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Literature DB >> 29605661

A Novel Mechanism to Drive Castration-Resistant Prostate Cancer.

Abstract

Androgen receptor signaling is critical for prostate adenocarcinoma, even after androgen deprivation therapy. Persistence of intratumoral androgens has been found in castration-resistant prostate cancer and attributed to increased in situ synthesis. Recently, Sharifi and colleagues reported an additional mechanism that can enhance local androgenic exposure: downregulation of an androgen-inactivating enzyme.

Entities: Chemical Disease Gene Mutation Species

Keywords: DHT; HSD17B4 variant 2; androgen receptor (AR) signaling; castration-resistant prostate cancer; testosterone

Mesh：

Substances：

Year: 2018 PMID： 29605661 PMCID： PMC5960430 DOI： 10.1016/j.tem.2018.03.006

Source DB: PubMed Journal: Trends Endocrinol Metab ISSN： 1043-2760 Impact factor: 12.015

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References

10 in total

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10 in total

A Novel Mechanism to Drive Castration-Resistant Prostate Cancer.

Review 1. Structure and function of human 17beta-hydroxysteroid dehydrogenases.

2. Deletions of the androgen-metabolizing UGT2B genes have an effect on circulating steroid levels and biochemical recurrence after radical prostatectomy in localized prostate cancer.

Review 3. HSD3B1 status as a biomarker of androgen deprivation resistance and implications for prostate cancer.

4. Distinct patterns of dysregulated expression of enzymes involved in androgen synthesis and metabolism in metastatic prostate cancer tumors.

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8. Next generation sequencing with copy number variant detection expands the phenotypic spectrum of HSD17B4-deficiency.

9. Meta-analysis reveals a lack of association between UGT2B17 deletion polymorphism and tumor susceptibility.

10. Loss of an Androgen-Inactivating and Isoform-Specific HSD17B4 Splice Form Enables Emergence of Castration-Resistant Prostate Cancer.