An appraisal of the Food and Drug Administration warning on urogynecologic surgical mesh.

Currently, there is no consensus on the use of mesh in transvaginal surgical repairs for the treatment of pelvic organ prolapse. This review recapitulates and assesses the recent U. S. Food and Drug Administration (FDA) warnings about the use of surgical mesh in transvaginal pelvic organ prolapse repair and summarizes the responses of the national organizations that represent the health care providers most invested in treating patients with transvaginal surgical mesh. Mesh exposure or extrusion through the vaginal wall, true mesh erosion into viscera, and infection are the major complications that are currently used to define the safety of synthetic mesh use. Other potential adverse postsurgical outcomes that can affect quality of life, sexual function, and patient satisfaction include dyspareunia, "hispareunia" (ie, complaints of a sexual partner), prosthetic contraction or prominence, vaginal shortening, pelvic pain, urinary dysfunction, and failure of the repair. These outcomes are frequently attributed to mesh use, and can result in expense, frustration, and the need for further medical and surgical interventions for patients undergoing treatment for pelvic floor disorders. Information regarding the FDA's reports on the use of surgical mesh in pelvic organ prolapse repair should be made available to patients at the time of surgical planning and should be used as an adjunct in the process of obtaining informed consent.

Prolactin overexpression by MDA-MB-435 human breast cancer cells accelerates tumor growth.

Prolactin (PRL) is an important hormone in mammary tumorigenesis in rodents but its involvement in human breast cancer has been controversial. A role for locally produced PRL in breast carcinogenesis is suggested by its mitogenic action on breast cancer cells and the expression of both PRL and its receptor (PRL-R) in breast carcinomas. Our objective was to examine whether PRL, overexpressed by breast cancer cells, forms an autocrine/paracrine loop that confers a growth advantage for tumors. MDA-MB-435 breast cancer cells overexpressing 23K human PRL were generated, and PRL production and secretion by the clones were confirmed by RT-PCR, western blotting, and the Nb2 bioassay; control clones contain vector only. In vitro the 23K PRL clones proliferated faster and expressed higher levels of the PRL-R protein than controls only when incubated in charcoal-stripped serum (CSS) devoid of lactogenic hormones. When injected into the mammary fatpad of female nude mice or subcutaneously into males, the PRL-overexpressing clones formed tumors that grew 2-4-fold faster than tumors derived from control clones or wild type MDA-MB-435 cells. Western analysis demonstrated significantly higher PRL, PRL-R, and bcl-2 levels in the tumors overexpressing PRL compared to control tumors. These data support a role for breast PRL as a growth/anti-apoptotic factor and suggest that it may serve as a novel therapeutic target for the treatment of breast cancer.