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      Cat Mammary Tumors: Genetic Models for the Human Counterpart

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          Abstract

          The records are not clear, but Man has been sheltering the cat inside his home for over 12,000 years. The close proximity of this companion animal, however, goes beyond sharing the same roof; it extends to the great similarity found at the cellular and molecular levels. Researchers have found a striking resemblance between subtypes of feline mammary tumors and their human counterparts that goes from the genes to the pathways involved in cancer initiation and progression. Spontaneous cat mammary pre-invasive intraepithelial lesions (hyperplasias and neoplasias) and malignant lesions seem to share a wide repertoire of molecular features with their human counterparts. In the present review, we tried to compile all the genetics aspects published (i.e., chromosomal alterations, critical cancer genes and their expression) regarding cat mammary tumors, which support the cat as a valuable alternative in vitro cell and animal model (i.e., cat mammary cell lines and the spontaneous tumors, respectively), but also to present a critical point of view of some of the issues that really need to be investigated in future research.

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          Most cited references144

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          Notch signalling in solid tumours: a little bit of everything but not all the time.

          The discovery of Notch in Drosophila melanogaster nearly a century ago opened the door to an ever-widening understanding of cellular processes that are controlled or influenced by Notch signalling. As would be expected with such a pleiotropic pathway, the deregulation of Notch signalling leads to several pathological conditions, including cancer. A role for Notch is well established in haematological malignancies, and more recent studies have provided evidence for the importance of Notch activity in solid tumours. As it is thought to act as an oncogene in some cancers but as a tumour suppressor in others, the role of Notch in solid tumours seems to be highly context dependent.
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            The role of cyclooxygenases in inflammation, cancer, and development.

            The cyclooxygenase (COX) enzymes catalyze a key step in the conversion of arachidonate to PGH2, the immediate substrate for a series of cell specific prostaglandin and thromboxane synthases. Prostaglandins play critical roles in numerous biologic processes, including the regulation of immune function, kidney development, reproductive biology, and gastrointestinal integrity. There are two COX isoforms, which differ mainly in their pattern of expression. COX-1 is expressed in most tissues, whereas COX-2 usually is absent, but is induced by numerous physiologic stimuli. Surprisingly, disruption of Cox1 (Ptgs1) in the mouse did not result in gastrointestinal abnormalities. cox-2 (Ptgs2) null mice show reproductive anomalies and defects in kidney development. Epidemiologic, animal, and human data indicate that NSAIDs, inhibitors of cyclooxygenase, are chemopreventive for colon cancer. COX-2 is overexpressed in 50% of benign polyps and 80-85% of adenocarcinomas. Offspring from cox-2 null by Apcdelta716 matings exhibit an 86% reduction in polyp number when compared to offspring from control animals, thus providing genetic evidence that COX-2 contributes to tumor formation or growth. The in vivo mechanism by which COX-2 affects tumor growth has not been determined. It is possible that both tumor and stromally derived COX-2 could influence tumor angiogenesis and/ or immune function.
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              Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis.

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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Vet Sci
                Vet Sci
                vetsci
                Veterinary Sciences
                MDPI
                2306-7381
                16 August 2016
                September 2016
                : 3
                : 3
                : 17
                Affiliations
                [1 ]Laboratory of Cytogenomics and Animal Genomics (CAG), Department of Genetics and Biotechnology (DGB), University of Trás-os-Montes and Alto Douro (UTAD), Vila Real 5001-801, Portugal; filadega@ 123456utad.pt (F.A.); borgesluisa@ 123456sapo.pt (A.B.)
                [2 ]Faculty of Sciences, BioISI—Biosystems & Integrative Sciences Institute, University of Lisboa, Campo Grande, Lisboa 1749-016, Portugal
                Author notes
                [* ]Correspondence: rchaves@ 123456utad.pt ; Tel.: +35-125-9350-936
                Article
                vetsci-03-00017
                10.3390/vetsci3030017
                5606576
                31ac045a-15ae-4b9a-8411-3ffe68a3bf54
                © 2016 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 07 May 2016
                : 11 August 2016
                Categories
                Review

                feline mammary carcinomas,cancer critical genes,chromosome rearrangements,cell and animal model,targeting therapies

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