Diagnosis of adenocarcinoma in prostate needle biopsy tissue

Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA.
Journal of Clinical Pathology (Impact Factor: 2.92). 02/2007; 60(1):35-42. DOI: 10.1136/jcp.2005.036442
Source: PubMed


Prostate cancer is a major public health problem throughout the developed world. For patients with clinically localised prostate cancer, the diagnosis is typically established by histopathological examination of prostate needle biopsy samples. Major and minor criteria are used to establish the diagnosis, based on the microscopic appearance of slides stained using haematoxylin and eosin. Major criteria include an infiltrative glandular growth pattern, an absence of basal cells and nuclear atypia in the form of nucleomegaly and nucleolomegaly. In difficult cases, basal cell absence may be confirmed by immunohistochemical stains for high-molecular-weight cytokeratins (marked with antibody 34betaE12) or p63, which are basal cell markers. Minor criteria include intraluminal wispy blue mucin, pink amorphous secretions, mitotic figures, intraluminal crystalloids, adjacent high-grade prostatic intraepithelial neoplasia, amphophilic cytoplasm and nuclear hyperchromasia. Another useful diagnostic marker detectable by immunohistochemistry is alpha-methylacyl coenzyme A racemase (AMACR), an enzyme selectively expressed in neoplastic glandular epithelium. Cocktails of antibodies directed against basal cell markers and AMACR are particularly useful in evaluating small foci of atypical glands, and in substantiating a diagnosis of a minimal adenocarcinoma. Reporting of adenocarcinoma in needle biopsy specimens should always include the Gleason grade and measures of tumour extent in the needle core tissue. Measures of tumour extent are (1) number of cores positive for cancer in the number of cores examined, (2) percentage of needle core tissue affected by carcinoma and (3) linear millimetres of carcinoma present.

    • "the cancer expressed antigen AMACR (Humphrey, 2007; Dabir et al., 2012). Given that prostate basal cells express ΔNp63, detecting these isoforms rather than pan-p63 staining shows higher specificity, although there are potential problems with antibody quality and background staining of the currently employed polyclonal reagents (Sailer et al., 2013). "
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    ABSTRACT: p63 and p73, the two other members of the p53 family, were identified almost 15 years ago. Here, we review their potential use for diagnosis, prognosis and prediction of response to therapy in various cancers. The two genes show distinct expression patterns in both normal and cancer tissues and each gene gives rise to multiple protein isoforms with different activities, including those with tumour-suppressor or oncogenic effects. Despite such complexity, some common themes emerge; p63 is commonly over-expressed as the ΔNp63 isoform and sometimes associated with TP63 amplification, whereas p73 is often reduced (by methylation or gene loss), or there is an increase in the ratio of ΔNp73 to TAp73. These generalisations do not apply universally; TAp63 is overexpressed in haematological malignancies, TP63 mis-sense mutations have been reported in squamous cancers and TP63 translocations occur in lymphomas and some lung adenocarcinomas. There are associations with disease prognosis and response to specific therapies in individual cancer types for both p63 and p73, making their analysis of clinical relevance. We also discuss their utility for aiding in differential diagnosis, which has been demonstrated for p63, but not yet for p73. Throughout, we highlight the discrepant nature of many studies due to the variable methodologies employed, the lack of systematic evaluation of isoforms and the problems of poor antibody characterization and cross-reactions within the p63/p73 family. Finally, we emphasize the value of recently developed isoform-specific reagents that have clear advantages for the study of p63 and p73 experimentally and clinically. (247 words).
    No preview · Article · Dec 2014 · Histology and histopathology
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    • "underdiagnosis of a small focus of prostatic adenocarcinoma might delay early treatment and cause severe adverse consequences for patients. Therefore, a PCa specific marker could be be of great importance and usefulness to adjunct to facilitate critical diagnostic decisions with high sensitivity and specificity [4]. "
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    ABSTRACT: Alpha-methylacyl-CoA racemase (AMACR) is a mitochondrial and peroxisomal enzyme that is overexpressed in prostate cancer. The aim of this study was to confirm and expand the findings that the PCa risk increased in men associated with AMACR expression across various geographic regions. A systematic search of databases was carried out and other relevant articles were also identified. Then the meta-analyses were conducted according to the standard guidelines. A total of 22 studies with 4,385 participants were included on the basis of inclusion criteria. AMACR by IHC was significantly associated with increased diagnosis of PCa (OR = 76.08; 95% CI, 25.53-226.68; P<0.00001). Subgroup-analysis showed that findings didn't substantially change when only Caucasians or Asians (OR = 51.23; 95% CI, 19.41-135.24; P<0.00001) were considered. Expression of AMACR by PCR in relation to PCa risk suggested that AMACR was associated with PCa (OR = 33.60; 95% CI, 4.67-241.77; P<0.00001). There was also no significant publication bias observed. Our findings provide further evidences that the expression of AMACR contribute to PCa risk. AMACR protein overexpression was found in prostate cancers, low expression in any of the normal tissues or in benign prostatic tissue. AMACR is potentially an important prostate tumor marker.
    Full-text · Article · Dec 2013 · PLoS ONE
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    • "It has been reported that, in prostate, putative stem/progenitor cells can reside in CK5(+) 8(−) basal cells. A diagnostic feature of human prostate cancer is the loss of basal cells [108], indicating cancer origin cells as basal cells. In BPH, CD133(+) cells expressed genes related to undifferentiated cells such as TDGF1 (teratocarcinoma-derived growth factor 1) and targets of the Wnt and Hedgehog developmental pathways, whereas CD133(−) cells showed upregulation of genes related to proliferation and metabolism. "
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    ABSTRACT: Benign Prostate hyperplasia (BPH) and prostate cancer (PCa) are the most common prostatic disorders affecting elderly men. Multiple factors including hormonal imbalance, disruption of cell proliferation, apoptosis, chronic inflammation, and aging are thought to be responsible for the pathophysiology of these diseases. Both BPH and PCa are considered to be arisen from aberrant proliferation of prostate stem cells. Recent studies on BPH and PCa have provided significant evidence for the origin of these diseases from stem cells that share characteristics with normal prostate stem cells. Aberrant changes in prostate stem cell regulatory factors may contribute to the development of BPH or PCa. Understanding these regulatory factors may provide insight into the mechanisms that convert quiescent adult prostate cells into proliferating compartments and lead to BPH or carcinoma. Ultimately, the knowledge of the unique prostate stem or stem-like cells in the pathogenesis and development of hyperplasia will facilitate the development of new therapeutic targets for BPH and PCa. In this review, we address recent progress towards understanding the putative role and complexities of stem cells in the development of BPH and PCa.
    Full-text · Article · Jul 2013
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