期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 160, 期 1, 页码 219-226出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)64365-9
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- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [P30HD018968] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [P01CA077739, R01CA064865] Funding Source: NIH RePORTER
- NCI NIH HHS [R01-CA-64865, R01 CA064865, P01 CA077739, P01-CA-77739] Funding Source: Medline
- NIA NIH HHS [R01-AG-11343] Funding Source: Medline
- NICHD NIH HHS [P30-HD-18968] Funding Source: Medline
Androgen receptor expression was analyzed in the CWR22 human prostate cancer xenograft model to better understand its role In prostate cancer recurrence after castration. In androgen-dependent tumors, 98.5% of tumor cell nuclei expressed androgen receptor with a mean optical density of 0.26 +/- 0.01. On day 2 after castration androgen deprivation decreased immunostained cells to 2% that stained weakly (mean optical density, 0.16 +/- 0.08). Cellular proliferation measured using Ki-67 revealed <1% immunostained cells on day 6. Androgen receptor immunostained cells increased to 63% on day 6 and 84% on day 32 although immunostaining remained weak. Cellular proliferation was undetectable beyond day 6 after castration until multiple foci of 5 to 20 proliferating cells became apparent on day 120. These foci expressed increased levels of prostate-specific antigen, an androgen receptor-regulated gene product. In tumors recurrent 150 days after castration androgen receptor-immunostaining intensity was similar to CWR22 tumors from Intact mice although the percentage of cells immunostained was more variable. The appearance of proliferating tumor cells that expressed androgen receptor and prostate-specific antigen 120 days after castration suggests that these cells represent the origin of recurrent tumors.
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