Toshiyuki Kamijo

Induction of apoptosis by cyclooxygenase-2 inhibitors in prostate cancer cell lines.

Abstract Prostaglandins are thought to play an important role in the proliferation of prostate cancer and are highly expressed in prostate cancer tissue. Cyclooxygenase‐2 (COX‐2), or prostaglandin endoperoxide synthase, is a key enzyme in the conversion of arachidonic acid into prostaglandin. In several cancers, COX‐2 contributes to the proliferation and metastasis of cancer cells. To assess the role of COX‐2 in prostate cancer, we investigated whether the inhibition of COX‐2 affected the proliferation of prostate cancer cells. The human prostate cancer cell lines, LNCaP and PC 3, and a normal prostate stromal cell line (PrSC) were treated with COX‐2 inhibitors NS 398 and Etodolac. The proliferation rate of the cell lines was examined using 3(4,5‐dimethylethiazoly 1‐2‐) 2,5‐diphonyl tetrazolium bromide (MTT) assays. A DNA fragmentation assay was also used for proof of apoptosis. COX‐2 inhibitors could suppress the proliferation of LNCaP and PC 3 cells. In contrast, PrSC was not affected by COX‐2 inhibitors. These suppressive effects occurred in a time‐ and dose‐dependent manner. One of mechanisms responsible for cell death was apoptosis. COX‐2 seems to play a significant role in the progression of prostate cancer. COX‐2 may be a therapeutic target for prostate cancer. Since COX‐2 inhibitors suppress proliferation and induce apoptosis in prostate cancer cells, and have no effect in normal prostate stromal cells, COX‐2 inhibitors will be useful for the treatment of prostate cancer.

Long‐term outcome of endoscopic biopsy and subsequent nephroureterectomy for upper urinary tract tumor

Abstract Background: Upper urinary tract tumors can be biopsied using a flexible ureterorenoscope. This study examined retrospectively possible adverse effects of this procedure on patient outcome.