Luteinizing hormone and follicle-stimulating hormone are called gonadotropins, because they stimulate the gonads - in males the testes and in females the ovaries. They are not necessary for life, but are essential for reproduction. In addition, the association of these hormones with prostate cancer has been the interest of many researchers. Their detection in the human prostate has been investigated using different methods, including immunologic and RT-PCR techniques. In addition, the increasing evidence of paracrine/autocrine functions of the gonadotropic glycoprotein hormones, their allocation to the superfamily of cystine knot growth factors, and luteinizing hormone/chorionic gonadotropin receptor gene expression in non-gonadal tissues led many researchers to investigate intraprostatic glycoprotein hormones and their receptor gene expression. We aim in this review to shed light on the physiology of the gonadotropins and their association with prostate cancer and highlight the future possibilities of their use as targets in treating this disease. Copyright (c) 2006 S. Karger AG, Basel.

The effects of irradiation are commonly evident in a range of specimens dealt with by pathologists in routine clinical practice. Radiotherapy is frequently employed in the treatment of human malignancies and often patients will subsequently require surgery or, at least, tissue sampling to assess complications or recurrent tumour. Therefore, it is critical that all those involved in reporting of these specimens are aware of the range of effects that may occur in cells or tissues after irradiation. The most consistent changes seen after irradiation can be separated into early and late groups. The former result primarily from direct cellular toxicity with apoptosis and necrosis together with small vessel damage leading to endothelial cell injury, increased vascular permeability and stromal oedema. The chronic or delayed effects are dominated by degeneration and repair when morphological cellular abnormalities such as epithelial nuclear atypia and multinucleate stromal fibroblasts develop. At this later stage the vascular damage becomes more severe with intimal thickening, medial hyalinization, fibrinoid necrosis, luminal thrombosis and endarteritis obliterans. The vascular damage leads to ischaemic compromise with further stromal collagenous fibrosis and parenchymal atrophy. Rarely, malignant tumours may develop in the irradiated tissue after a latent period of several years. More detailed descriptions of specific tissue damage and mechanisms of radiation-induced injury are discussed.