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D F Gleason

Publications and source records attributed to D F Gleason.

At least 37 records · Page 2Linked to original sources
PubMed1989

Immunohistochemical localization of laminin in the basement membranes of normal, hyperplastic, and neoplastic human prostate.

We examined the effects of fixatives and antibody sources on the immunohistologic localization of laminin in normal and cancer-containing human prostates and studied the localization patterns in carcinomas of varying degrees of histologic differentiation. Two different polyclonal antibodies were localized in paraffin-embedded or cryostat sections of fixed (alcohol, formalin, and paraformaldehyde) or unfixed tissue, using the immunofluorescence (IF) or immunoperoxidase (IP) techniques, with positive and negative controls. We found that the IF reactions were more intense in unfixed or alcohol-fixed sections than in paraformaldehyde-fixed specimens. IP reactions were very weak or absent in fixed and paraffin-embedded sections, but pepsin treatment of these sections resulted in more intense and uniform IP reaction products, stronger than in unfixed or ethanol-fixed cryostat sections. With the IP technique, laminin localization was intense and uniform in the basement membranes (BM) of acini, blood vessels, smooth muscle, and nerve fibers in normal prostate, benign hyperplasia (BPH), and well-differentiated carcinomas. The BM of poorly differentiated carcinomas showed widespread absence of laminin reactivity. In normal BPH and well-differentiated tumors, occasional epithelial cells and their surface and acinar lumina had laminin reactivity. However, in higher grade tumors, numerous neoplastic cells had laminin reactivity in cytoplasm, their surface, and secretory material. Some macrophages and neutrophils also contained laminin reactivity, presumably of degraded laminin. In some moderately and poorly differentiated tumors, the BM of small capillaries did not contain laminin. The BM of larger vessels always had laminin reactivity, even in the higher grade tumors.

Adenocarcinoma↗
PubMed1988

Relationship of prostatic acid phosphatase localization in human prostate by a monoclonal antibody with the Gleason grading system.

Prostatic acid phosphatase (PAP) was localized in human prostate with a monoclonal antibody prepared against PAP isoenzyme II to determine patterns of its expression in normal, hyperplastic (BPH), and cancerous glands. The monoclonal antibody reacted with both isoenzymes II and IV in immunoblot studies. Formalin-fixed, paraffin-embedded tissue was used from patients who had not been treated with hormones or chemotherapy. In normal glands and BPH, there was marked variation in the intensity of PAP staining in morphologically otherwise similar epithelial cells. There was similar heterogeneity of staining in the adenocarcinomas. Rough quantification of the intensity patterns in the clinical groups indicated a slight shift to more intense staining in BPH and well-differentiated carcinomas but a progressive decline in the PAP staining in the moderately and poorly differentiated tumors. This decrease in intracellular staining with decreasing differentiation is not inconsistent with the clinical observation that serum levels of acid phosphatase generally increase with higher grade and disseminated tumors, since the enzyme is simply more accessible to the circulatory system in those cases. The same decrease may explain the few disseminated tumors that are not associated with elevated serum levels.

Acid Phosphatase↗
PubMed1988

Histologic grade, clinical stage, and patient age in prostate cancer.

The highly variable and often prolonged clinical course of prostate cancer poses difficult problems. Some patients appear to be at such low risk that overtreatment should be avoided. Many patients must be studied for many years before 2 treatments can be compared. If the patients could be sorted into groups with predictably different survival rates, such studies could be completed in less time and/or with fewer patients. Accumulated experience indicates that the survival rates for patients with a diagnosis of prostate cancer are determined largely by three factors: the clinical stage, histologic grade of the tumor, and the patient's age. Treatment is a fourth variable factor that requires further study. In this paper, the relationships are interactions among grade, stage, and age are analyzed and discussed, and ways are suggested in which they can be combined to enhance stratification and discrimination in clinical trials of treatment. The information can also be applied broadly to the management of individual patients, but it is painfully obvious that we need a much larger body of accumulated treatment data that must include more uniform clinical staging, uniform histologic grading, and detailed patient-age reporting. These data would help adjust for the nonuniform mixture of patients in different studies. The problem of variable patient selection processes before admission to a study affects the results of many reported studies and remains a difficult problem.

Adult↗
PubMed1987

Immunoelectron microscopic localization of prostatic-specific antigen in human prostate by the protein A-gold complex.

Human prostate specimens from 25 patients provided 15 normal, four benign prostatic hypertrophy (BPH), and seven adenocarcinoma samples which were studied using a polyclonal antibody against prostatic specific antigen (PSA) and protein A-gold complex. Our study showed the presence of gold particles in cytoplasmic vesicles and granules, rough endoplasmic reticulum, and occasional lysosomal dense bodies in columnar or cuboidal cells of acini from normal, BPH and well-differentiated cancerous specimens, but not in the acinar basal cells. Some moderately differentiated and most poorly differentiated tumors contained undifferentiated neoplastic cells in which PSA localizations often were associated with membranous structures since specific cytoplasmic organelles were not differentiated. In prostatic stroma, invasive cells which were of differentiated type localized gold particles. In addition, some neutrophils and macrophages also localized PSA suggesting their role in phagocytosis of extracellularly released PSA in the stroma of BPH and cancerous samples. Thus far, the authors have not observed neutrophils and macrophages with gold particles in normal prostate. We suggest that neutrophils and macrophages were involved in transport of some extracellularly released PSA from the prostatic stroma or other metastatic sites to sera in BPH and cancer patients.

Adenocarcinoma↗
PubMed1986

Analysis of fixation effects on immunohistochemical localization of prostatic specific antigen in human prostate.

We studied human prostatic specific antigen (PSA) localization in human prostate to investigate the possibility that the previously reported variations in the intensity of antigen staining were due to fixation and embedding methods. We have evaluated the effects of physical and several chemical fixatives on prostate samples obtained immediately after prostatectomies and radical cystectomies. Our analysis of fixation effects and immunohistochemical staining of polyclonal antibody to PSA indicates that the formalin fixation and paraffin embedding methods used previously did provide optimum localization of the antigen and the variations in the intensity of PSA staining could not be attributed to the methodology. Although PSA staining was relatively uniform in the lower grade neoplastic tumors, the higher grade, moderately to poorly differentiated tumors showed intense-through-weak PSA localization or no PSA staining suggesting that PSA staining intensity was not uniformly related to tumor differentiation.

Adenocarcinoma↗
PubMed1975

Bacterial endocarditis in idiopathic hypertrophic subaortic stenosis.

Bacterial endocarditis complicating idiopathic hypertrophic subaortic stenosis (IHSS) is uncommon but endocarditis may be the first clinical manifestation of IHSS. In this report of such a case, the aortic and the mitral valves were the sites of the bacterial infection. Many chordae tendineae to the mitral valve were ruptured from the extension of the infectious process. The endothelial lesions, which served as the seat for the bacterial infection on the anterior mitral leaflet, likely resulted from its abutting action against the septal prominence. Damage to the aortic valve leaflet may have resulted from abnormal valve motion caused by IHSS and created an environment conducive to endocarditis. This patient developed aortic insufficiency during the course of bacterial endocarditis, suggesting that the occasional association of aortic insufficiency in patients with IHSS may be secondary to healed endocarditis of the aortic valve.

Adult↗
PubMed1965

pH measurements.

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Acid-Base Equilibrium↗