From HPV Infection to Oncogenesis: A Brief Review of the Complex Immunobiological Events

Stern, Peter L.; Einstein, Mark H.

doi:10.2174/157339410791202565

Cited by 6 publications

(6 citation statements)

References 68 publications

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“…This subnetwork might have an important role in prostate cancer. In fact, we found that this network demonstrates a very strong correlation among others; with the "Proliferation_positive regulation cell proliferation" which further validates that genes in this network may serve in the process of oncogenesis [ 45 , 46 ] (Additional File 4 , Figure S8). In addition, among GO molecular functions, "growth factor activity" was found to be significantly activated indicating, that this network may stimulate growth of cancer cells (Additional File 4 , Figure S9).…”

Section: Resultssupporting

confidence: 64%

Differential C3NET reveals disease networks of direct physical interactions

et al. 2011

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BackgroundGenes might have different gene interactions in different cell conditions, which might be mapped into different networks. Differential analysis of gene networks allows spotting condition-specific interactions that, for instance, form disease networks if the conditions are a disease, such as cancer, and normal. This could potentially allow developing better and subtly targeted drugs to cure cancer. Differential network analysis with direct physical gene interactions needs to be explored in this endeavour.ResultsC3NET is a recently introduced information theory based gene network inference algorithm that infers direct physical gene interactions from expression data, which was shown to give consistently higher inference performances over various networks than its competitors. In this paper, we present, DC3net, an approach to employ C3NET in inferring disease networks. We apply DC3net on a synthetic and real prostate cancer datasets, which show promising results. With loose cutoffs, we predicted 18583 interactions from tumor and normal samples in total. Although there are no reference interactions databases for the specific conditions of our samples in the literature, we found verifications for 54 of our predicted direct physical interactions from only four of the biological interaction databases. As an example, we predicted that RAD50 with TRF2 have prostate cancer specific interaction that turned out to be having validation from the literature. It is known that RAD50 complex associates with TRF2 in the S phase of cell cycle, which suggests that this predicted interaction may promote telomere maintenance in tumor cells in order to allow tumor cells to divide indefinitely. Our enrichment analysis suggests that the identified tumor specific gene interactions may be potentially important in driving the growth in prostate cancer. Additionally, we found that the highest connected subnetwork of our predicted tumor specific network is enriched for all proliferation genes, which further suggests that the genes in this network may serve in the process of oncogenesis.ConclusionsOur approach reveals disease specific interactions. It may help to make experimental follow-up studies more cost and time efficient by prioritizing disease relevant parts of the global gene network.

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Section: Resultssupporting

confidence: 64%

Differential C3NET reveals disease networks of direct physical interactions

et al. 2011

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“…The presence of these defined tumor-specific antigens forms an excellent basis for the development of strategies aiming to reinforce the immune response to combat cancer. It has long been known that the adaptive immune response, in particular T cells, confer protection against HPV-induced diseases [35,36]. However, it is likely that in some cases the natural immune response against these HPV proteins may have been compromised, e.g., in a chronic HPV infection or cancer by systemic and/or local immune regulatory or escape factors [37,38].…”

Section: Development Of Novel Treatmentsmentioning

confidence: 99%

Therapy of Human Papillomavirus-Related Disease

Stern

Burg

Hampson

et al. 2012

Vaccine

157

124

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This chapter reviews the current treatment of chronic and neoplastic HPV-associated conditions and the development of novel therapeutic approaches. Surgical excision of HPV-associated lower genital tract neoplasia is very successful but largely depends on secondary prevention programmes for identification of disease. Only high-risk HPV-driven chronic, preneoplastic lesions and some very early cancers cannot be successfully treated by surgical procedures alone. Chemoradiation therapy of cervical cancer contributes to the 66–79% cervical cancer survival at 5 years. Outlook for those patients with persistent or recurrent cervical cancer following treatment is very poor. Topical agents such as imiquimod (immune response modifier), cidofovir (inhibition of viral replication; induction apoptosis) or photodynamic therapy (direct damage of tumour and augmentation of anti-tumour immunity) have all shown some useful efficacy (~50–60%) in treatment of high grade vulvar intraepithelial neoplasia. Provider administered treatments of genital warts include cryotherapy, trichloracetic acid, or surgical removal which has the highest primary clearance rate. Patient applied therapies include podophyllotoxin and imiquimod. Recurrence after “successful” treatment is 30–40%. Further improvements could derive from a rational combination of current therapy with new drugs targeting molecular pathways mediated by HPV in cancer. Small molecule inhibitors targeting the DNA binding activities of HPV E1/E2 or the anti-apoptotic consequences of E6/E7 oncogenes are in preclinical development. Proteasome and histone deacetylase inhibitors, which can enhance apoptosis in HPV positive tumour cells, are being tested in early clinical trials. Chronic high-risk HPV infection/neoplasia is characterised by systemic and/or local immune suppressive regulatory or escape factors. Recently two E6/E7 vaccines have shown some clinical efficacy in high grade VIN patients and this correlated with strong and broad systemic HPV-specific T cell response and modulation of key local immune factors. Treatments that can shift the balance of immune effectors locally in combination with vaccination are now being tested. This article forms part of a special supplement entitled “Opportunities for comprehensive control of HPV infections and related diseases” Vaccine Volume 30, Supplement X, 2012.

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“…The result is the release of E2F, which can bind and activate its DNA targets to promote cell cycle progression. With these efects, E6 and E7 are truly oncoproteins and are also responsible for cell transformation [36]. Expression of these oncogenes appears to be a critical step in the maintenance of the transformed stage and progression to invasive carcinoma.…”

Section: Vaccinesmentioning

confidence: 99%

Prophylactic and Therapeutic Vaccines against Human Papillomavirus Infections

Rosales¹,

Rosales²

2017

Vaccines

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Human papillomaviruses (HPVs) are a large family of double-strand DNA viruses comprising more than 180 types. Infection with HPV is associated with benign and malignant proliferation of skin and mucosae. Low-risk HPVs produce warts, whereas high-risk viruses induce tumors. Because there are no anti-viral drugs for HPV infection, there is a lot of interest in vaccines that can prevent the infection and also in vaccines that can be used to treat established infections and HPV-related tumors. Two prophylactic vaccines have been approved for preventing HPV infection. They seem to be efective when very young people are vaccinated. Unfortunately, many older people are still at risk of infection, mainly in countries where vaccination coverage is not eicient and for those people, novel therapeutic vaccines are being developed. This chapter describes the properties of HPV vaccines used today and the current status of several therapeutic vaccines been developed to treat HPV-induced lesions.

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From HPV Infection to Oncogenesis: A Brief Review of the Complex Immunobiological Events

Cited by 6 publications

References 68 publications

Differential C3NET reveals disease networks of direct physical interactions

Differential C3NET reveals disease networks of direct physical interactions

Therapy of Human Papillomavirus-Related Disease

Prophylactic and Therapeutic Vaccines against Human Papillomavirus Infections

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