Prostate adenocarcinoma is the second most frequent cancer worldwide and is one of the leading causes of male cancer-related deaths. However, it varies greatly in its behaviour, from indolent non-progressive disease to metastatic cancers with high associated mortality. The aim of this study was to identify predictive biomarkers for patients with localised prostate tumours most likely to progress to aggressive disease, to facilitate future tailored clinical treatment and identify novel therapeutic targets. The expression of 602 genes was profiled using oligoarrays, across three prostate cancer cell lines: CA-HPV-10, LNCaP and PC3, qualitatively identifying several potential prognostic biomarkers. Of particular interest was six transmembrane epithelial antigen of the prostate (STEAP) 1 and STEAP 2 which was subsequently analysed further in prostate cancer tissue samples following optimisation of an RNA extraction method from laser captured cells isolated from formalin-fixed paraffin-embedded biopsy samples. Quantitative analysis of STEAP1 and 2 gene expression were statistically significantly associated with the metastatic cell lines DU145 and PC3 as compared to the normal prostate epithelial cell line, PNT2. This expression pattern was also mirrored at the protein level in the cells. Furthermore, STEAP2 up-regulation was observed within a small patient cohort and was associated with those that had locally advanced disease. Subsequent mechanistic studies in the PNT2 cell line demonstrated that an over-expression of STEAP2 resulted in these normal prostate cells gaining an ability to migrate and invade, suggesting that STEAP2 expression may be a crucial molecule in driving the invasive ability of prostate cancer cells.
Objectives To determine the incidence of testicular microlithiasis in men presenting for testicular ultrasonography, to identify any associated pathology (with particular reference to testicular neoplasia) and to report the follow‐up of those patients in whom testicular microlithiasis was identified. Patients and methods In this retrospective study, the results of all testicular ultrasonography undertaken between July 1995 and March 1998 in a district general hospital were reviewed. The records of all patients diagnosed ultrasonographically to have testicular microlithiasis were retrieved and the pathology database was accessed for all testicular tumours diagnosed in the same period. Results During the study period 2215 scans were taken; 34 cases of testicular microlithiasis were identified, giving an incidence of 1.4%. Thirty‐one testicular tumours were removed during the same period. Of the 34 cases with testicular microlithiasis, five had histologically confirmed testicular tumours (15%). The incidence of testicular tumours in the scans showing no microlithiasis was 26 in 2181 (1.1%). The differential incidence of tumours in the two groups is statistically significant (P < 0.001, chi‐square analysis). Patients with testicular microlithiasis but no tumour were followed up for a median (range) of 41 (19–54) months; no interval tumours have developed to date. Conclusion This study confirms an incidence of testicular microlithiasis comparable with that in other reported series, albeit in a selected population. There was a strong association between testicular microlithiasis and testicular tumours. Whether this is a causal relationship has yet to be determined. Careful clinical and ultrasonographic follow‐up of these patients is therefore recommended until the significance of testicular microlithiasis is clear.
These findings indicate that a model in which there is increasing in situ dysplasia before the development of stromal invasion is incorrect for breast carcinoma. Rather, in most cases, well-differentiated DCIS probably gives rise to low grade invasive breast carcinoma with a better long term clinical outcome. These data suggest that many of the important prognostic biologic and genetic characteristics of breast carcinoma are already established in the neoplastic clones of malignant cells at the preinvasive stage of the disease.
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