Reprint of: Cancer “Causation” by Infections—Individual Contributions and Synergistic Networks

Hausen, Harald zur; Villiers, Ethel Michele De

doi:10.1053/j.seminoncol.2015.02.019

Cited by 16 publications

(11 citation statements)

References 131 publications

(125 reference statements)

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“…In the 1930s, Rous and Beard first described malignant changes to benign CRPV skin warts in infected domestic rabbits (Rous & Beard, 1935; Rous, Kidd et al, 1936). Further studies demonstrated that various carcinogenic compounds could accelerate malignant progression rates (Rous & Kidd, 1938) and provided an important preview into the subsequent connection between several high-risk HPV types and cervical cancer (reviewed in zur Hausen & de Villiers, 2015). More recent studies in the CRPV model have shown that increasing the ratio of common to rare synonymous codons in the viral oncogenes E6 and E7 can accelerate malignant progression rates (Cladel, Budgeon et al, 2013b; Cladel, Hu et al, 2008b).…”

Section: Preclinical Models (In Vivo)mentioning

confidence: 99%

Recent advances in preclinical model systems for papillomaviruses

et al. 2017

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Preclinical model systems to study multiple features of the papillomavirus life cycle have greatly aided our understanding of Human Papillomavirus (HPV) biology, disease progression and treatments. The challenge to studying HPV in hosts is that HPV along with most PVs are both species and tissue restricted. Thus, fundamental properties of HPV viral proteins can be assessed in specialized cell culture systems but host responses that involve innate immunity and host restriction factors requires preclinical surrogate models. Fortunately, there are several well-characterized and new animal models of papillomavirus infections that are available to the PV research community. Old models that continue to have value include canine, bovine and rabbit PV models and new rodent models are in place to better assess host-virus interactions. Questions arise as to the strengths and weaknesses of animal PV models for HPV disease and how accurately these preclinical models predict malignant progression, vaccine efficacy and therapeutic control of HPV-associated disease. In this review, we examine current preclinical models and highlight the strengths and weaknesses of the various models as well as provide an update on new opportunities to study the numerous unknowns that persist in the HPV research field.

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Section: Preclinical Models (In Vivo)mentioning

confidence: 99%

Recent advances in preclinical model systems for papillomaviruses

et al. 2017

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“…However, increased population densities and contact between different species in urban areas can create opportunities for increased disease transmission and act as a proliferation source of novel diseases [11]. Infectious agents have been increasingly recognized as causes of cancer; they are presently accepted as aetiological agents for about 20% of human cancer [37]. Candidate pathogens have been correlated with most of the remaining 80% of human cancers, but their causal role has not yet been determined.…”

Section: Infections Urban Habitat Alterations and Cancermentioning

confidence: 99%

Urban environment and cancer in wildlife: available evidence and future research avenues

et al. 2019

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While it is generally known that the risk of several cancers in humans is higher in urban areas compared with rural areas, cancer is often deemed a problem of human societies with modern lifestyles. At the same time, more and more wild animals are affected by urbanization processes and are faced with the need to adapt or acclimate to urban conditions. These include, among other things, increased exposure to an assortment of pollutants (e.g. chemicals, light and noise), novel types of food and new infections. According to the abundant literature available for humans, all of these factors are associated with an increased probability of developing cancerous neoplasias; however, the link between the urban environment and cancer in wildlife has not been discussed in the scientific literature. Here, we describe the available evidence linking environmental changes resulting from urbanization to cancer-related physiological changes in wild animals. We identify the knowledge gaps in this field and suggest future research avenues, with the ultimate aim of understanding how our modern lifestyle affects cancer prevalence in urbanizing wild populations. In addition, we consider the possibilities of using urban wild animal populations as models to study the association between environmental factors and cancer epidemics in humans, as well as to understand the evolution of cancer and defence mechanisms against it.

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“…From this point of view, cancerous cells differ from their normal counterparts within the same individual in the set of genetic mutations they harbour during lifetime. Despite genomic instability fulfils a fundamental role in generating the genetic diversity that sustains and expedites cancer features, several other mechanisms have been reported to underlie cancer initiation and progression, including deregulated epigenetic control of gene transcription [15], altered energy metabolism [16] and signalling pathways activation [17], chronic inflammation/evasion of immune surveillance [18,19], perturbation of tissue microenvironment [20], infections [21] and many others. Of course, not all, but rather only specific cell types can progress into malignancy, and, hence, have been called "cancer cells of origin".…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

Role of Environmental Chemicals, Processed Food Derivatives, and Nutrients in the Induction of Carcinogenesis

Persano

Zagoura

Louisse

et al. 2015

Stem Cells and Development

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In recent years it has been hypothesized that cancer stem cells (CSCs) are the actual driving force of tumor formation, highlighting the need to specifically target CSCs to successfully eradicate cancer growth and recurrence. Particularly, the deregulation of physiological signaling pathways controlling stem cell proliferation, self-renewal, differentiation, and metabolism is currently considered as one of the leading determinants of cancer formation. Given their peculiar, slow-dividing phenotype and their ability to respond to multiple microenvironmental stimuli, stem cells appear to be more susceptible to genetic and epigenetic carcinogens, possibly undergoing mutations resulting in tumor formation. In particular, some animal-derived bioactive nutrients and metabolites known to affect the hormonal milieu, and also chemicals derived from food processing and cooking, have been described as possible carcinogenic factors. Here, we review most recent literature in this field, highlighting how some environmental toxicants, some specific nutrients and their secondary products can induce carcinogenesis, possibly impacting stem cells and their niches, thus causing tumor growth.

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Reprint of: Cancer “Causation” by Infections—Individual Contributions and Synergistic Networks

Cited by 16 publications

References 131 publications

Recent advances in preclinical model systems for papillomaviruses

Recent advances in preclinical model systems for papillomaviruses

Urban environment and cancer in wildlife: available evidence and future research avenues

Role of Environmental Chemicals, Processed Food Derivatives, and Nutrients in the Induction of Carcinogenesis

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