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)

The detection rate of organ-confined prostate cancer by digital rectal examination (DRE), serum prostate-specific antigen (PSA), and transrectal ultrasound (TRUS) of the prostate, as well as the value of a directed, guided transrectal core biopsy for the prostate (TRUS-guided biopsy) combined with systematic biopsy, were evaluated. The subjects were 171 patients with urinary symptoms suggestive of prostatic disease excluding those with clinical stage C and D prostate cancer. Twenty-five patients (14.6%) had prostate cancer, 127 (74.2%) had benign prostate hypertrophy, four (2.3%) had prostatic intraepithelial neoplasia, eleven (6.4%) had inflammation, and four (2.3%) had normal prostate tissue. The incidence of detection of hypoechoic findings by TRUS in the patients in whom nodules were detected by DRE or who had elevated serum PSA was higher than that in patients with negative diagnostic findings. In 22 of the 25 patients with prostate cancer, the cancer was detected by recognition of a hypoechoic area on TRUS. In 10 of these 22 patients, prostate cancer was also detected by systematic biopsy in isoechoic areas. Prostate cancer was detected by systematic biopsy in three patients without hypoechoic findings. The positive predictive value for patients with abnormal findings on all three tests was 64.3%, which is significantly higher than that for patients with any other combination of findings (p < 0.05). Our results indicate that the combination of DRE, serum PSA and TRUS is useful for the detection of organ-confined prostate cancer, and that TRUS and TRUS-guided prostate biopsy combined with systematic biopsy should be performed in patients with abnormal findings for both DRE and PSA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of digital rectal examination, serum prostate-specific antigen, transrectal ultrasonography and systematic prostate biopsy for the detection of organ-confined prostate cancer. 755 83

The pathogenetic relationship between high-grade prostatic intraepithelial neoplasia (PIN), prostatic carcinoma, and metastases is poorly understood. We used fluorescence in situ hybridization (FISH) with centromere-specific probes for chromosomes 7, 8, 10, 12, and Y to evaluate numeric chromosomal anomalies in PIN (68 foci), localized prostatic carcinoma (78 foci), and lymph node metastases (8 foci) in 40 whole-mount radical prostatectomy and pelvic lymphadenectomy specimens. Chromosomal anomalies were found in 50, 51, and 100% of the foci of PIN, carcinoma, and metastases, respectively. The mean numbers of abnormal chromosomes per focus were 0.66 in PIN, 1.09 in carcinoma, and 3.75 in metastases. The most frequent anomaly in PIN was a gain of chromosome 8 (32% of foci), followed by gains of chromosomes 10 (13%), 7 (10%), 12 (4%), and Y (4%). The most frequent anomalies in foci of carcinoma were gains of chromosomes 7 and 8 (28% and 30% of foci, respectively), followed by gains of chromosomes 10 (23%), 12 (9%), and Y (9%). There was a positive correlation of the gain of chromosome 8 with the pathological stage and Gleason score (both P < 0.05). Usually, carcinoma foci contained more anomalies than paired PIN foci, but five prostates contained one or more foci of PIN with more anomalies than carcinoma. Among the cases with metastases, usually one or more foci of the primary tumor shared chromosomal anomalies with the matched metastases. Our results indicate that PIN and prostatic carcinoma foci have similar proportions of chromosomal anomalies, but foci of carcinoma usually have more alterations. This observation supports the hypothesis that PIN is often a precursor of carcinoma, although there are some carcinoma foci that have few or no apparent chromosomal alterations, whereas concurrent PIN foci have multiple alterations. A gain of chromosome 8 was the most common numerical alteration and was associated with increasing cancer stage and grade, suggesting that it may play a role in the initiation and progression of prostatic carcinoma. Usually, one or more foci of the primary tumor shared chromosomal anomalies with associated lymph node metastases, suggesting that, often, just a single focus of carcinoma gives rise to metastases.
Cancer Res 1995 Nov 15
PMID:Chromosomal anomalies in prostatic intraepithelial neoplasia and carcinoma detected by fluorescence in situ hybridization. 758 10

The development and progression of human prostate cancer is associated with genetic abnormalities in tumor cells. Inactivation of tumor suppressor genes due to allelic loss is thought to be an important mechanism of gene alteration in prostatic neoplasms. In this study we examined allelic loss on chromosome 8p12-21 in microdissected samples of normal prostatic epithelium, high grade prostatic intraepithelial neoplasia (PIN), and invasive prostate carcinoma from the same patients. Tissue microdissection under direct microscopic visualization procures pure populations of cells of interest, including small lesions such as PIN. Among 30 patients with concomitant cancer and PIN, we found loss of heterozygosity on chromosome 8p12-21 in 63% (34 of 54) of foci of PIN examined and 90.6% (29 of 32) of tumors, suggesting that abnormalities on chromosome 8p12-21 may be important in the early stages of prostatic carcinoma development. Several cases in which multiple foci of PIN from the same patient were sampled showed different patterns of allelic loss. Fifty-five % (16 of 29) of the prostate carcinomas contained a potential precursor PIN focus based on allelic loss pattern. Our results are consistent with the hypothesis that PIN arises multifocally within the prostate gland, and that a subset of these lesions progress to become carcinoma.
Cancer Res 1995 Jul 15
PMID:Allelic loss on chromosome 8p12-21 in microdissected prostatic intraepithelial neoplasia. 760 9

To assess interobserver reproducibility in the categorization of prostatic intraepithelial neoplasia (PIN) seven pathologists reviewed 25 lesions. Rather than classic or consecutive examples of PIN, cases were selected to represent the full spectrum of diagnostic issues in this field. Lesions were classified into one of six categories: (a) benign prostate tissue, (b) PIN1, (c) PIN2, (d) PIN3, (e) PIN3 cannot rule out associated cancer, and (f) PIN3 plus cancer. Following evaluation of the slides, data were also analyzed by combining several of the groups into three categories: (a) benign/PIN1; (b) PIN2/PIN3/PIN cannot rule out cancer; and (c) PIN plus cancer. The level of agreement was fair (Kappa = 0.33) for the six categories and substantial (Kappa = 0.61) for the three groups. In no case was there a uniform diagnosis of PIN1; in all cases at least some pathologists considered the biopsies to be normal. This finding provides support for not commenting on PIN1 in biopsy material. In general, there was good distinction between low-grade PIN (PIN1) and high-grade PIN (PIN2-3). Among the seven cases for which there was a consensus that the lesion represented high-grade PIN, there was no case in which there was uniform agreement as to whether the lesion represented PIN2 or PIN3. This finding supports combining PIN2 and PIN3 into high-grade PIN. Cases classified as low-grade PIN by some and as high-grade PIN by others were those with pleomorphism but without prominent nucleoli. Difficulties in distinguishing "high-grade PIN" from "high grade PIN cannot rule out cancer" were those with cribriform glands, glands with necrosis, and where high-grade PIN was associated with only a few adjacent small atypical glands. These same histologies caused the participating pathologists difficulty in distinguishing "high-grade PIN cannot rule cancer" from "high grade PIN plus cancer."
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PMID:Interobserver reproducibility in the diagnosis of prostatic intraepithelial neoplasia. 761 34

"Incidental" cancer refers to predominantly well differentiated cancer that arises in the transition zone and is found by chance in TURP chips. These tumours are frequently small and may be completely resected by TURP, although a significant number have an additional tumour that is unreachable with a resectoscope. These tumours often co-exist with benign prostatic hyperplasia. Putative precursors of incidental carcinoma include high grade PIN and AAH, and these lesions are frequently found in the transition zone in prostatectomies for cancer. The single most significant question in treating incidental adenocarcinoma is how to separate tumours that will progress from those that will not progress during the expected lifetime of the patient. The 1992 revision of the TNM staging system separated non-aggressive (T1a) and aggressive (T1b) incidental cancer according to the number of foci of cancer, using more than three foci as the cutpoint to identify more aggressive cancer. However, 8-37% of patients with T1 a cancer will develop cancer progression within 10 years if untreated, with the risk of progression increasing with additional years of follow-up. Important prognostic factors include the patient's age, tumour location (peripheral zone v. transition zone), tumour grade, tumour volume, serum PSA concentrations and morphometric factors such as nuclear roundness. Studies directed at early detection allow discovery of increasingly smaller cancers.
Cancer Surv 1995
PMID:The pathology of incidental carcinoma. 762 75

We investigated the association between expression of a novel M(r) 32,000 nuclear phosphoprotein (pp32) and cell proliferation in vivo using the well-characterized physiological model of androgen-dependent regeneration of prostate in orchiectomized rats, pp32 is expressed at high levels in neoplastic cell lines and in certain anatomically defined stem cell compartments of normal human tissues such as intestinal crypt epithelial cells. Immunohistochemistry and in situ hybridization were used to monitor pp32 expression in rat ventral prostatic epithelium following castration and androgen restoration. Castrated rats retained only 6% of prostate wet weight compared to intact controls but were capable of complete gland restoration upon androgen replacement. In intact controls, pp32 expression localized to small acini at the periphery of the gland and to rare basal cells in the central regions. Ten days following castration, there was a 3,5-fold enrichment in the frequency of pp32-positive cells with greater than 56% of remaining epithelial cells expressing pp32 protein. In situ hybridization showed that all remaining epithelial cells contained pp32 mRNA. Upon testosterone replacement, pp32 expression and localization returned to that of intact controls. In order to determine the association between pp32 expression and cell division, DNA synthesis was monitored by bromodeoxyuridine incorporation during prostate involution and regeneration. Bromodeoxyuridine incorporation peaked 3 days after androgen replacement and occurred diffusely throughout the gland. Thus, pp32-positive cells are anatomically distinguishable from the population of terminally differentiating cells undergoing rapid expansion. Preliminary immunohistochemical studies of human prostatic neoplasia demonstrated increased expression of pp32 in human prostatic adenocarcinoma and prostatic intraepithelial neoplasia compared to benign prostatic hypertrophy and normal human prostate. The highest degree of expression occurred in the higher Gleason grades and prostatic intraepithelial neoplasia. This work suggests that pp32 is a nuclear protein which has a selective but presently undefined role in cells competent for self-renewal.
Cancer Res 1993 Oct 01
PMID:A novel M(r) 32,000 nuclear phosphoprotein is selectively expressed in cells competent for self-renewal. 769 3

Prostatic cancer is the second most frequent cancer in men in industrialised countries. The histological analysis of its initial development demonstrates the existence of precancerous lesions, PIN. The initial presence of several different cell populations accounts for the development of contingents of hormone-sensitive and hormone-resistant cells. The presence of numerous neuroendocrine cells appears to be a factor of poor prognosis. Hormones are intimately involved in the development of prostatic cancer and are an integral part of its treatment. Progress in molecular biology has furthered out knowledge of this disease. In particular, growth factors such as EGF and FGF are particularly involved and are starting to have a clinical application. The oncogene and anti-oncogene system is currently being explored (particularly p53 abd BCL 2). They are the basis for carcinogenesis and analysis of these factors will allow a better approach to the mechanisms of tumour induction and development.
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PMID:[Cancer of the prostate. 2. Physiology and cellular development]. 771 57

The relationship of prostatic intraepithelial neoplasia (PIN) and invasive carcinoma of the prostate is not fully understood. It is generally accepted that HGPIN is a probable preinvasive malignant change or at least a marker lesion for carcinoma. The prevalence of HGPIN in younger men is not known. Two hundred and forty nine entirely processed prostates from men aged 20-69 were thoroughly evaluated for the presence of PIN and carcinoma. The histologic diagnosis of all positive cases was confirmed by two pathologists. Our results are summarized as follows: Seventy seven percent of the prostates with HGPIN harbored adenocarcinoma, whereas the frequency of cancer in prostates without HGPIN was 24%. HGPIN was encountered in 0, 5, 10, 41 and 63% of men in the 3rd, 4th, 5th and 7th decades, respectively. The corresponding figures for invasive carcinoma were 2, 29, 32, 55, and 64% respectively.
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PMID:High grade prostatic intraepithelial neoplasia (HGPIN) and prostatic adenocarcinoma between the ages of 20-69: an autopsy study of 249 cases. 780 31

Chemoprevention trials usually target healthy populations and employ non-toxic chemicals in an effort to eliminate, reduce, or reverse premalignant lesions or early cancer. Recent efforts have been directed at short-term Phase II trials which rely on changes in surrogate endpoint biomarkers rather than cancer incidence reduction as an endpoint. Chemopreventive agents are chosen that are likely to produce a modulating effect on one or more biomarkers in prostate cancer, including extent and grade of morphometric, genetic, proliferative, differentiative, and regulatory biomarkers. Five target populations appear to have the greatest promise in chemoprevention trials for prostate cancer: (1) Patients with high-grade prostatic intraepithelial neoplasia, a microscopic lesion which is the likely precursor of some prostate cancers; (2) patients with early cancer treated by watchful waiting; (3) patients with cancer waiting for prostatectomy; (4) men at high risk of developing prostate cancer; and (5) men from the general population (normal risk of prostate cancer).
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PMID:Target populations and strategies for chemoprevention trials of prostate cancer. 782 91

Chemoprevention trials in prostate cancer would involve excessively long follow-up if conventional endpoints of efficacy are used. Prostatic intraepithelial neoplasia (PIN) may be an appropriate surrogate endpoint for monitoring outcome during prostate cancer chemoprevention studies. To address the question of whether PIN could be stratified into "stable" PIN and PIN likely to progress to invasive cancer, we selected patients with a single focus of peripheral zone cancer with ipsilateral and contralateral high-grade PIN. Sixteen patients met these criteria from a series of 550 patients treated by radical prostatectomy. We examined the rate of apoptosis in PIN and prostate cancer tissues by quantifying the number of apoptotic bodies per hundred cells (apoptotic index) on hematoxylin and eosin stained histological sections. Significant differences (ANOVA: p < 0.05) were detected between foci of prostatic intraepithelial neoplasia contralateral to the cancer and the cancer itself. There was no difference in the apoptotic index between a given cancer and a focus of PIN ipsilateral to the tumor in the same section. However, the range of apoptotic indices overlapped in all categories. Apoptotic indices appear to parallel the biological activity of PIN and malignant prostatic tissue, but may be of little benefit when used alone in monitoring the outcome of chemopreventive therapy in an individual patient.
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PMID:Apoptotic index as a biomarker in prostatic intraepithelial neoplasia (PIN) and prostate cancer. 782 93


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