Use of tissue ink to maintain identification of individual cores on needle biopsies of the prostate.

BACKGROUND: There is an increasing necessity to extract the maximum amount of information, beyond even a cancer diagnosis, from prostate biopsies. Thus, maintaining site-specific information regarding individual biopsy cores might be critical. AIM: To evaluate the applicability of employing tissue ink to maintain the identity of individual prostatic biopsy cores. METHOD: In this ongoing study, 12 core prostate biopsy specimens are sent to the laboratory in individual pots labelled according to anatomical site. The specimens are placed in two separate multi-compartment cassettes. They are inked with different colours to identify the site of origin from each lobe. The cassettes are then processed with a single paraffin block for each side; the six cores from each side can be mounted on a single slide. RESULTS: The different colours used adhere well to the biopsy cores, thus maintaining the identity of each core. Six cores from each side are embedded in a single paraffin block and examined on a single slide, making it cost-effective, while maintaining high quality, accurate histopathological information. CONCLUSION: Differential inking of prostate biopsy cores is an easily applicable method that is cost-effective and provides tumour location information. Prostate biopsy data archived to maintain individual core information might be used to determine applicability of such information to predict extra-capsular extension by correlating with imaging and radical prostatectomy findings, and for treatment planning.

Torsion of the epididymis: a rare cause of acute scrotum.

Acute scrotum is a common clinical problem and establishing its etiology can be difficult, often necessitating scrotal exploration. We report here a very rare case of acute scrotum: torsion of the epididymis. Only one such case has been reported previously in the literature.

Loss of HLA class I expression in prostate cancer: implications for immunotherapy.

OBJECTIVES: There is currently no reliable predictor of the metastatic potential of apparently localized prostate cancer in an individual patient or satisfactory treatment for patients with advanced disease. One of the factors that may influence tumor progression is the cellular arm of the immune response, and central to this is the human leukocyte antigen (HLA) system, which acts to restrict T-cell recognition of potential tumor antigens. It has been reported in some cancers that down regulation of HLA class I expression by the tumor cells is associated with poor prognosis. In this report, HLA class I and II expression have been investigated in both benign and malignant prostate disease, first to define the extent of altered HLA expression and second to assess whether HLA expression may be related to disease progression. METHODS: HLA expression was assessed by immunohistochemistry utilizing a set of monoclonal antibodies that recognize both monomorphic determinants and the commoner HLA class I allelic products. RESULTS: In contrast to the normal HLA class I expression of the benign tissue, complete loss of HLA class I expression occurred in 34% of primary prostate cancers and 80% of lymph node metastases. When individual allelic expression was assessed, the minimum estimate of down regulation was 85% in the primary prostate cancers and 100% of the metastases. CONCLUSIONS: This investigation has demonstrated a higher rate of HLA class I loss than has been reported in other tumors and would suggest that the immune system may have an important role in the progression of prostate cancer, as well as having implications for the design and success of immunotherapy regimens in advanced disease.

Feedback effects of steroids and gonadotrophin control in adult rats with streptozotocin-induced diabetes mellitus.

The effects of long-and short-term streptozotocin-induced diabetes mellitus on the control of gonadotrophin secretion have been investigated in adult intact rats. A high dose of streptozotocin (80 mg/kg), administered intraperitoneally 3 days before experimentation, inhibited ovulation and reduced the pituitary luteinizing hormone response to luteinizing hormone releasing hormone in proestrous rats. A lower dose (40 mg/kg) did not inhibit ovulation but abolished the luteinizing hormone releasing hormone-priming effect on the pituitary which normally occurs on proestrus, prior to ovulation. Oestrous cyclicity was lost when diabetes was induced for 14 or 56 days, but there was no effect on pituitary responsiveness to luteinizing hormone-releasing hormone compared with control animals. Similar observations were made with rats placed on a food-restricted diet. In all experiments there was no difference between diabetic and control animals in the pituitary luteinizing hormone content, the hypothalamic content of luteinizing hormone-releasing hormone or the ovarian weights. Ovariectomized rats treated with streptozotocin (40 mg/kg) were used to investigate the effects of diabetes on steroid feedback mechanisms. There was an attenuated luteinizing hormone response to ovariectomy in diabetic compared with control animals, and an impaired positive feedback effect of progesterone in oestrogen-primed animals. The results show that streptozotocin-induced diabetes mellitus inhibits feedback action of gonadal steroids and this could account for both the loss of oestrous cyclicity and the reduced pituitary sensitivity to luteinizing hormone-releasing hormone.