Gonadotropin levels in ovarian cyst fluids: a predictor of malignancy?

Gonadotropins can stimulate ovarian cancer growth in cell cultures. Corresponding LH/hCG receptors have been demonstrated in ovarian cancer. However, reduction of elevated serum gonadotropins by GnRH analogs in ovarian cancer patients did not lead to growth restriction, which means that serum levels of gonadotropins may not play the most important role in ovarian cancer. We therefore analyzed the LH and FSH concentrations in cyst fluids of ovarian cancer. Patients with preoperatively diagnosed cystic ovarian tumors were eligible for the study. Serum samples of the patients were obtained during surgery, while the fluids within the cysts were aspirated after surgical removal of the tumor. FSH and LH levels in serum and cyst fluids were measured using single antibody EIA (Boehringer Mannheim GmbH, Germany). Cyst fluids and sera of 108 patients were evaluated. While there were no significant differences in the FSH and LH serum concentrations, highly significant differences in the FSH and LH levels in cyst fluids were found. Only cancer cysts contained FSH and LH, while the corresponding concentrations in benign cysts were always below the measuring range of the assays. This clear division between high gonadotropin levels in cysts of serous ovarian cancer and low or absent concentrations in benign ovarian tumors further supports the hypothesis that FSH and LH may play a role in ovarian cancer; however, explanations for this surprising finding are still lacking.

The liver eliminates T cells undergoing antigen-triggered apoptosis in vivo.

Deletion of mature peripheral T cells may result from TCR ligation by bacterial enterotoxins, endogenous provirus-encoded superantigens, and peptide antigens. But the ultimate fate of deleted T cells is not clear. Using a line of T cell receptor transgenic mice injected with antigenic peptide, we have documented that peripheral deletion is accompanied by the induction of abortive T cell activation followed by the disappearance of transgene-positive T cells. As these T cells disappear from the lymph nodes and spleen, they accumulate in the liver, where they undergo apoptosis. This is likely to be a general clearance pathway for T cells that are programmed to undergo apoptosis in vivo, and it may further explain the expansion of the intrahepatic T cell pool in mice with genetic defects in the T cell apoptosis mechanism, such as the lpr mutant.