The objective of this work was to assess the correlation between microvessel density (MVD), pathological stage and disease recurrence in a series of patients who underwent radical prostatectomy for prostate cancer. Pathological material from 75 consecutive radical prostatectomies performed before 1994 without neoadjuvant treatment, in which sufficient follow-up data were available, was reexamined. Paraffin embedded material was re-cut and hematoxylin and eosin (H&E) stained. Areas of maximal angiogenesis within tumor were identified. Expression of CD34 was investigated by using the monoclonal antibody MY 10. Within the areas of maximal angiogenesis, microvessels expressing CD34 were counted and specimens were divided into two groups, one showing a count of less than 90 microvessels per microscopic field at 2006magnification (MVD < 90), the second more than 90 microvessels (MVD > 90). The MVD was then related to pathological stage, Gleason score (GS) and outcome of the disease. Mean followup was 84 months. Clinical or biochemical progression was observed in 38.6% of patients. In low GS cases, MVD was always < 90, whereas in GS 5 -6, half had MVD < 90 and half were > 90. In high GS MVD was always > 90. MVD was positively associated with a higher pathological stage. Progression of the disease was observed in 20% of MVD < 90 and in 51% in MVD > 90 (P ¼ 0.006). MantelHaensz test showed a correlation between MVD and time to progression (P < 0.05). Although problems exist in methods of counting and in the cut-off number of vessels, which can discriminate the risk categories, it may be concluded that microvessel counts, using CD34 monoclonal antibody, can accurately predict the outcome of radical prostatectomy.

Gonadotropin-releasing hormone (GnRH), which is a well-known regulator of gonadotroph function, has recently been considered to be a paracrine factor involved in the control of somatotroph, lactotroph, and corticotroph cells. GnRH action is initiated by binding to a specific cell surface receptor, the gonadotropin-releasing hormone receptor (GnRHR), which is expressed by follicle-stimulating hormone/luteinizing hormone (FSH/LH) cells. Using in situ hybridization techniques, GnRHR messenger ribonucleic acid (mRNA) has recently been detected in normal human anterior pituitary gland and in various pituitary adenomas, including FSH/LH-cell, growth hormone (GH)-cell, adrenocorticotropic hormone (ACTH)-cell, and null-cell adenomas. However, immunohistochemical studies indicating the specific cell distribution of GnRHR in normal pituitary cells have never been reported. The aim of the present investigation was to evaluate the immunohistochemical expression of GnRHR in different types of normal pituitary cells and related tumors. Using double-label immunohistochemical techniques on formalin-fixed and paraffin-embedded tissues and specific antibodies directed against pituitary hormones and GnRHR, we found GnRHR immunoreactivity not only in FSH/LH cells, but also in GH- and thyroid-stimulating hormone (TSH) cells. GnRHR was detected in FSH/LH-cell, GH-cell, mixed GH- and prolactin (PRL)-cell, and alpha-subunit (alpha-SU)/null-cell adenomas. The findings of this study suggest that the interaction between GnRH and GnRHR may play a role in paracrine/autocrine regulation of different types of normal pituitary cells and pituitary adenomas.

criteria reduced the list to nine that were significantly over-expressed and 23 that were under-expressed. These significant genes belonged to the families of oncogenes, growth factors, interleukins, receptors, immune system components, cytoskeleton, matrix proteins and intracellular modulators, or they coded for proteins involved in DNA transcription and RNA translation, DNA repair, protein turnover, and metabolism of carbohydrates and lipids. There were differences in gene expression according to the presence or absence of granular cells and according to tumour grade. Using quantitative real-time PCR there was overexpression of epidermal growth factor receptor, c-myc , transforming growth factor-α , vascular endothelial growth factor and vimentin, and under-expression of TYRO3 protein tyrosine kinase. The von HippelLindau gene was under-expressed but not significantly. CONCLUSIONSA procedure for collecting and storing fresh renal tissue and subsequent gene expression profiling of RCC and normal renal tissue was established. A commercially available DNA macroarray coupled with the significance analysis of macroarrays allowed the identification of sets of differentially expressed cancer-related genes that were characteristic of RCC, compared with apparently normal renal tissue, and which distinguished among subgroups divided according to tumour grade and histological subtype. Quantitative PCR is important to validate the results of macroarray experiments.

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