Workgroup 4: Spontaneous prostate carcinoma in dogs and nonhuman primates

Waters, David J.; Sakr, Wael; Hayden, D. W.; Lang, C. Max; McKinney, LuAnn; Murphy, Gerald P.; Radinsky, Robert; Ramoner, Rheinhold; Richardson, Ralph C.; Tindall, Donald J.

doi:10.1002/(sici)1097-0045(19980615)36:1<64::aid-pros12>3.0.co;2-g

Cited by 88 publications

(26 citation statements)

References 9 publications

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“…Both species display late onset of disease, high propensity for skeletal metastasis, and share the heterogeneous nature of tumor lesions. The similarities also extend to the nature of metastatic spread with canine secondaries commonly localizing to regional lymph nodes, lung, and bone [6], the latter being especially useful for evaluating therapies targeting bone metastases. Unlike humans, castration at an early age does not confer an additional survival benefit in dogs, possibly due to lack of functional AR, which may suggest the fundamentally different nature of canine prostate carcinogenesis [7].…”

Section: Canine Modelsmentioning

confidence: 92%

Modeling prostate cancer: a perspective on transgenic mouse models

Jeet

Russell

Khatri

2010

Cancer Metastasis Rev

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Despite considerable success in treatment of early stage localized prostate cancer (PC), acute inadequacy of late stage PC treatment and its inherent heterogeneity poses a formidable challenge. Clearly, an improved understanding of PC genesis and progression along with the development of new targeted therapies are warranted. Animal models, especially, transgenic immunocompetent mouse models, have proven to be the best ally in this respect. A series of models have been developed by modulation of expression of genes implicated in cancer-genesis and progression; mainly, modulation of expression of oncogenes, steroid hormone receptors, growth factors and their receptors, cell cycle and apoptosis regulators, and tumor suppressor genes have been used. Such models have contributed significantly to our understanding of the molecular and pathological aspects of PC initiation and progression. In particular, the transgenic mouse models based on multiple genetic alterations can more accurately address the inherent complexity of PC, not only in revealing the mechanisms of tumorigenesis and progression but also for clinically relevant evaluation of new therapies. Further, with advances in conditional knockout technologies, otherwise embryonically lethal gene changes can be incorporated leading to the development of new generation transgenics, thus adding significantly to our existing knowledge base. Different models and their relevance to PC research are discussed.

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Section: Canine Modelsmentioning

confidence: 92%

Modeling prostate cancer: a perspective on transgenic mouse models

Jeet

Russell

Khatri

2010

Cancer Metastasis Rev

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“…Furthermore, most are not suitable for studying XMRV in the context of prostate cancer. For instance, nonhuman primates rarely develop prostatic lesions or prostate cancer [97]; in fact, canine is the only other species presently known to naturally develop spontaneous prostate cancer [98]. A rodent model may be a viable option due to the availability of several rodent models of prostate cancer [99].…”

Section: Future Directionsmentioning

confidence: 99%

Biology and pathophysiology of the new human retrovirus XMRV and its association with human disease

Rusmevichientong

Chow

2010

Immunol Res

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Xenotropic murine leukemia virus-related virus (XMRV) is a new human retrovirus originally identified in prostate cancer patients with a deficiency in the antiviral enzyme RNase L. XMRV has been detected with varying frequencies in cases of prostate cancer and chronic fatigue syndrome (CFS), as well as in a small proportion of healthy individuals. An etiologic link between XMRV infection and human disease, however, has yet to be established. Here, we summarize existing knowledge regarding the characteristics of XMRV replication, association of XMRV with prostate cancer and CFS, and potential mechanisms of XMRV pathophysiology. We also highlight several areas, such as the establishment of standardized assays and the development of animal models, as future directions to advance our current understanding of XMRV and its relevance to human disease.

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“…However, the disease is locally invasive in both species with a comparable progression, metastatic pattern and histopathology [2], [4].…”

Section: Introductionmentioning

confidence: 99%

“…Besides man, the dog is the only known domesticated mammalian species developing spontaneous prostate cancer with considerable interest [2].…”

Section: Introductionmentioning

confidence: 99%

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Generation and Characterisation of a Canine EGFP-HMGA2 Prostate Cancer In Vitro Model

et al. 2014

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The architectural transcription factor HMGA2 is abundantly expressed during embryonic development. In several malignant neoplasias including prostate cancer, high re-expression of HMGA2 is correlated with malignancy and poor prognosis. The let-7 miRNA family is described to regulate HMGA2 negatively. The balance of let-7 and HMGA2 is discussed to play a major role in tumour aetiology. To further analyse the role of HMGA2 in prostate cancer a stable and highly reproducible in vitro model system is precondition. Herein we established a canine CT1258-EGFP-HMGA2 prostate cancer cell line stably overexpressing HMGA2 linked to EGFP and in addition the reference cell line CT1258-EGFP expressing solely EGFP to exclude EGFP-induced effects. Both recombinant cell lines were characterised by fluorescence microscopy, flow cytometry and immunocytochemistry. The proliferative effect of ectopically overexpressed HMGA2 was determined via BrdU assays. Comparative karyotyping of the derived and the initial CT1258 cell lines was performed to analyse chromosome consistency. The impact of the ectopic HMGA2 expression on its regulator let-7a was analysed by quantitative real-time PCR. Fluorescence microscopy and immunocytochemistry detected successful expression of the EGFP-HMGA2 fusion protein exclusively accumulating in the nucleus. Gene expression analyses confirmed HMGA2 overexpression in CT1258-EGFP-HMGA2 in comparison to CT1258-EGFP and native cells. Significantly higher let-7a expression levels were found in CT1258-EGFP-HMGA2 and CT1258-EGFP. The BrdU assays detected an increased proliferation of CT1258-HMGA2-EGFP cells compared to CT1258-EGFP and native CT1258. The cytogenetic analyses of CT1258-EGFP and CT1258-EGFP-HMGA2 resulted in a comparable hyperdiploid karyotype as described for native CT1258 cells. To further investigate the impact of recombinant overexpressed HMGA2 on CT1258 cells, other selected targets described to underlie HMGA2 regulation were screened in addition. The new fluorescent CT1258-EGFP-HMGA2 cell line is a stable tool enabling in vitro and in vivo analyses of the HMGA2-mediated effects on cells and the development and pathogenesis of prostate cancer.

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Workgroup 4: Spontaneous prostate carcinoma in dogs and nonhuman primates

Cited by 88 publications

References 9 publications

Modeling prostate cancer: a perspective on transgenic mouse models

Modeling prostate cancer: a perspective on transgenic mouse models

Biology and pathophysiology of the new human retrovirus XMRV and its association with human disease

Generation and Characterisation of a Canine EGFP-HMGA2 Prostate Cancer In Vitro Model

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