Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0282612 (PIN)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinically benign, whole untrimmed prostates were obtained from 104 patients at autopsy, completely sectioned, and examined microscopically. The histological and gross findings of the prostate were correlated with premortem prostatic acid phosphatase levels (PAP, enzymatic method, ACA, Dupont Co.) to determine how often carcinoma of the prostate (CAP) affected PAP levels and to identify other findings within the prostate associated with elevated PAP levels. Sixty (58%) prostates did not have CAP, 34 (33%) had CAP smaller than 1 ml in volume, and 10 (10%) had CAP larger than 1 ml in volume. PAP levels were elevated (greater than 1 U/L) in 8 of 60 (13%) prostates without CAP, in 2 of the 34 (6%) prostates with CAP smaller than 1 ml, and in 1 of the 10 (10%) prostates with CAP larger than 1 ml. These differences were not statistically significant. Likewise, a statistically significant correlation between PAP levels and patient age, patient race, severe inflammation, of high grade prostatic intraepithelial neoplasia (PIN) was not found. However, there was a statistically significant correlation between PAP levels and prostate weight (p < 0.0001). This study suggest that PAP cannot distinguish between patients with clinically undetected CAP and patients without CAP. Furthermore, elevated PAP levels are often not due to metastatic CAP and additional evidence should be present, even in patients with known CAP, before an elevated PAP level is considered to be conclusive evidence of metastatic CAP.
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PMID:Prostatic acid phosphatase levels (enzymatic method) from completely sectioned, clinically benign, whole prostates. 861 55

Biopsy or fine-needle aspiration cytology are the only appropriate methods for detection of prostatic intraepithelial neoplasia (PIN). PIN has been suggested to be a principal precursor of invasive carcinoma of the prostate. Most reports on an association of PIN and invasive prostatic cancer have a follow-up of less than 1 year, indicating that the successively diagnosed cancer most probably was present at the time of diagnosis of PIN. The natural history of PIN is unknown and detection of PIN should therefore not influence therapeutic decisions. If coexistent carcinoma is not found, close surveillance is recommended to identify a possible subsequent cancer at an early stage. Follow-up examinations should be performed at 6-month intervals for 2 years and thereafter annually.
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PMID:Follow-up of prostatic intraepithelial neoplasia. 887 8

Prostatic carcinoma is increasingly diagnosed on small foci of core needle biopsy specimens. What constitutes adequate sampling of this tissue has not been investigated. Two hundred twenty-nine cases were reviewed, which included 47 cores with atypical foci, 22 with high-grade prostatic intraepithelial neoplasia (PIN), and 533 diagnostic of carcinoma. Six core specimens were obtained for each case, and two blocks were prepared containing three cores each. At least three slides containing multiple serial sections were prepared from each block. Ninety-seven percent of atypical foci, 0% of high-grade PIN foci, and 25% of carcinomatous foci comprised less than 5% of the tissue in the core and measured less than 1 mm in greatest dimension. Thirteen percent of atypical foci, 0% of high-grade PIN foci, and 3% of carcinomatous foci were not present on the first slide. In every case, the tissue containing the focus was not present on the first slide. Thirteen percent of atypical foci and 3% of carcinomatous foci are not present on the first slide of prostate core needle biopsy specimens because the tissue containing these foci simply is not cut. As proposed in this report, at least three slides are necessary to detect all lesions.
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PMID:Adequate tissue sampling of prostate core needle biopsies. 929 62

Many anticipate that application of findings in molecular genetics will help to achieve greater precision in defining high-risk populations that may benefit from chemopreventive interventions. We must recognize, however, that genetic susceptibility, environmental factors, and complex gene-environment interactions are all likely to be risk determinants for most cancers. Cohort studies of twins and cancer indicate that having "identical" genes is generally not a very accurate predictor of cancer incidence. Data from twin studies support the suggestion that environmental factors such as tobacco use significantly influence cancer risk. The complexities of the genetic contribution to disease risk are exemplified by the development of Duchenne muscular dystrophy in only one of monozygotic twin girls, hypothesized to be the result of X chromosome inactivation, with the distribution patterns of the X chromosome being skewed to the female X in the manifesting twin and to the male X in the normal twin. Evidence from transgenic and genetic-environmental studies in animals support the possibility of genetic-environmental interactions. Calorie restriction modifies tumor expression in p53 knockout mice; a high-fat, low-calcium, low-vitamin D diet increases prepolyp hyperplasia formation in Apc-mutated mice; and calorie restriction early in life influences development of obesity in the genetically obese Zucker rat (fafa). Such environmental modulation of gene expression suggests that chemoprevention has the potential to reduce risk for both environmentally and genetically determined cancers. In view of the growing research efforts in chemoprevention, the NCI has developed a Prevention Trials Decision Network (PTDN) to formalize the evaluation and approval process for large-scale chemoprevention trials. The PTDN addresses large trial prioritization and the associated issues of minority recruitment and retention; identification and validation of biomarkers as intermediate endpoints for cancer; and chemopreventive agent selection and development. A comprehensive database is being established to support the PTDN's decision-making process and will help to determine which agents investigated in preclinical and early phase clinical trials should move to large-scale testing. Cohorts for large-scale chemoprevention trials include individuals who are determined to be at high risk as a result of genetic predisposition, carcinogenic exposure, or the presence of biomarkers indicative of increased risk. Current large-scale trials in well-defined, high-risk populations include the Breast Cancer Prevention Trial (tamoxifen), the Prostate Cancer Prevention Trial (finasteride), and the N-(4-hydroxyphenyl) retinamide (4-HPR) breast cancer prevention study being conducted in Milan. Biomarker studies will provide valuable information for refining the design and facilitating the implementation of future large-scale trials. For example, potential biomarkers are being assessed at biopsy in women with ductal carcinoma in situ (DCIS). The women are then randomized to either placebo, tamoxifen, 4-HPR, or tamoxifen plus 4-HPR for 2-4 weeks, at which time surgery is performed and the biomarkers reassessed to determine biomarker modulation by the interventions. For prostate cancer, modulation of prostatic intraepithelial neoplasia (PIN) by 4-HPR and difluoromethylornithine is being investigated; similar studies are being planned for oltipraz, dehydroepiandrosterone, and vitamin E plus selenomethionine. The validation of biomarkers as surrogate endpoints for cancer incidence in high-risk cohorts will allow more agents to be evaluated in shorter studies that use fewer subjects to achieve the desired statistical power.
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PMID:Cancer risk factors for selecting cohorts for large-scale chemoprevention trials. 902 95

Primary prostatic duct adenocarcinoma, initially labeled as endometrioid carcinoma of the prostate, is a rare neoplasm that displays exophytic growth into the prostatic urethra with involvement of prostatic ducts. Because this tumour arises from preexisting epithelia, there is a possibility that a remnant basal epithelium may be seen in association with these tumours. If this hypothesis is correct, then prostatic duct adenocarcinoma may possibly be mistaken for high-grade prostatic intraepithelial neoplasia (PIN) on needle biopsies. The distribution of basal cells in this tumour has not been described previously. Nine cases of prostatic duct adenocarcinoma and prostatic adenocarcinoma with focal ductal differentiation were studied immunohistochemically with antibodies specifying cytokeratin 34 beta E12, prostate-specific antigen (PSA), and prostatic acid phosphatase (PAP). All cases were positive for PSA and PAP. In some areas of the tumour in eight cases there was a continuous and discontinuous layer of basal cells surrounding islands of carcinoma. This was found with cribriform, comedo, solid, and papillary components of ductal type adenocarcinoma. It is necessary to be aware of the presence of basal cells in association with primary prostatic duct adenocarcinoma. Differentiation of high-grade PIN from this lesion should depend on complex architectural characteristics and Cytologic features rather than presence of a basal cell layer. This finding confirms that the solid, cribriform, papillary, and comedo components initially grow intraluminally within ducts before invasion into surrounding stroma occurs.
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PMID:Distribution pattern of basal cells detected by cytokeratin 34 beta E12 in primary prostatic duct adenocarcinoma. 913 Sep 90

High-grade prostatic intraepithelial neoplasia (HGPIN) is the most likely precursor proliferation of peripheral zone, moderately to poorly differentiated prostatic adenocarcinomas. The usual cell type of the epithelial lining of HGPIN is a glandular epithelial cell with characteristic nuclear abnormalities. Here we report nine cases of unusual types of HGPIN, including three cases of signet-ring cell HGPIN, one case of small cell neuroendocrine HGPIN, and five cases of HGPIN with distinctive mucinous features. The three examples of signet-ring cell PIN were all associated with an invasive primary signet-ring cell carcinoma of the prostate. The HGPIN assumed a classical tufted and micropapillary architectural growth pattern, with the constituent cells exhibiting a morphologic appearance identical to that of the invasive signet-ring cells. The intraepithelial and invasive signet-ring cells were mucin negative and were immunoreactive for prostate-specific antigen (PSA). A fourth case displayed a mixed intraepithelial glandular-small cell neoplastic proliferation, where intraepithelial small cells were histologically identical to surrounding invasive small cell carcinoma cells. The small cell HGPIN and invasive small cell carcinoma cells were positive for the neuroendocrine markers chromogranin, synaptophysin, and neuron-specific enolase. In five cases, mucinous distension of HGPIN glands, producing a flat pattern of the epithelial lining layer, comprised the third unusual pattern of HGPIN. These blue mucinous secretions were readily detected by hematoxylin and eosin staining and were composed of both neutral (periodic acid-Schiff-positive) and acidic (alcian blue-positive) mucins. Herein we document the existence of an intraepithelial proliferation of neoplastic cell types-small cell neuroendocrine and signet-ring cell-that are usually considered as stromal-invasive cells in the prostate. The presence of these rare prostatic cell types in both HGPIN and invasive carcinoma provides further support for a close relationship between HGPIN and invasive carcinoma of the prostate. All three unusual types of HGPIN-signet-ring cell, small cell neuroendocrine, and mucinous-are important to diagnostically recognize because of the strength of association of HGPIN with invasive carcinoma.
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PMID:Unusual histologic types of high-grade prostatic intraepithelial neoplasia. 933 Dec 95

Prostate cancer screening and early detection efforts have resulted in the identification of smaller volume carcinomas of the prostate. We evaluated the diagnostic features of minimal (< 1 mm) carcinoma in sextant needle biopsy specimens of the prostate and in follow-up analyzed the features of the corresponding carcinomas in the whole gland. We reviewed specimens from 50 consecutive patients who had minimal carcinoma in needle biopsy tissue and who had undergone radical prostatectomy. Histologic grade, tumor size, pathologic stage, and margin status of the 50 carcinomas in the whole gland in which the carcinoma size was minimal in the sextant needle biopsy specimen were compared with those of 50 carcinomas in the whole gland in which carcinoma size was greater than 1 mm in the needle biopsy specimen. The most common morphologic features of these minimal carcinomas were nucleomegaly (96%), infiltrative growth pattern (88%), intraluminal secretions (78%), prominent nucleoli (64%), associated high-grade prostatic intraepithelial neoplasia (40%), amphophilic cytoplasm (36%), hyperchromatic nuclei (30%), and intraluminal crystalloids (22%). Perineural invasion (2%), collagenous micronodules (2%) and mitotic figures (2%) were uncommon. The mean tumor volume in the whole gland of carcinomas corresponding to minimal carcinoma in a needle biopsy specimen was significantly smaller (P=.029) at 1.1 mL than it was in carcinomas with tumor greater than 1 mm in the needle biopsy specimen at 1.6 mL, but other pathologic features of carcinoma in the whole gland were not significantly different. In conclusion, a constellation of morphologic attributes is important for establishment of a diagnosis of minimal carcinoma of the prostate in needle biopsy specimen. Most (82%) of the corresponding prostate cancers in the whole gland were pathologically significant.
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PMID:Minimal carcinoma in prostate needle biopsy specimens: diagnostic features and radical prostatectomy follow-up. 979 35

Small acinar lesions of the prostate may mimic prostate cancer. In the central and transition zone of the prostate, atypical adenomatous hyperplasia (AAH) must be differentiated from low grade carcinoma (Gleason score 2-5). In the dorso-peripheral zone, high grade prostatic intraepithelial neoplasia (PIN) and atypical small acinar proliferations (ASAP) are the most important lesions mimicking carcinoma. Further differentiation is necessary between high grade PIN and intraductal carcinoma. ASAP, on the other hand, may mimic low grade carcinoma. The significance of basal cell type cytokeratin immunohistochemistry (IHC) in the differentiation between ASAP and low grade carcinoma of the prostate was substantiated by additional MIB-1 IHC. The status of the basal cell layer in ASAP was found to be variable (complete, fragmented and absent). Independent of the status of the basal cell layer, the mean MIB-1 proliferation index of ASAP was significantly higher than that of clearly benign lesions and did not differ from that of low grade carcinoma. As carcinoma is frequently detected in rebiopsies, close clinical follow up of patients with ASAP is advisable.
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PMID:Atypical acinar proliferations of the prostate. 1063 13

A variety of small acinar lesions of the prostate may mimick prostate cancer. In the central and transition zone of the prostate atypical adenomatous hyperplasia (AAH) has to be differentiated from low grade carcinoma (Gleason score 2-6). In the dorso-peripheral zone high grade PIN (prostatic intraepithelial neoplasie) and ASAP (atypical small acinar proliferations) represent the most important mimicers of carcinoma. High grade PIN has to be differentiated from intraductal carcinoma, ASAP on the other hand may mimic low grade carcinoma. The significance of basal cell type cytokeratin immunhistochemistry (IHC) in the differentiation between ASAP and low grade carcinoma of the prostate is assessed by additional MIB-1 IHC. The status of the basal cell layer in ASAP was shown to be variable (complete, fragmented and partial loss). Independently from the status of the basal cell layer the mean MIB-1 proliferation index of ASAP was significantly higher than of clearly benign lesions and did not differ from that of low grade carcinoma. Taking into account the high detection rate of carcinoma in repeat biopsies, close clinical follow up of patients with ASAP should be recommended.
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PMID:[Suspicious acinar proliferations of the prostate]. 1071 7

Prior meetings of the International Conference on Neoadjuvant Hormonal Therapy in Prostate Cancer identified areas of concern in the pathologic analysis of post-treatment specimens. In response, a pathology subcommittee was formed to address the questions that had been raised. Recommendations are made here concerning pretreatment biopsy review and reporting, handling and reporting of radical prostatectomy specimens, Gleason scoring of treated cancer, grading of therapy effect, role of immunohistochemistry procedures, and the significance of high-grade prostatic intraepithelial neoplasia. Neoadjuvant trials with both surgery and radiation therapy were considered in drawing up these recommendations.
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PMID:Pathologic Handling and Reporting of Prostate Tissue Specimens in Patients Receiving Neoadjuvant Hormonal Therapy: Report of the Pathology Committee. 1085 23


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