Retinal Tumor Induction by Ocular Inoculation of Human Adenovirus in 3-Day-Old Rats

Mukai, Noritsugu; Murao, Tsuyoshi

doi:10.1097/00005072-197501000-00003

Cited by 17 publications

(3 citation statements)

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“…Proc. 24: 174, 1965) and induces tumors in a number of rodents (21,31,32,34,45,46). Neuronal tumors in different animals demonstrate a remarkably uniform phenotype (for a review, see reference 30).…”

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confidence: 99%

Adenovirus type 12-induced rat tumor cells of neuroepithelial origin: persistence and expression of the viral genome

Ibelgaufts¹,

Doerfler²,

Scheidtmann³

et al. 1980

J Virol

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MATERIALS AND METHODS Animals. BDIX rats (9) used in the experiments came from a colony which has been maintained as a closed brother-sister-mated colony for more than 2 years at the Max-Planck-Institute for Brain Research in Cologne, Germany. Athymic nude mice (BALB/c nu/nu) were obtained specific pathogen-free from Bomholtgard, Ry, Denmark. Virus propagation and purification. Human Adl2, Huie strain, and Ad2 were propagated in sus-423

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confidence: 99%

Adenovirus type 12-induced rat tumor cells of neuroepithelial origin: persistence and expression of the viral genome

Ibelgaufts¹,

Doerfler²,

Scheidtmann³

et al. 1980

J Virol

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“…That was first described by Huebner and colleagues in 1963, who showed that HAdV-A12 infections induce peritoneal tumors in rats with 30% efficiency [ 98 ]. Interestingly, HAdV-A12-induced sarcomas and even retinoblastomas have been observed by other groups [ 32 , 99 , 100 , 101 ]. In contrast, HAdV-D9 has been shown to cause tumors in rats more efficiently, as investigated in a series of papers by Javier and colleagues.…”

Section: Main Textmentioning

confidence: 88%

Animal Models in Human Adenovirus Research

Bertzbach

Dobner

2021

Biology

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Human adenovirus (HAdV) infections cause a wide variety of clinical symptoms, ranging from mild upper respiratory tract disease to lethal outcomes, particularly in immunocompromised individuals. To date, neither widely available vaccines nor approved antiadenoviral compounds are available to efficiently deal with HAdV infections. Thus, there is a need to thoroughly understand HAdV-induced disease, and for the development and preclinical evaluation of HAdV therapeutics and/or vaccines, and consequently for suitable standardizable in vitro systems and animal models. Current animal models to study HAdV pathogenesis, persistence, and tumorigenesis include rodents such as Syrian hamsters, mice, and cotton rats, as well as rabbits. In addition, a few recent studies on other species, such as pigs and tree shrews, reported promising data. These models mimic (aspects of) HAdV-induced pathological changes in humans and, although they are relevant, an ideal HAdV animal model has yet to be developed. This review summarizes the available animal models of HAdV infection with comprehensive descriptions of virus-induced pathogenesis in different animal species. We also elaborate on rodent HAdV animal models and how they contributed to insights into adenovirus-induced cell transformation and cancer.

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“…Prior to the discovery in the late 1980s that viral oncoproteins bind RB family proteins, it was shown that adenovirus can induce retinal tumors in the mouse, rat or baboon eye [95][96][97] . Subsequently, retinoblastomalike tumors were observed in transgenic mice in which the SV40 large T antigen (Tag) was under the control of the ␤ -luteinizing hormone promoter (LH ␤ -Tag) [98] .…”

Section: Retinoblastoma In Transgenic Mice Expressing Viral Oncoproteinsmentioning

confidence: 99%

The RB Protein Family in Retinal Development and Retinoblastoma: New Insights from New Mouse Models

Bremner

Chen²,

Pacal³

et al. 2004

Dev Neurosci

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The Rb gene was isolated almost 20 years ago, but fundamental questions regarding its role in retinal development and retinoblastoma remain. What is the normal function of RB protein in retinogenesis? What is the cell-of-origin of retinoblastoma? Why do retinoblastoma tumors have recurrent genetic lesions other than Rb inactivation? Why is retinoblastoma not induced by defects in cell cycle regulators other than Rb? Why is the retina so sensitive to Rb loss? Recently developed conditional Rb knockout models provide new insight into some of these issues. The data suggest that RB protein may not control the rate of progenitor division, but is critical for cell cycle exit when dividing retinal progenitors differentiate into postmitotic transition cells. This finding focuses attention on the ectopically dividing transition cell, rather than the progenitor, as the cell-of-origin. Cell-specific analyses in the RB-deficient retina reveal that ectopically dividing photoreceptors, bipolar and ganglion cells die, but amacrine, horizontal and Müller cells survive and stop dividing when they terminally differentiate. Rare amacrine transition cells escape cell cycle exit and generate tumors. These data suggest that post-Rb mutations are required to overcome growth arrest associated with terminal differentiation, rather than apoptosis as previously suggested. To explain why perturbing cell cycle regulators other than RB does not initiate retinoblastoma, we speculate that mutations in other components of the RB pathway perturb cell cycle arrest, but only RB loss triggers genome instability in retinal transition cells, which may be critical to facilitate post-Rb mutations necessary for transformation. Cell-specific differences in the effect of Rb loss on genome stability may contribute to the tremendous sensitivity of retinal transition cells to tumorigenesis. The new mouse models of retinoblastoma will be invaluable for testing these possibilities.

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Retinal Tumor Induction by Ocular Inoculation of Human Adenovirus in 3-Day-Old Rats

Cited by 17 publications

References 0 publications

Adenovirus type 12-induced rat tumor cells of neuroepithelial origin: persistence and expression of the viral genome

Adenovirus type 12-induced rat tumor cells of neuroepithelial origin: persistence and expression of the viral genome

Animal Models in Human Adenovirus Research

The RB Protein Family in Retinal Development and Retinoblastoma: New Insights from New Mouse Models

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