SARS-CoV-2 and cancer: the intriguing and informative cross-talk

Goubran, Hadi; Stakiw, Julie; Seghatchian, Jerard; Ragab, Gaafar; Burnouf, Thierry

doi:10.1016/j.transci.2022.103488

Cited by 6 publications

(2 citation statements)

References 52 publications

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“…Additionally, some major signaling pathways have been recognized at the cross-talk between SARS-CoV-2 and cancer cells, frequently stimulating the tumor progression or modifying the response of the tumor to therapy. However, the causal relationship between SARS-CoV-2 and cancer and the effective role of the virus in oncogenesis still represents an open question, considering the observed reactivation of oncogenic viruses following COVID-19 in some cases and the paradoxical response of certain tumors to the immune modulation induced by the infection in others [80].…”

Section: The Oncogenic Potential Of Sars-cov-2mentioning

confidence: 99%

Deciphering the Relationship between SARS-CoV-2 and Cancer

Costanzo

Giglio

Roviello

2023

IJMS

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Some viruses are known to be associated with the onset of specific cancers. These microorganisms, oncogenic viruses or oncoviruses, can convert normal cells into cancer cells by modulating the central metabolic pathways or hampering genomic integrity mechanisms, consequently inhibiting the apoptotic machinery and/or enhancing cell proliferation. Seven oncogenic viruses are known to promote tumorigenesis in humans: human papillomavirus (HPV), hepatitis B and C viruses (HBV, HCV), Epstein-Barr virus (EBV), human T-cell leukemia virus 1 (HTLV-1), Kaposi sarcoma-associated herpesvirus (KSHV), and Merkel cell polyomavirus (MCPyV). Recent research indicates that SARS-CoV-2 infection and COVID-19 progression may predispose recovered patients to cancer onset and accelerate cancer development. This hypothesis is based on the growing evidence regarding the ability of SARS-CoV-2 to modulate oncogenic pathways, promoting chronic low-grade inflammation and causing tissue damage. Herein, we summarize the main relationships known to date between virus infection and cancer, providing a summary of the proposed biochemical mechanisms behind the cellular transformation. Mechanistically, DNA viruses (such as HPV, HBV, EBV, and MCPyV) encode their virus oncogenes. In contrast, RNA viruses (like HCV, HTLV-1) may encode oncogenes or trigger host oncogenes through cis-/-trans activation leading to different types of cancer. As for SARS-CoV-2, its role as an oncogenic virus seems to occur through the inhibition of oncosuppressors or controlling the metabolic and autophagy pathways in the infected cells. However, these effects could be significant in particular scenarios like those linked to severe COVID-19 or long COVID. On the other hand, looking at the SARS-CoV-2─cancer relationship from an opposite perspective, oncolytic effects and anti-tumor immune response were triggered by SARS-CoV-2 infection in some cases. In summary, our work aims to recall comprehensive attention from the scientific community to elucidate the effects of SARS-CoV-2 and, more in general, β-coronavirus infection on cancer susceptibility for cancer prevention or supporting therapeutic approaches.

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Section: The Oncogenic Potential Of Sars-cov-2mentioning

confidence: 99%

Deciphering the Relationship between SARS-CoV-2 and Cancer

Costanzo

Giglio

Roviello

2023

IJMS

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“…The potential causal relationship between SARS-CoV-2 and cancer, as well as the virus's actual contribution to oncogenesis, remains an unresolved inquiry. This uncertainty arises from instances of oncoviruses reactivating post-COVID-19 and the puzzling reactions of certain tumors to immune modulation [61].…”

Section: Discussionmentioning

confidence: 99%

High Risk of Heart Tumors after COVID-19

Mitrofanova,

Makarov,

Goncharova

et al. 2023

Life

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An emergence of evidence suggests that severe COVID-19 is associated with an increased risk of developing breast and gastrointestinal cancers. The aim of this research was to assess the risk of heart tumors development in patients who have had COVID-19. Methods: A comparative analysis of 173 heart tumors was conducted between 2016 and 2023. Immunohistochemical examination with antibodies against spike SARS-CoV-2 was performed on 21 heart tumors: 10 myxomas operated before 2020 (the control group), four cardiac myxomas, one proliferating myxoma, three papillary fibroelastomas, two myxofibrosarcomas, one chondrosarcoma resected in 2022–2023. Immunohistochemical analysis with antibodies against CD34 and CD68 was also conducted on the same 11 Post-COVID period heart tumors. Immunofluorescent examination with a cocktail of antibodies against spike SARS-CoV-2/CD34 and spike SARS-CoV-2/CD68 was performed in 2 cases out of 11 (proliferating myxoma and classic myxoma). Results: A 1.5-fold increase in the number of heart tumors by 2023 was observed, with a statistically significant increase in the number of myxomas. There was no correlation with vaccination, and no significant differences were found between patients from 2016–2019 and 2021–2023 in terms of gender, age, and cardiac rhythm dis-orders. Morphological examination revealed the expression of spike SARS-CoV-2 in tumor cells, endothelial cells, and macrophages in 10 out of 11 heart tumors. Conclusion: The detection of SARS-CoV-2 persistence in endothelium and macrophages as well as in tumor cells of benign and malignant cardiac neoplasms, the increase in the number of these tumors, especially cardiac myxomas, after the pandemic by 2023 may indicate a trend toward an increased risk of cardiac neoplasms in COVID-19 patients, which re-quires further research on this issue and a search for new evidence.

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Analysis of a reaction-diffusion oncolytic SARS-CoV-2 model

Al Agha

2024

Model. Earth Syst. Environ.

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SARS-CoV-2 and cancer: the intriguing and informative cross-talk

Cited by 6 publications

References 52 publications

Deciphering the Relationship between SARS-CoV-2 and Cancer

Deciphering the Relationship between SARS-CoV-2 and Cancer

High Risk of Heart Tumors after COVID-19

Analysis of a reaction-diffusion oncolytic SARS-CoV-2 model

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