentioning

confidence: 99%

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

et al. 2021

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Background This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. Methods This case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay. Results The EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18–45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Conclusion The HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors.

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Section: Introductionmentioning

confidence: 99%

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

et al. 2021

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“…Chronic in ammation and infection may be associated with the development of cancer in various organs including the thyroid, breast, stomach, liver, cervix and colon. Reportedly, an adult prostate can be prone to in ammation [3][4][5][6][7]. In ammation of the prostate can occur as a result of a variety of factors, including poor diet, hormonal changes, cell damage, and infection (especially sexually transmitted infections).…”

Section: Introductionmentioning

confidence: 99%

Anoikis Resistance and Development in Prostate Cancer: The Possible Role of HPV/EBV Coinfection

Nahand

Khanaliha

Mirzaei

et al. 2021

Preprint

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Background: This study aimed to evaluate the possible role of EBV/HPV co-infection as an etiologic factor in prostate cancer (PCa) development.Methods: The present case‐control research was conducted on 67 cases with prostate cancer and 40 controls. The expression of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantitated using ELISA and qRT-PCR.Results: The EBV/HPV co-infection was reported in 14.9% of case group and 7.5% of control group. The high-risk type of HPV, including HPV 16 and 18, were responsible for 50% and 30% of 10 HPV/EBV co-infected PCa samples, respectively. According to the results, a significant relationship was not observed between the PCa and HPV/EBV co-infection (OR=2.9, 95%CI=0.18-45.2, P=0.31). However, the highest percentage of HPV genome integration was found in HPV/EBV coinfected PCa group (8/10, 80%). Moreover, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS and RNS), anti-apoptotic mediators (Bcl-2 and Survivin), and anti-anoikis factors (TWIST, N-cad) were higher significantly in the HPV/EBV co-infected PCa cases when comparing with the non-coinfected PCa samples. Nevertheless, the tumor suppressor proteins (p53 and Rb) and the E-cad (inhibiting anoikis resistance) had a significant downregulation in the HPV/EBV co-infected PCa cases than in the non-coinfected PCa samples. Conclusion: HPV/EBV co-infection probably can act as an etiologic factor in PCa through modulation of cellular behavior.

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“…El-Naby et al and Shahi et al [130,139] reported a higher nodal status in EBV-positive patients. Mostafaei et al [135] reported higher levels of inflammatory markers such as TNF𝛼 in patients with EBV+ breast cancer than in controls.…”

Section: Ebvmentioning

confidence: 99%

The Role of Oncogenic Viruses in the Pathogenesis of Sporadic Breast Cancer: A Comprehensive Review of the Current Literature

Rossi,

Inzani,

Cesari

et al. 2024

Pathogens

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Breast cancer is the most common malignancy in the female sex; although recent therapies have significantly changed the natural history of this cancer, it remains a significant challenge. In the past decade, evidence has been put forward that some oncogenic viruses may play a role in the development of sporadic breast cancer; however, data are scattered and mostly reported as sparse case series or small case–control studies. In this review, we organize and report current evidence regarding the role of high-risk human papillomavirus, mouse mammary tumor virus, Epstein–Barr virus, cytomegalovirus, bovine leukemia virus, human polyomavirus 2, and Merkel cell polyomavirus in the pathogenesis of breast cancer.

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The role of Epstein‐Barr virus‐expressed genes in breast cancer development

Cited by 9 publications

References 5 publications

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

Anoikis Resistance and Development in Prostate Cancer: The Possible Role of HPV/EBV Coinfection

The Role of Oncogenic Viruses in the Pathogenesis of Sporadic Breast Cancer: A Comprehensive Review of the Current Literature

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