Hormonal and Stromal Regulation of Normal and Neoplastic Prostatic Growth

Ricke, William A.; Wang, Yuzhuo; Kurita, Takeshi; Hayward, Simon W.; Cunha, Gerald R.

doi:10.1007/3-540-27671-8_8

Cited by 9 publications

(7 citation statements)

References 117 publications

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“…These results show that Tag expression in the stroma is a critical step in lesion progression in the TRAMP model and emphasize the important role of the tumor microenvironment, and in particular the stromal cells, in control of tumor cell growth. 22 These transplantation studies of prostate tissue from TRAMP mice support a separate and distinct lineage of origin for neuroendocrine carcinomas.…”

Section: Tumorigenic Potential Of Early-stage Epithelial Lesions Frommentioning

confidence: 77%

Dissociation of Epithelial and Neuroendocrine Carcinoma Lineages in the Transgenic Adenocarcinoma of Mouse Prostate Model of Prostate Cancer

Chiaverotti

Couto

Donjacour

et al. 2008

The American Journal of Pathology

208

242

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The transgenic adenocarcinoma of mouse prostate (TRAMP) model is widely used in prostate cancer research because of rapid tumor onset and progression. The transgenic mouse is on a C57BL/6 (B6) background and expresses SV40 T-antigen under the probasin promoter. The strong genetic component of susceptibility to prostate cancer in humans prompted us to investigate the effect of mouse strain background (FVB and B6) on incidence, progression, and pathology of prostate cancer in this model. Because TRAMP lesions are unique but differ from conventional prostatic intraepithelial neoplasia because the epithelium and stroma are affected diffusely, we designated them as "atypical hyperplasia of Tag." Although the incidence and severity of atypical hyperplasia of Tag is similar, FVB-TRAMP mice live significantly shorter lives than B6-TRAMP mice because of the rapid development and progression of neuroendocrine carcinomas. This is associated with an increased frequency of neuroendocrine precursor lesions in young TRAMP mice, detectable at 4 weeks after birth. These lesions show properties of bipotential stem cells and co-express markers of epithelial (E-cadherin) and neuroendocrine (synaptophysin) lineages, as well as the transcription factors Foxa1 and Foxa2. Transplantation studies using TRAMP prostatic ducts suggested that neuroendocrine carcinomas arise independently from atypical hyperplasias or other epithelial lesions. Adenocarcinomas were not seen in our cohort. Thus, neuroendocrine Prostate cancer is the most frequently diagnosed cancer in men living in the United States and the second leading cause of cancer-related mortality, accounting for more than 29,000 deaths annually. The causes of this high incidence are unknown, but include both environmental factors and a genetic component.

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Section: Tumorigenic Potential Of Early-stage Epithelial Lesions Frommentioning

confidence: 77%

Dissociation of Epithelial and Neuroendocrine Carcinoma Lineages in the Transgenic Adenocarcinoma of Mouse Prostate Model of Prostate Cancer

Chiaverotti

Couto

Donjacour

et al. 2008

The American Journal of Pathology

208

242

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“…Although the complete pathophysiology of BPH and PC has not yet been completely understood, several mechanisms seem to be implicated. Th ese involve age-related tissue remodelling [18], hormonal [19] and metabolic alterations [20] and more recently immune response [4,5]. Th ere is accumulating evidence that infl ammation may be a central mechanism in pathogenesis of BPH and PC [5][6][7][8].…”

Section: Discussionmentioning

confidence: 99%

Comparative study of frequency of different lymphocytes subpopulation in peripheral blood of patients with prostate cancer and benign prostatic hyperplasia

Sotošek

Tokmadžić

Mrakovčić-Šutić

et al. 2011

Wien Klin Wochenschr

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“…The nutritional uptake and blood supply from surrounding and endothelial cells are very important in PCa cell growth and invasion [7,71]. The inflammatory cells also infiltrate the prostate and can cause prostatitis, which can alter PCa cell growth and metastasis.…”

Section: In Vivo Tissue Recombination Modelmentioning

confidence: 99%

“…However, the AR continues to be expressed in most cells of the HRPCs [5], and the detailed mechanisms involved in the conversion from androgen dependence (AD) to androgen independence in PCa remain unclear. Several papers [2,[6][7][8] have proposed possible mechanisms for this transition, such as: (1) AR mutation, with AR acquiring promiscuous binding to other steroids; (2) imbalance of AR co-regulators, causing abnormal alteration of AR transactivation; (3) alteration of selective androgen/AR signal transduction pathways through nonandrogen induction; and (4) changes in the surrounding 40 npg microenvironment and stromal cells.…”

Section: Introductionmentioning

confidence: 99%

The diverse and contrasting effects of using human prostate cancer cell lines to study androgen receptor roles in prostate cancer

Yu¹,

Lai²,

Xia³

et al. 2008

Asian J Androl

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The androgen receptor (AR) plays an important role in the development and progression of prostate cancer (PCa). Androgen deprivation therapy is initially effective in blocking tumor growth, but it eventually leads to the hormonerefractory state. The detailed mechanisms of the conversion from androgen dependence to androgen independence remain unclear. Several PCa cell lines were established to study the role of AR in PCa, but the results were often inconsistent or contrasting in different cell lines, or in the same cell line grown under different conditions. The cellular and molecular alteration of epithelial cells and their microenvironments are complicated, and it is difficult to use a single cell line to address this important issue and also to study the pathophysiological effects of AR. In this paper, we summarize the different effects of AR on multiple cell lines and show the disadvantages of using a single human PCa cell line to study AR effects on PCa. We also discuss the advantages of widely used epithelium-stroma co-culture systems, xenograft mouse models, and genetically engineered PCa mouse models. The combination of in vitro cell line studies and in vivo mouse models might lead to more credible results and better strategies for the study of AR roles in PCa.

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Hormonal and Stromal Regulation of Normal and Neoplastic Prostatic Growth

Cited by 9 publications

References 117 publications

Dissociation of Epithelial and Neuroendocrine Carcinoma Lineages in the Transgenic Adenocarcinoma of Mouse Prostate Model of Prostate Cancer

Dissociation of Epithelial and Neuroendocrine Carcinoma Lineages in the Transgenic Adenocarcinoma of Mouse Prostate Model of Prostate Cancer

Comparative study of frequency of different lymphocytes subpopulation in peripheral blood of patients with prostate cancer and benign prostatic hyperplasia

The diverse and contrasting effects of using human prostate cancer cell lines to study androgen receptor roles in prostate cancer

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