| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
1) We investigated corrlation of androgen receptor (AR) , proliferating cell marker (Ki-67) and histologic grade in prostatic carcinoma using a computer-assisted image analysis system. There was a significant correlation between the histologic grade, and AR and Ki-67 ; however, there was no correlation between the clinical stage and AR or Ki-67.
2) Endocrine differentiation in prostatic carcinoma cells has been considered one of the causes of worse prognosis because of unresponsiveness for hormone therapy. We measured plasma levels of chromogranin A (CgA) by ELISA as an indicator of endocrine differentiation in patients with neuroendocrine tumors (NET), and prostatic carcinoma (PC) and benign prostatic hyperplasia (BPE). There were significant differences between plasma levels of CgA in BPH and NET (P<0.001), and between the levels in PC and NET (P<0.01). of the 33 patients with prostatic carcinoma, five had elevated CgA in which only one had elevated PSA.We concluded that CgA is an excellent marker for NET,and measurement of CgA is also useful to detect prostatic carcinoma in patients whose PSA is not elevated.
3) We analyzed growth factors ; IGF-1, EGFR,BMP2, and TIMP-II in prostatic carcinomas in 50 prostatic carcinomas. IGF-I was detected in both tumor cells and stromal cells. EGFR was detected only in the epithelial cells, especially strong in the basal cells. BMP2 and TIMP-II were detected in only the stromal cells. In conclusion, all above growth factors mediate growth of prostatic carcinoma.
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