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      Transgenic Models in Retinoblastoma Research

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          Abstract

          Understanding the mechanism of retinoblastoma (Rb) tumor initiation, development, progression and metastasis in vivo mandates the use of animal models that mimic this intraocular tumor in its genetic, anatomic, histologic and ultrastructural features. An early setback for developing mouse Rb models was that Rb mutations did not cause tumorigenesis in murine retinas. Subsequently, the discovery that the p107 protein takes over the role of pRb in mice led to the development of several animal models that phenotypically and histologically resemble the human form. This paper summarizes the transgenic models that have been developed over the last three decades.

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          Enumeration of the simian virus 40 early region elements necessary for human cell transformation.

          William C. Hahn, Scott Dessain, Mary Brooks … (2002)
          While it is clear that cancer arises from the accumulation of genetic mutations that endow the malignant cell with the properties of uncontrolled growth and proliferation, the precise combinations of mutations that program human tumor cell growth remain unknown. The study of the transforming proteins derived from DNA tumor viruses in experimental models of transformation has provided fundamental insights into the process of cell transformation. We recently reported that coexpression of the simian virus 40 (SV40) early region (ER), the gene encoding the telomerase catalytic subunit (hTERT), and an oncogenic allele of the H-ras gene in normal human fibroblast, kidney epithelial, and mammary epithelial cells converted these cells to a tumorigenic state. Here we show that the SV40 ER contributes to tumorigenic transformation in the presence of hTERT and oncogenic H-ras by perturbing three intracellular pathways through the actions of the SV40 large T antigen (LT) and the SV40 small t antigen (ST). LT simultaneously disables the retinoblastoma (pRB) and p53 tumor suppressor pathways; however, complete transformation of human cells requires the additional perturbation of protein phosphatase 2A by ST. Expression of ST in this setting stimulates cell proliferation, permits anchorage-independent growth, and confers increased resistance to nutrient deprivation. Taken together, these observations define the elements of the SV40 ER required for the transformation of human cells and begin to delineate a set of intracellular pathways whose disruption, in aggregate, appears to be necessary to generate tumorigenic human cells.
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            Differentiated horizontal interneurons clonally expand to form metastatic retinoblastoma in mice.

            Itsuki Ajioka, Rodrigo A.P. Martins, Ildar T Bayazitov … (2007)
            During neurogenesis, the progression from a progenitor cell to a differentiated neuron is believed to be unidirectional and irreversible. The Rb family of proteins (Rb, p107, and p130) regulates cell-cycle exit and differentiation during retinogenesis. Rb and p130 are redundantly expressed in the neurons of the inner nuclear layer (INL) of the retina. We have found that in the adult Rb;p130-deficient retinae p107 compensation prevents ectopic proliferation of INL neurons. However, p107 is haploinsufficient in this process. Differentiated Rb(-/-);p107(+/-);p130(-/-) horizontal interneurons re-entered the cell cycle, clonally expanded, and formed metastatic retinoblastoma. Horizontal cells were not affected in Rb(+/-);p107(-/-);p130(-/-) or Rb(-/-);p107(-/-);p130(+/-), retinae suggesting that one copy of Rb or p130 was sufficient to prevent horizontal proliferation. We hereby report that differentiated neurons can proliferate and form cancer while maintaining their differentiated state including neurites and synaptic connections.
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              Coexpression of normally incompatible developmental pathways in retinoblastoma genesis.

              Zsofia Nemeth, Cori Bradley, L. Fu … (2011)
              It is widely believed that the molecular and cellular features of a tumor reflect its cell of origin and can thus provide clues about treatment targets. The retinoblastoma cell of origin has been debated for over a century. Here, we report that human and mouse retinoblastomas have molecular, cellular, and neurochemical features of multiple cell classes, principally amacrine/horizontal interneurons, retinal progenitor cells, and photoreceptors. Importantly, single-cell gene expression array analysis showed that these multiple cell type-specific developmental programs are coexpressed in individual retinoblastoma cells, which creates a progenitor/neuronal hybrid cell. Furthermore, neurotransmitter receptors, transporters, and biosynthetic enzymes are expressed in human retinoblastoma, and targeted disruption of these pathways reduces retinoblastoma growth in vivo and in vitro. Copyright © 2011 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (publisher-id): OOP
                Journal ID (pmc): OOP
                Journal ID (doi): 10.1159/issn.2296-4657
                Title: Ocular Oncology and Pathology
                Publisher: S. Karger AG
                ISBN: 978-3-318-05306-7
                ISBN: 978-3-318-05307-4
                ISSN (Print): 2296-4681
                ISSN (Electronic): 2296-4657
                Publication date Subscription-year: 2015
                Publication date (Print): April 2015
                Publication date (Electronic): 09 April 2015
                Volume: 1
                Issue: 3
                Pages: 207-213
                Affiliations
                School of Medical Sciences, University of Hyderabad, Hyderabad, India
                Author notes
                *Prof. Geeta K. Vemuganti, MD, DNB, FAMS, FICP, Dean, School of Medical Sciences, University of Hyderabad, Prof. C.R. Rao Road, Gachibowli, Hyderabad 500046 (India), E-Mail deanmd@uohyd.ernet.in
                Article
                Publisher ID: 370157 Pmcid ID: PMC4847202 Other ID: Ocul Oncol Pathol 2015;1:207-213
                DOI: 10.1159/000370157
                PMC ID: PMC4847202
                PubMed ID: 27171579
                SO-VID: 398c9890-d23a-4dce-b179-834baca2b546
                Copyright © © 2015 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 05 November 2014
                Date accepted : 26 November 2014
                Page count
                Figures: 1, Tables: 1, References: 47, Pages: 7
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Vision sciences,Ophthalmology & Optometry,Pathology
                Keywords: Knockout models,LHβ-Tag,Retinoblastoma,Transgenic models,Tumorigenesis
                Data availability:
                ScienceOpen disciplines: Vision sciences, Ophthalmology & Optometry, Pathology
                Keywords: Knockout models, LHβ-Tag, Retinoblastoma, Transgenic models, Tumorigenesis

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