Apoptosis or retinoblastoma: alternative fates of photoreceptors expressing the HPV-16 E7 gene in the presence or absence of p53.

@article{Howes1994ApoptosisOR,
  title={Apoptosis or retinoblastoma: alternative fates of photoreceptors expressing the HPV-16 E7 gene in the presence or absence of p53.},
  author={K. Howes and N. Ransom and D. Papermaster and J. Lasudry and D. Albert and J. Windle},
  journal={Genes \& development},
  year={1994},
  volume={8 11},
  pages={
          1300-10
        }
}
A transgenic mouse model for retinoblastoma was produced previously by directing SV40 T antigen expression to retinal photoreceptor cells using the promoter of the interstitial retinol-binding protein (IRBP) gene. This gene becomes active prior to the terminal differentiation of photoreceptors. Because T antigen-transforming activity is attributable, at least in part, to the inactivation of the retinoblastoma (pRb) and p53 tumor suppressor proteins, we addressed the role of p53 in the… Expand
APOPTOSIS OF PHOTORECEPTORS AND LENS FIBER CELLS WITH CATARACT AND MULTIPLE TUMOR FORMATION IN THE EYES OF TRANSGENIC MICE LACKING THE P53 GENE AND EXPRESSING THE HPV 16 E7 GENE UNDER THE CONTROL OF THE IRBP PROMOTER
TLDR
The lack of the p53 gene does not eliminate apoptosis of either the retina or the lens in these transgenic mice although the rate of destruction of photoreceptors is slightly delayed, and the retinal tumors apparently arise from precursors that survive amid a dying cell layer. Expand
Tumor formation in mice with somatic inactivation of the retinoblastoma gene in interphotoreceptor retinol binding protein-expressing cells
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The Cre-LoxP mediated somatic inactivation of Rb in a subset of neuroendocrine cells, including photoreceptor cells is described, highlighting the important differences that exist in tumor susceptibility between mice and man and question the photorecept cell origin of human retinoblastoma. Expand
Inhibition of cell death by lens-specific overexpression of bcl-2 in transgenic mice.
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Surprisingly, overexpression of bcl-2 was sufficient to interfere with normal fiber cell differentiation, inducing cataracts, microphakia, vacuolization, fiber cell disorganization, and inhibition of fiber cell denucleation, and these experiments show that the lenses of transgenic mice represent a valuable in vivo setting for studies of both induction and inhibited cell death. Expand
Temporally distinct patterns of p53-dependent and p53-independent apoptosis during mouse lens development.
TLDR
A similarity between the mechanism regulating E7-induced, p53-independent apoptosis and the apoptotic-like developmental process of fiber cell denucleation is suggested, and the mechanisms through which E6 suppresses both processes are suggested. Expand
The proliferative and apoptotic activities of E2F1 in the mouse retina
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The concept that cross-talk occurs between different retinal cell types and that multiple genetic pathways must become dysregulated for the full oncogenic transformation of neuronal retinal cells is supported. Expand
p107 is a suppressor of retinoblastoma development in pRb-deficient mice.
TLDR
Findings provide formal proof for the role of loss of Rb in retinoblastoma development in the mouse and the first in vivo evidence that p107 can exert a tumor suppressor function. Expand
p53 and p21waf-1 expression correlates with apoptosis or cell survival in poorly differentiated, but not well-differentiated, retinoblastomas.
TLDR
It is postulated that oxygen and cell "survival/growth factors" delivered via blood vessels protect retinoblastoma cells from apoptosis, and p53 varies its expression (and by implication its function) with altered differentiation in retinOBlastomas. Expand
Nuclear exclusion of wild-type p53 in immortalized human retinoblastoma cells.
TLDR
Some immortalized retinoblastoma cells may exhibit p53 dysfunction through nuclear exclusion of wild-type p53 protein through fusion with immortalized p53 messenger RNA. Expand
Inactivation of retinoblastoma family proteins by SV40 T antigen results in creation of a hepatocyte growth factor/scatter factor autocrine loop associated with an epithelial-fibroblastoid conversion and invasiveness.
TLDR
It is shown that LT causes loss of epithelial differentiation and induces invasiveness in Madin-Darby canine kidney epithelial cells, and results demonstrate that inactivation of RB family proteins in these cells is at the origin of a HGF/SF autocrine loop. Expand
p 53 and p 21 waf-1 Expression Correlates with Apoptosis or Cell Survival in Poorly Differentiated , but not Well-Differentiated , Retinoblastomas 1
In human retinoblastomas, rare genetic mutations of the retinoblastoma gene cause massive cell proliferation, altered differentiation, and tumor formation; but paradoxically, this is accompanied byExpand
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