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Literature DB >> 26446945

Germline Variants in Asporin Vary by Race, Modulate the Tumor Microenvironment, and Are Differentially Associated with Metastatic Prostate Cancer.

Paula J Hurley¹, Debasish Sundi², Brian Shinder², Brian W Simons³, Robert M Hughes², Rebecca M Miller², Benjamin Benzon², Sheila F Faraj⁴, George J Netto⁴, Ismael A Vergara⁵, Nicholas Erho⁵, Elai Davicioni⁵, R Jeffrey Karnes⁶, Guifang Yan², Charles Ewing², Sarah D Isaacs², David M Berman⁷, Jennifer R Rider⁸, Kristina M Jordahl⁸, Lorelei A Mucci⁸, Jessie Huang⁹, Steven S An¹⁰, Ben H Park¹¹, William B Isaacs², Luigi Marchionni¹², Ashley E Ross¹³, Edward M Schaeffer¹⁴.

Abstract

PURPOSE: Prostate cancers incite tremendous morbidity upon metastatic growth. We previously identified Asporin (ASPN) as a potential mediator of metastatic progression found within the tumor microenvironment. ASPN contains an aspartic acid (D)-repeat domain and germline polymorphisms in D-repeat-length have been associated with degenerative diseases. Associations of germline ASPN D polymorphisms with risk of prostate cancer progression to metastatic disease have not been assessed. EXPERIMENTAL
DESIGN: Germline ASPN D-repeat-length was retrospectively analyzed in 1,600 men who underwent radical prostatectomy for clinically localized prostate cancer and in 548 noncancer controls. Multivariable Cox proportional hazards models were used to test the associations of ASPN variations with risk of subsequent oncologic outcomes, including metastasis. Orthotopic xenografts were used to establish allele- and stroma-specific roles for ASPN D variants in metastatic prostate cancer.
RESULTS: Variation at the ASPN D locus was differentially associated with poorer oncologic outcomes. ASPN D14 [HR, 1.72; 95% confidence interval (CI), 1.05-2.81, P = 0.032] and heterozygosity for ASPN D13/14 (HR, 1.86; 95% CI, 1.03-3.35, P = 0.040) were significantly associated with metastatic recurrence, while homozygosity for the ASPN D13 variant was significantly associated with a reduced risk of metastatic recurrence (HR, 0.44; 95% CI, 0.21-0.94, P = 0.035) in multivariable analyses. Orthotopic xenografts established biologic roles for ASPN D14 and ASPN D13 variants in metastatic prostate cancer progression that were consistent with patient-based data.
CONCLUSIONS: We observed associations between ASPN D variants and oncologic outcomes, including metastasis. Our data suggest that ASPN expressed in the tumor microenvironment is a heritable modulator of metastatic progression. ©2015 American Association for Cancer Research.

Entities: CellLine Chemical Disease Gene Species

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Year: 2015 PMID： 26446945 PMCID： PMC4715968 DOI： 10.1158/1078-0432.CCR-15-0256

Source DB: PubMed Journal: Clin Cancer Res ISSN： 1078-0432 Impact factor: 12.531

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2. Expression pattern and gene characterization of asporin. a newly discovered member of the leucine-rich repeat protein family.

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5. Natural history of progression after PSA elevation following radical prostatectomy.

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8. Correlation of pathologic findings with progression after radical retropubic prostatectomy.

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Review 9. Explaining racial differences in prostate cancer in the United States: sociology or biology?

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10. TGF-beta signaling in fibroblasts modulates the oncogenic potential of adjacent epithelia.

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2. Asporin Restricts Mesenchymal Stromal Cell Differentiation, Alters the Tumor Microenvironment, and Drives Metastatic Progression.

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3. Asporin Interacts With HER2 to Promote Thyroid Cancer Metastasis via the MAPK/EMT Signaling Pathway.

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4. Prognostic Utility of a New mRNA Expression Signature of Gleason Score.

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5. The dual role of asporin in breast cancer progression.

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