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At least 1,117 records · Page 62Linked to original sources
PubMed1983

Neuron-specific enolase in neuroendocrine tumors of the thymus, bronchus, and skin.

In order to better define the use of neuron-specific enolase (NSE) as a marker for neuroendocrine neoplasms, we studied 11 thymic carcinoid tumors, three bronchial small-cell carcinomas (all with cutaneous metastases), and 10 trabecular carcinomas of the skin for its presence, using the peroxidase-antiperoxidase (PAP) technic with an antiserum directed at NSE. All 11 carcinoid tumors stained positively, as did two of the bronchial small-cell carcinomas and seven of the trabecular carcinomas. We conclude that PAP staining for NSE content may be a useful adjunct to morphologic analysis in diagnostically identifying the tumors we studied and that our results support the concept of a functionally unified APUD system, as reflected in the tumors originating from it. Nevertheless, because of the vagaries of the PAP method, exemplified by the results in our small series, it cannot be relied upon as a sole indicator that a tumor contains NSE and is therefore neuroendocrine. Also, since it is hypothesized that NSE is present in all tumors of this type, staining for its presence would seem to be of little benefit in distinguishing primary from secondary neuroendocrine tumors or in identifying the origin of metastatic lesions that have a neuroendocrine histologic appearance.

Bronchial Neoplasms↗
PubMed2004

DNA adducts in tumour, normal peripheral lung and bronchus, and peripheral blood lymphocytes from smoking and non-smoking lung cancer patients: correlations between tissues and detection by 32P-postlabelling and immunoassay.

Smoking is a major risk factor for lung cancer. This comparative study of smoking-related carcinogen-DNA adducts in pulmonary tissues and peripheral blood lymphocytes aims to further explore the primary DNA damaging processes by cigarette smoke in target and surrogate tissues. Samples of tumour and normal peripheral lung tissue, normal bronchial tissue and peripheral blood lymphocytes were obtained from a total of 85 lung cancer patients who underwent lung resection. Bulky DNA adducts were determined by 32P-postlabelling, and polycyclic aromatic hydrocarbon (PAH)-DNA adducts were detected by (+/-)-7beta, 8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene-DNA chemiluminescence immunoassay (BPDE-DNA CIA) in smaller subsets of tissue samples subject to availability of DNA. Bulky DNA adduct levels ranged between 0.3 and 27.8 adducts/10(8) nucleotides (nt) with mean adduct levels between 2.8 and 11.5 adducts/10(8) nt. Mean PAH-DNA adduct levels were 2.6-6.2 adducts/10(8) nt. Significantly higher bulky DNA adduct levels were detected in smokers' lungs as compared with non-smokers' (P < 0.02). PAH-DNA adduct levels appeared higher in the lungs of smokers compared with non-smokers but the difference was not significant. Lung tumour contained on average a 50% lower DNA adduct level compared with normal lung tissue. A statistically significant positive correlation was found between the DNA adduct levels of the corresponding tumour and normal lung tissue samples in both smokers and non-smokers using both methodologies. Bulky DNA adduct levels in normal lung and blood lymphocytes correlated significantly in non-smokers only (r = 0.55, P = 0.023). In lung tumour DNA samples there was a weak correlation between values obtained by 32P-postlabelling and by the BPDE-DNA immunoassay (r = 0.27, P = 0.054). However, with normal lung DNA samples, values obtained by the two assays did not correlate.

Adult↗
PubMed1994

Epithelial-myoepithelial tumor of the bronchus.

A primary bronchial tumor with a histological pattern similar to that of epithelial-myoepithelial tumor of the salivary gland is reported in a 55-year-old woman. The tumor was well delimited, although not encapsulated, and showed a polypoid growth. The tumor was composed of two types of neoplastic cells: epithelial cells displaying tubules and myoepithelial cells that either formed compact masses or surrounded the tubular formations. Immunohistochemical study confirmed positive immunoreaction to both high- and low-molecular-weight cytokeratins in the epithelial cells and positive immunoreaction to vimentin, S-100 protein, and myosin in the myoepithelial cells.

Bronchial Neoplasms↗
PubMed2001

Epithelial-myoepithelial carcinomas of the bronchus.

Epithelial-myoepithelial carcinomas are very rare in the lung, and little is known about the relationship of their histologic features to prognosis. We describe five primary pulmonary epithelial-myoepithelial carcinomas with details on clinical presentation, histology, and immunohistochemical profiles. We also reviewed the literature to detail further their prognosis. The patients' ages ranged from 33 to 57 years (average 51 years). The tumors were all endobronchial and the patients presented with symptoms or imaging features of airway obstruction. The tumors were completely resected; none showed nodal involvement. All five patients are alive and free of disease 4 months to 8 years (average 4.2 years) after surgery. Four tumors showed a mixed pattern of glands lined by a dual layer of cells and solid sheets of either spindle cells or clear cells, the glandular and solid components being present in variable proportions. The fifth tumor comprised purely spindle cells. The mitotic rate was <1/20 high power fields in both the glandular and spindle/clear cell components. In one case there was focal nuclear pleomorphism. The inner layer of the glands stained for cytokeratins and epithelial membrane antigen, and the outer layer for S-100 and smooth muscle actin. In one case the spindle cells stained for CD34. A review of published cases shows the majority of tumors behave in an indolent fashion, the rare aggressive tumors being predominantly myoepitheliomatous. Nevertheless, the term epithelial-myoepithelial carcinoma is preferred because of their malignant potential. A high mitotic rate, tumoral necrosis, and nuclear pleomorphism appear to be adverse prognostic factors.

Actins↗