1,721,197 research outputs found
Reflection on the past, present and future of analytical and quantitative cytology and histology
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HER-2 expression and gene amplification in high-grade PIN and prostate cancer.
No full textThe aim of the current study was to analyze HER-2 expression and gene amplification in prostate cancer and HGPIN incidentally detected in cystoprostatectomies. Eighty prostate cases were used. Group 1 (incidental): nineteen cystoprostatectomy specimens with prostate cancer and HGPIN and no residual urothelial carcinoma in the prostate. Group 2 (untreated): twenty-five radical prostatectomy specimens with prostate cancer Group 3 (hormonally treated): nineteen radical prostatectomy specimens with prostate cancer. All the patients were under total androgen ablation therapy for three months before surgery. Group 4 (hormone-independent): nine TURP specimens with locally recurrent androgen independent prostate cancer Group 5 (normal reference): eight cystoprostatectomy specimens without HGPIN and without prostate cancer, and no residual urothelial carcinoma. None of the patients belonging to Groups 1, 2, and 5 had received chemotherapy, hormone therapy, or radiation therapy before surgery. Weak to moderate HER-2 membrane immunoreactivity was observed in most of the basal cells but not in the secretory cells of normal prostatic ducts and acini both in the cystoprostatectomies and in the radicals of the untreated patients. High-grade PIN. HER-2 overexpression was present in the secretory cells in 26% of HGPIN cases in the CyP group, 40% in the untreated clinically detected cancer group, and 83% in the treated group. Prostate cancer HER-2 overexpression was seen in 16% of cases in the CyP group, 36% in the untreated group and 47.5% in the treated group. HER-2 overexpression was present in 78% of cases with androgen independent PCa. Association of HER-2 overexpression and gene amplification. When considering HGPIN the lowest proportion of cases with HER-2 overexpression and with nuclei with gene amplification was seen in the CyP specimens (7%), whereas the highest was in the treated material (28%). As far as the cancers were concerned, the proportions were slightly higher than in HGPIN, the lowest value being in the CyP specimens (9%) and the highest in the hormone independent PCa (62.5%). A statistically significant difference in the number of cases with both overexpression and amplification was only seen between CyP and hormone-independent cancers (p = 0.007)
Prostatic intraepithelial neoplasia and prostate cancer.
No full textProstatic intraepithelial neoplasia (PIN) is composed of dysplastic cells with a luminal cell phenotype, expressing the androgen receptor as well as prostate specific antigen. PIN is characterized by progressive abnormalities of phenotype which are intermediate between normal prostatic epithelium (NP) and cancer, indicating impairment of cell differentiation and regulatory control with advancing stages of carcinogenesis. High-grade PIN is considered the most likely precursor of prostatic carcinoma (PCa), according to virtually all available evidence. Androgen deprivation decreases the prevalence and extent of PIN and the degree of capillary vascularization (e.g., angiogenesis) in the surrounding stroma via the suppression of vascular endothelial growth factor (VEGF) production. It is likely that PCa might also arise from precursor lesions other than high-grade PIN (low-grade PIN, atypical adenomatous hyperplasia, malignancy-associated foci, and atrophy)
Assessment and reporting of pathological findings of penile specimens.
No full textThe correct assessment of penile specimens may provide clinically relevant diagnostic and prognostic data. This protocol is intended to assist pathologists in providing useful information to the clinicians and urologists and to uniform the examination of the penis by a standardized approach
Precancerous lesions and conditions of the prostate: from morphological and biological characterization to chemoprevention
No full textMeningioma: the impact of new techniques for the diagnosis and prognosis
No full textOur knowledge of meningioma has expanded considerably in the last few years. Immunohistochemistry, cytogenetics and molecular biology have given an important contribution to this improvement. Meningiomas can have almost endless variations in cellular morphology, architectural patterns and metaplastic changes. The majority of them have no prognostic implications. But a few variants should be recognised because of peculiar clinico-pathologic correlations or biological behavior. Histological features useful in distinguishing benign from potentially aggressive meningiomas have been identified. According to the WHO classification meningiomas are classified as benign (Grade 1), atypical (Grade 2) and anaplastic (Grade 3). Since histological appearance fails to predict accurately the clinical behaviour in a significant percentage of meningiomas, the attention has turned from tumor histology to tumor biology. Proliferative indices can be used, together with other histologic features, in assessing the prognosis as well as the postoperative management of the patients. Karyotyping may be of use to identify a subgroup of patients at higher risk for recurrence who may need special follow-up and treatment. The most consistent chromosome aberration in meningiomas seems to be a monosomy 22. As the karyotype becomes progressively abnormal, the tumor becomes more aggressive. Molecular genetic analysis has shown that TP53 gene mutation may be considered as a marker for malignant transformation in meningioma. P53 immunoreactivity is not always associated with the gene mutation but is not detectable in benign meningiomas
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