A “hit-and-run” affair – A possible link for cancer progression in virally driven cancers

Ferreira, Danyelle Assis; Tayyar, Yaman; Idris, Adi; McMillan, Nigel A.J.

doi:10.1016/j.bbcan.2020.188476

Cited by 39 publications

(33 citation statements)

References 105 publications

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“…Viruses such as Epstein–Barr virus, human herpesvirus 8, also called Kaposi’s sarcoma-associated herpesvirus, hepatitis B and C viruses, Merkel cell polyomavirus, human T-cell leukemia virus type 1virus; human papillomaviruses (HPVs) are distinctly recognizable as human tumor viruses. They are responsible for approximately 12% of all human cancers ( Ferreira et al, 2021 , Niller et al, 2011 Jun 28 ). HPVs are responsible for the majority of cervical, vaginal and vulvar cancers.…”

Section: Discussionmentioning

confidence: 99%

“…The late genes encode two late proteins (L1, L2), whereas the early genes produce six early proteins (E1, E2, E4, E5, E6, E7) ( Lee et al, 2016 ). HPV oncogenes associated with cellular transformation are E6 (degrades tumor suppressor p53) and E7 (inhibits tumor suppressor pRb) ( Ferreira et al, 2021 , Lee et al, 2016 ). HPV initiates to the basal epithelial layer through micro-lesion of the tissues and activates the late viral genes, which produce capsid protein formation and viral DNA replication.…”

Section: Discussionmentioning

confidence: 99%

“…It has been established that vulvar intraepithelial neoplasia and HPV are the dominant pathways of VC occurrence in young women ( Hajeer et al, 2020 ). HPV is double-stranded DNA virus, which belongs to the Papillomaviridae family and it is classified into 5 groups: alpha, beta, gamma, mu, and nu ( Mitra et al, 2018 , Ferreira et al, 2021 , Rollison et al, 2019 ). Over 200 types have been described of which HPV 16 and 33 subtypes are predominant and account for 55.5% of all HPV-related vulvar cancers ( Mitra et al, 2018 , Ferreira et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

“…The “hit and run” theory has been a subject of longstanding curiosity in tumor virology ( Niller et al, 2011 ). The “hit and run” scenario suggests that viruses have an activating role in cancer development and the viral genome may disappear after the host cell accumulates numerous mutations ( Ferreira et al, 2021 ). Herein, a case of HPV- positive SVC in a young patient with a possible “hit and run” scenario, is presented.…”

Section: Introductionmentioning

confidence: 99%

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A case of human papillomavirus infection and vulvar cancer in a young patient – “hit and run” theory

Kostov¹,

Dzhenkov

Metodiev

et al. 2021

Gynecologic Oncology Reports

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Highlights Squamous vulvar cancer is often associated with human papillomavirus infection. Vulvar cancer located in the Bartholini gland area should be distinguished from Bartholini gland carcinoma. The “hit and run” theory states that the viral genome may disappear after the host cell accumulates numerous mutations. The “hit and run” theory suggests that viruses might cause more cancers than previously thought .

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A case of human papillomavirus infection and vulvar cancer in a young patient – “hit and run” theory

Kostov¹,

Dzhenkov

Metodiev

et al. 2021

Gynecologic Oncology Reports

View full text Add to dashboard Cite

show abstract

“…However, it must be mentioned that there are examples where the viral components may become dispensable to the tumor phenotype. There are recent postulations for a ‘hit-and-run’ hypothesis suggesting that the accumulation of other genomic mutations could supersede the tumor’s dependence on the viral oncogenes resulting in a virus-independent tumor (Reviewed in [ 130 ]). This virus-independence has been observed with the spontaneous loss of EBV episomes in a Burkitt’s lymphoma (BL) cell line [ 131 ], or KSHV transformed cell lines that are episome negative but still tumorigenic in mice [ 132 ], and even in instances of HPV-related cancers, often considered a clear example of oncogenic addiction, known HPV18 transformed cell lines can lack HPV DNA [ 133 ].…”

Section: ‘Hit-and-run’ Virally Driven Cancersmentioning

confidence: 99%

Designer nucleases to treat malignant cancers driven by viral oncogenes

Scott

Morris

2021

Virol J

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Viral oncogenic transformation of healthy cells into a malignant state is a well-established phenomenon but took decades from the discovery of tumor-associated viruses to their accepted and established roles in oncogenesis. Viruses cause ~ 15% of know cancers and represents a significant global health burden. Beyond simply causing cellular transformation into a malignant form, a number of these cancers are augmented by a subset of viral factors that significantly enhance the tumor phenotype and, in some cases, are locked in a state of oncogenic addiction, and substantial research has elucidated the mechanisms in these cancers providing a rationale for targeted inactivation of the viral components as a treatment strategy. In many of these virus-associated cancers, the prognosis remains extremely poor, and novel drug approaches are urgently needed. Unlike non-specific small-molecule drug screens or the broad-acting toxic effects of chemo- and radiation therapy, the age of designer nucleases permits a rational approach to inactivating disease-causing targets, allowing for permanent inactivation of viral elements to inhibit tumorigenesis with growing evidence to support their efficacy in this role. Although many challenges remain for the clinical application of designer nucleases towards viral oncogenes; the uniqueness and clear molecular mechanism of these targets, combined with the distinct advantages of specific and permanent inactivation by nucleases, argues for their development as next-generation treatments for this aggressive group of cancers.

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Analysis of a hit‐and‐run tumor model by HPV in oropharyngeal cancers

Ferreira

Idris

McMillan

2022

Journal of Medical Virology

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Several viruses are known to be associated with the development of certain cancers, including human papilloma virus (HPV), an established causative agent for a range of anogenital and head and neck cancers. However, the causality has been based on the presence of the virus, or its genetic material, in the sampled tumors. We have long wondered if viruses cause cancer via a “hit and run” mechanism such that they are no longer present in the resulting tumors. Here, we hypothesize that the absence of viral genes from the tumor does not necessarily exclude the viral aetiology. To test this, we used an HPV‐driven oropharyngeal cancer (OPC) tumor model and CRISPR to delete the viral oncogene, E7. Indeed, the genetic removal of HPV E7 oncogene eliminates tumors in vivo. Remarkably, E7 deleted tumors recurred over time and develop new mutations not previously seen in HPV+ OPC tumors. Importantly, a number of these new mutations are found to be already present in HPV− OPC tumors.

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A “hit-and-run” affair – A possible link for cancer progression in virally driven cancers

Cited by 39 publications

References 105 publications

A case of human papillomavirus infection and vulvar cancer in a young patient – “hit and run” theory

A case of human papillomavirus infection and vulvar cancer in a young patient – “hit and run” theory

Designer nucleases to treat malignant cancers driven by viral oncogenes

Analysis of a hit‐and‐run tumor model by HPV in oropharyngeal cancers

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