Expression of cyclin D1, CDK4 and p27KIP1 is associated with the p16MTS1 gene status in human esophageal carcinoma cell lines.

p16MTS1/INK4A negatively regulates cell cycle progression by inhibiting the cyclin D/CDK4 complex that phosphorylates pRb. Frequent homozygous deletions of the p16 gene were recently found in various tumor cell lines. We examined the relationship between the genetic status of p16 and the expression of the cell cycle regulating molecules in human esophageal carcinoma cell lines.

[Low-dose FP (5-FU+low-dose CDDP) therapy for far advanced upper gastro-intestinal carcinoma].

Low-dose FP therapy was undertaken in 25 patients with far advanced or recurrent carcinoma (13 stomach, 7 esophagus, 3 colon, 1 gallbladder, 1 pancreas). This therapy consisted of intermittent infusion of CDDP (10 mg/body X 5 days) and continuous infusion of 5-FU (500 mg/body X 5 days) for 5 days with 2-day intervals. Patients were treated with at least 2 courses of low-dose FP therapy.

Xanthogranulomatous cholecystis. Cell composition and a possible pathogenetic role of cell-mediated immunity.

Thirty-three cases of xanthogranulomatous cholecystitis (XGC) exhibiting the typical morphologic features were studied by light and electron microscopy and immunohistochemical techniques. Incidence of XGC was 4.2% of the surgically resected gallbladder diseases.

Biomodulation by hyperthermia of topoisomerase II-targeting drugs in human colorectal cancer cells.

We examined whether heat stress could enhance the sensitivity of human colon cancer WiDr cells to topoisomerase II-targeting anticancer agents, etoposide (VP-16) and teniposide (VM-26), and also determined the most effective timing for the drug administration after exposure to hyperthermia. Both topoisomerase II contents and topoisomerase II activity were significantly increased in WiDr cells 3 to 12 h after heat stress at 43 degrees C for 1 h, in comparison with those immediately after the heat stress. Cytotoxicity by VP-16 was most significantly enhanced 3 to 12 h after exposure to 43 degrees C for 1 h, but no synergistic effect was observed when the drug was administered immediately after the heat stress.