Role of the stromal microenvironment in carcinogenesis of the prostate.
| Title: | Role of the stromal microenvironment in carcinogenesis of the prostate. |
|---|---|
| Authors: | Gerald R. Cunha, Simon W. Hayward, Y.Z. Wang |
| Source: | International Journal of Cancer; 10/20/2003, Vol. 107 Issue 1, p1, 10p |
| Subject Terms: | ANDROGENS, PROSTATITIS, ENDOCRINOLOGY, PROSTATE diseases |
| Abstract: | The topic of this review is the role of stromal-epithelial interactions in normal and malignant prostatic growth. Because cell-cell interactions and androgens play such key roles in the prostate, the goal of this review will be to apply endocrinologic and developmental concepts to the understanding of normal and malignant prostatic growth. Prostatic development is induced by androgens, which act via androgen receptors. Androgens elicit prostatic epithelial growth during fetal and prepubertal periods, and in adulthood androgens act via reciprocal homeostatic stromal-epithelial interactions to maintain functional differentiation and growth quiescence. During carcinogenesis, these reciprocal homeostatic stromal-epithelial interactions are disrupted. In this review, 2 models of prostatic carcinogenesis will be reviewed, both of which emphasize the role of the stromal microenvironment in the carcinogenic process. Hormonal carcinogenesis of the prostate can be elicited by treatment of rats and mice with testosterone plus estradiol (T+E2). Using an immortalized but nontumorigenic human prostatic epithelial cell line (BPH-1), tissue recombinant studies were employed to explore the cellular mechanisms of prostatic carcinogenesis. Accordingly, human BPH-1 prostatic epithelial cells were combined with rat UGM, and the resultant UGM+BPH1 recombinants were grown in adult male nude mouse hosts. In untreated mouse hosts, UGM+BPH1 recombinants produced solid branched epithelial cords and ductal structures exhibiting benign growth. In T+E2-treated hosts, UGM+BPH1 recombinants formed invasive carcinomas. Since BPH-1 cells lack androgen and estrogen receptors, whereas rat UGM expresses both of these receptors, it is proposed that hormonal carcinogenesis is elicited by T+E2 via paracrine mechanisms mediated by the stromal microenvironment. During prostatic carcinogenesis in rats and humans, the periepithelial stroma undergoes progressive loss in smooth muscle with the appearance of carcinoma-associated fibroblasts (CAFs). This abnormal stroma was shown to promote carcinogenesis in genetically abnormal but nontumorigenic epithelial cells. CAF+BPH-1 tissue recombinants grown in male hosts formed carcinomas, whereas benign growth and orderly tissue architecture developed in recombinants composed of normal prostatic stroma+BPH-1. Malignant transformation triggered by CAF was associated with additional genetic alterations and changes in gene expression in the BPH-1 cells. Thus, the stromal microenvironment is a critical determinant of benign versus malignant growth. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR] |
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| Database: | Complementary Index |
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| Items | – Name: Title Label: Title Group: Ti Data: Role of the stromal microenvironment in carcinogenesis of the prostate. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Gerald+R%2E+Cunha%22">Gerald R. Cunha</searchLink><br /><searchLink fieldCode="AR" term="%22Simon+W%2E+Hayward%22">Simon W. Hayward</searchLink><br /><searchLink fieldCode="AR" term="%22Y%2EZ%2E+Wang%22">Y.Z. Wang</searchLink> – Name: TitleSource Label: Source Group: Src Data: International Journal of Cancer; 10/20/2003, Vol. 107 Issue 1, p1, 10p – Name: Subject Label: Subject Terms Group: Su Data: <searchLink fieldCode="DE" term="%22ANDROGENS%22">ANDROGENS</searchLink><br /><searchLink fieldCode="DE" term="%22PROSTATITIS%22">PROSTATITIS</searchLink><br /><searchLink fieldCode="DE" term="%22ENDOCRINOLOGY%22">ENDOCRINOLOGY</searchLink><br /><searchLink fieldCode="DE" term="%22PROSTATE+diseases%22">PROSTATE diseases</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: The topic of this review is the role of stromal-epithelial interactions in normal and malignant prostatic growth. Because cell-cell interactions and androgens play such key roles in the prostate, the goal of this review will be to apply endocrinologic and developmental concepts to the understanding of normal and malignant prostatic growth. Prostatic development is induced by androgens, which act via androgen receptors. Androgens elicit prostatic epithelial growth during fetal and prepubertal periods, and in adulthood androgens act via reciprocal homeostatic stromal-epithelial interactions to maintain functional differentiation and growth quiescence. During carcinogenesis, these reciprocal homeostatic stromal-epithelial interactions are disrupted. In this review, 2 models of prostatic carcinogenesis will be reviewed, both of which emphasize the role of the stromal microenvironment in the carcinogenic process. Hormonal carcinogenesis of the prostate can be elicited by treatment of rats and mice with testosterone plus estradiol (T+E2). Using an immortalized but nontumorigenic human prostatic epithelial cell line (BPH-1), tissue recombinant studies were employed to explore the cellular mechanisms of prostatic carcinogenesis. Accordingly, human BPH-1 prostatic epithelial cells were combined with rat UGM, and the resultant UGM+BPH1 recombinants were grown in adult male nude mouse hosts. In untreated mouse hosts, UGM+BPH1 recombinants produced solid branched epithelial cords and ductal structures exhibiting benign growth. In T+E2-treated hosts, UGM+BPH1 recombinants formed invasive carcinomas. Since BPH-1 cells lack androgen and estrogen receptors, whereas rat UGM expresses both of these receptors, it is proposed that hormonal carcinogenesis is elicited by T+E2 via paracrine mechanisms mediated by the stromal microenvironment. During prostatic carcinogenesis in rats and humans, the periepithelial stroma undergoes progressive loss in smooth muscle with the appearance of carcinoma-associated fibroblasts (CAFs). This abnormal stroma was shown to promote carcinogenesis in genetically abnormal but nontumorigenic epithelial cells. CAF+BPH-1 tissue recombinants grown in male hosts formed carcinomas, whereas benign growth and orderly tissue architecture developed in recombinants composed of normal prostatic stroma+BPH-1. Malignant transformation triggered by CAF was associated with additional genetic alterations and changes in gene expression in the BPH-1 cells. Thus, the stromal microenvironment is a critical determinant of benign versus malignant growth. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR] – Name: Abstract Label: Group: Ab Data: <i>Copyright of International Journal of Cancer is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1002/ijc.11335 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 10 StartPage: 1 Subjects: – SubjectFull: ANDROGENS Type: general – SubjectFull: PROSTATITIS Type: general – SubjectFull: ENDOCRINOLOGY Type: general – SubjectFull: PROSTATE diseases Type: general Titles: – TitleFull: Role of the stromal microenvironment in carcinogenesis of the prostate. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Gerald R. Cunha – PersonEntity: Name: NameFull: Simon W. Hayward – PersonEntity: Name: NameFull: Y.Z. Wang IsPartOfRelationships: – BibEntity: Dates: – D: 20 M: 10 Text: 10/20/2003 Type: published Y: 2003 Identifiers: – Type: issn-print Value: 00207136 Numbering: – Type: volume Value: 107 – Type: issue Value: 1 Titles: – TitleFull: International Journal of Cancer Type: main |
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