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PubMedDate not supplied

[Mortality study of a cohort of insulation workers].

Cause specific mortality was investigated in a cohort of insulators employed by a company which operated in various parts of Italy. Follow-up covered the years 1960-1996. The cohort, which included 893 subjects, was derived from company files of relatively poor quality, which resulted in a high rate of lost to follow-up (10.1%) and of deaths with unknown cause (12.4%). The mortality experience of the cohort was contrasted with that of the Italian population. Overall mortality (SMR 141, 90% CI 118-167, 97 observed), and cancer mortality (SMR 165, 90% CI 123-216, 38 observed) were significantly increased. Among neoplasms, significant increases were observed for lung cancer (SMR 202, 90% CI 124-311, 15 observed), pleural neoplasms (SMR 2667, CI 90% 911-6103, 4 observed), and peritoneal neoplasms (SMR 1853, 90% CI 329-5832, 2 observed). The excess mortality for lung cancer was especially pronounced in subjects with latency time longer than ten years (SMR 237.1, 90% CI 140-377, 13 observed).

Adult↗
PubMed1992

Expression of the protein kinase p-68 recognized by the monoclonal antibody TJ4C4 in human lung neoplasms.

P68 is a protein kinase expressed by eukaryotic cells, which is inducible by alpha interferon, and is believed to be an important factor in the regulation of viral and cellular protein synthesis. We have previously reported on a monoclonal antibody, TJ4C4, which is able to specifically detect p68 in formalin-fixed, paraffin-embedded tissue. Because of its important role in regulating cellular protein synthesis, we hypothesized that p68 expression would vary among lung neoplasms with level of differentiation and degree of biosynthetic activity. A total of 246 untreated primary pulmonary and pleural neoplasms were studied. The frequency and relative intensity of p68 expression was determined by light microscopic evaluation of ABC immunoperoxidase stained specimens. All categories of tumors studied demonstrated a spectrum of p68 expression. Expression of p68 correlated well with degree of differentiation in squamous cell carcinomas (SQCC) and acinar adenocarcinomas (AAC). Papillary adenocarcinoma (PAC) and bronchioalveolar carcinoma (BAC) expressed low levels of p68, despite their well differentiated appearance. Expression of the antigen in large cell carcinoma (LCC) was higher than that seen in either poorly differentiated AAC or SQCC. Neuroendocrine tumors generally showed low levels of p68 expression with the intermediate variant of small cell carcinoma expressing higher levels of p68 than the classic "oat cell" form (SCC). Carcinoid tumors expressed higher levels of p68 than did atypical carcinoid tumors. Mesotheliomas showed weak expression of p68, limited primarily to areas of glandular differentiation in the epithelioid form.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1994

Mesothelioma-like tumors of the pleura: a review of 72 autopsy cases.

The 72 mesothelioma-like tumors of the pleura (MLTP) found among 33 500 autopsy cases collected over more than 30 years are reviewed. MLTP have a worse prognosis than the 106 cases of pleural mesothelioma autopsied in our institutes with regard to survival time and metastatic spread. In MLTP, adenocarcinomas predominate with a wide range of histological and cytological variation and prominent development of connective tissue having its origin in the periphery of the lung. These intrapulmonary primary tumors often fulfill the criteria of pulmonary scar cancer. Etiologically, there is no correlation between the origin of this tumor and smoking or exposure to asbestos. The absence of mucus formation and glandular differentiation, together with the presence of spindle-shaped carcinoma components and strong mesothelial or stroma proliferation, can make the differential diagnosis between this tumor type and mesothelioma difficult. Immunohistological investigations were performed on 11 cases with antibodies against intermediate filament proteins, vascular endothelium, collagen IV, macrophage antigens, carcinoembryonic antigen (CEA), LeuM1, and the antibody BerEP4. Our investigation shows that a battery of several tumor markers, such as antibodies against LeuM1, CEA, and the antibody BerEP4, as well as staining with periodic acid/Schiff/diastase discriminate primary from secondary pleural neoplasms, whilst intermediate filament proteins alone are of little diagnostic value.

Adult↗
PubMed2003

Giant benign fibrous tumor of the pleura in a pregnant woman: report of a case.

While most pleural neoplasms are malignant and associated with asbestos exposure, benign tumors may also occur. Benign fibrous tumors of the pleura are rare and, unless diagnosed and resected early, they may reach an enormous size and cause severe symptoms. We report the case of a pregnant woman with a giant benign fibrous tumor localized in the pleura.

Adult↗
PubMed2004

Case-control study on cancer risk associated to residence in the neighbourhood of a petrochemical plant.

The aim of the present study is to investigate cancer mortality and residence in the neighbourhood of the petrochemical plant located in Brindisi, South-eastern Italy. Cases were all subjects resident in Brindisi and in three neighbouring municipalities who died in the study area in 1996-1997 from lung cancer, pleural neoplasm, bladder cancer and lymphohematopoietic malignancies. Controls were subjects resident in the same area and deceased in 1996-1997 for any cause except those listed for the cases. Next of kin's of all study subjects were visited by an interviewer who collected anamnestic information. The main residence of each subject, defined as the longest held residence with exclusion of the last 10 years, was reported on a digitalized map of the study area (MapInfo). The study included 144 cases and 176 controls; response rate was 98%. Residence within 2 km from the centre of the petrochemical plant was associated with a 3 fold increase of the Odds ratios (OR) for lung cancer, which did not reach statistical significance. Living close to the petrochemical plant was associated with moderate increases of OR for bladder cancer and lymphohematopoietic neoplasms which did not reach statistical significance. In conclusion the present study has shown moderate increases in risk for lung, bladder and lymphohematopoietic neoplasms in the population resident within 2 km from the centre of the petrochemical plant in Brindisi. These figures were confirmed after adjusting for smoking habit, occupation and school level. Random misclassification may have somehow resulted in risk underestimation.

Adult↗
PubMedDate not supplied

Mucin-positive epithelial mesotheliomas: a histochemical, immunohistochemical, and ultrastructural comparison with mucin-producing pulmonary adenocarcinomas.

Pathologists routinely use histochemistry, immunohistochemistry, and electron microscopy to differentiate epithelial mesotheliomas from pulmonary adenocarcinomas. Epithelial mesotheliomas are usually mucicarmine-, PAS-diastase, and carcinoembryonic antigen-negative, whereas about 60-75% of pulmonary adenocarcinomas are mucicarmine- and PAS-diastase-positive, and about 90% express polyclonal carcinoembryonic antigen. During a pathologic evaluation of pleural neoplasms between 1975 and 1990, 10 epithelial mesotheliomas were identified that were mucicarmine- and in some instances PAS-diastase-positive (diagnosis of mesothelioma confirmed by ultrastructural examination), with four mesotheliomas focally expressing carcinoembryonic antigen. The mucicarmine, PAS-diastase, and carcinoembryonic antigen staining were usually eradicated or reduced in intensity by pretreatment of the tissue sections with hyaluronidase, suggesting that hyaluronic acid was responsible for the positive mucin reactions. In three cases the epithelial mesotheliomas showed focal regions of mucicarmine, PAS-d-, and Alcian blue-hyaluronidase-resistant staining. In contrast, 10 mucicarmine-, PAS-diastase-, Alcian blue-, and carcinoembryonic antigen-positive pulmonary adenocarcinomas were not affected by hyaluronidase pretreatment of the tissue. Besides the usual ultrastructural features of well- to moderately well-differentiated epithelial mesotheliomas, the mucin-positive epithelial mesotheliomas often showed medium-electron-dense secretory material covering the microvilli, aggregates of medium electron-dense material in association with the microvilli, producing an ultrastructural morphology that has been observed only in epithelial mesotheliomas.

Adenocarcinoma↗
PubMed2006

Animal models of malignant mesothelioma.

Animal models of diffuse malignant mesothelioma have historically been used to assess carcinogenicity of various fiber types and to study the pathogenesis of this unusual neoplasm. Pleural and peritoneal mesotheliomas have been induced in rodents following exposure to erionite or asbestos fibers, radionuclides, particulate nickel compounds, and chemicals such as 3-methylcholanthrene. The role of SV40 virus as a cofactor with asbestos fibers in the development of diffuse malignant mesotheliomas in humans has been explored in animal models. SV40 virus alone induces mesotheliomas in hamsters. Generation of new transgenic mouse strains with targeted expression of SV40 large T and small t antigens in the mesothelium would be very useful for mechanistic studies. Human malignant mesotheliomas frequently show hypermethylation or deletions at the Cdkn2a/Arf and Cdkn2b gene loci and deletions or mutations at the NF2 gene locus. Heterozygous Nf2 (+/-) mice exposed to crocidolite asbestos fibers exhibited accelerated development of malignant mesotheliomas compared to wild-type littermates. Loss of the wild-type Nf2 allele, leading to biallelic inactivation, was observed in nine mesothelioma cell lines derived from Nf2 (+/-) mice. Similar to human malignant mesotheliomas, tumors from Nf2 (+/-) mice showed frequent homozygous deletions of the Cdkn2a/Arf locus and adjacent Cdkn2b tumor suppressor gene. As in the human disease, murine mesotheliomas also showed constitutive activation of Akt. This murine model of asbestos carcinogenesis recapitulates the molecular and histopathological features of the human disease and has significant implications for preclinical testing of novel preventive or therapeutic modalities.

Animals↗
PubMed2002

Inhibitor of apoptosis protein-1 promotes tumor cell survival in mesothelioma.

Malignant pleural mesothelioma (MPM) is a highly lethal pleural neoplasm that is often resistant to chemotherapeutic drugs, including cisplatin, and for which little is known regarding carcinogenic pathways. We used differential display to compare gene expression patterns in mesothelioma, normal pleura and normal lung, in order to better understand MPM pathobiology, and to search for genes that may facilitate drug resistance in this cancer. The human inhibitor of apoptosis protein-1 gene (IAP-1/MIHC/cIAP2) was discovered to be highly expressed in MPM. We confirmed overexpression of IAP-1 mRNA and protein in 39 additional human MPM tumor specimens and 3/5 (60%) MPM cell lines by multiple methods, including real time quantitative reverse transcription-PCR and western blot analysis. Using an antisense targeting approach, we found that attenuation of IAP-1 mRNA levels decreases baseline cell viability and increases the sensitivity of MPM cell lines to cisplatin by nearly 20-fold. Reduced IAP-1 gene expression also results in a concordant increase of the pro-apoptotic cleavage product of caspase 9 and a reduction in the number of viable tumor cells. Our observations strongly suggest that IAP-1 is at least partly responsible for promoting carcinogenesis and mediating resistance to cisplatin in many MPM tumors and that further study of this apoptotic pathway is warranted.

Cell Survival↗