Posts Tagged ‘Pulmonary’

Exposure to Pulmonary Carcinogens and Mesothelioma

Exposure to Pulmonary Carcinogens and Mesothelioma

When pieces of asbestos are inhaled or swallowed, they can lead to life threatening diseases.  To date, over 730,000 people have filed claims for asbestos related injuries in the United States alone. One interesting study that examples the link between exposure and Mesothelioma disease is called, “Analysis of asbestos fibers and asbestos bodies in tissue samples from human lung. An international interlaboratory trial.” by Gylseth B, Churg A, Davis J.M., Johnson N, Morgan A, Mowe G, Rogers A, Roggli V. – Scand J Work Environ Health. 1985 Apr;11(2):107-10.  Here is an excerpt: “Abstract – In order to compare methods of counting asbestos fibers in lung tissue, seven laboratories participated in an interlaboratory trial in which tissue samples from five human lungs were analyzed. In some laboratories, fiber concentrations were assessed with the light microscope and, in others, with either scanning or transmission electron microscopes. Within each laboratory the ranking of the results was similar, but there were marked differences in the absolute values obtained by the different laboratories. It is concluded that the laboratories participating in this trial appear to produce internally consistent results, but there is difficulty in directly comparing results from one laboratory to the next.”

A second study is called, “Reduced Fhit protein expression and loss of heterozygosity at FHIT gene in tumours from smoking and asbestos-exposed lung cancer patients.” By Pylkkanen L, Wolff H, Stjernvall T, Tuominen P, Sioris T, Karjalainen A, Anttila S, Husgafvel-Pursiainen K.  Int J Oncol. 2002 Feb;20(2):285-90.  Here is an excerpt: “Abstract – The FHIT gene, at 3p14.2, has been suggested to form a molecular target to damage induced by human lung carcinogens. We examined aberrant expression of the Fhit protein and allele loss at the FHIT gene in a series of lung cancer cases, mainly of non-small cell carcinoma (NSCLC) histology. We had detailed data on tobacco smoke exposure and occupational asbestos exposure available for the cases. The principal aim of the present study was to investigate whether absent or reduced Fhit expression or FHIT allele loss was associated with exposure to these pulmonary carcinogens. We detected reduced Fhit expression in 62% (33/53) of the cases analysed. Prevalence of allele loss at the FHIT locus was 22% (20/89). Reduced protein expression was common both in the asbestos-exposed (67%) and non-exposed cases (59%); [odds ratio (OR) 1.4, 95% confidence interval (CI) 0.4-4.9]. LOH frequencies differed somewhat between the two groups and were 25% vs. 16%, respectively (OR 1.8; 95% CI 0.5-5.9). Absent or reduced expression was common in smokers, with no significant difference found between current smokers and non-smokers (mainly former smokers) (OR 1.4, 95% CI 0.5-4.5). NSCLCs with squamous cell histology exhibited both aberrant [removed]OR 3.1, 95% CI 0.9-10.3) and allele loss (OR 3.3, 95% CI 0.9-12.7) more frequently than adenocarcinoma. Finally, we found that FHIT allele loss was increased in stage II or more advanced disease (OR 2.5, 95% CI 0.9-7.4), and in poorly differentiated tumours (grade 3, OR 2.6, 95% CI 0.8-8.1). In conclusion, our present data support significance of FHIT inactivation in development of lung cancer.”

A third study is called, “Effects of crocidolite and chrysotile asbestos on cellular uptake and metabolism of benzo(a)pyrene in hamster tracheal epithelial cells.” Environ Health Perspect. 1983 September; 51: 331 by B. T. Mossman, A. Eastman, J. M. Landesman, and E. Bresnick.  Here is an excerpt: “Abstract – The incidence of bronchogenic carcinoma is increased substantially in asbestos workers who smoke. We used several approaches to determine possible mechanisms of synergism at the cellular level between asbestos and the polycyclic aromatic hydrocarbon (PAH), benzo(a)pyrene (BaP), a chemical carcinogen in cigarette smoke. Specifically, we hypothesized that cellular uptake and metabolism of BaP might be facilitated when the hydrocarbon was coated on asbestos. In addition, we were interested in whether asbestos, alone or in combination with BaP, caused single strand breakage of DNA in epithelial cells of the airway. UICC reference samples of crocidolite and chrysotile were coated with 3H-BaP before their addition to monolayers of hamster tracheal epithelial cells. In comparative studies, 3H-BaP at identical amounts was added to cells in culture medium. At intervals thereafter, uptake of BaP by cells was documented by scintillation spectrometry and by autoradiography. In addition, cells and media were assayed by use of high pressure liquid chromatography (HPLC) to demonstrate the water-soluble metabolites of BaP. The integrity of DNA was monitored by alkaline elution at intervals after exposure of tracheal cells to various concentrations of asbestos, BaP and BaP-coated asbestos. A rapid transfer of BaP to cells occurred after addition of BaP-coated asbestos to cultures. When BaP was adsorbed to both types of fibers before their addition to cultures, 70% of the total BaP introduced entered the cell within 1 hr; 50% remained intracellular after 8 hr.”

If you found any of these studies interesting, please read them in their entirety.  We all owe a great deal of thanks to the people who are researching these important issues.

Monty Wrobleski is the author of this article, for more information please visit the following links Nephrogenic Systemic Fibrosis,

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Pulmonary Toxicity and Malignant Mesotheliomas

Pulmonary Toxicity and Malignant Mesotheliomas

Another interesting study is called, “Potential Role of Histone Deacetylase Inhibitors in Mesothelioma: Clinical Experience with Suberoylanilide Hydroxamic Acid
Clinical Lung Cancer” – Chest Surg Clin N Am. 1994 Feb;4(1):113-26 – Allen KB, Faber LP, Warren WH.  Here is an excerpt: “Abstract – Diffuse malignant pleural mesothelioma is an uncommon, uniformly fatal malignancy. Controversy continues to surround the optimal surgical procedure, both extrapleural pneumonectomy or pleurectomy, which should be utilized in conjunction with post-operative chemotherapy and/or radiotherapy. This retrospective study reviews a single institution’s experience with extrapleural pneumonectomy and pleurectomy in the multimodality treatment of diffuse malignant pleural mesothelioma.

Another interesting study is called, “Phase II trial of mitomycin in malignant mesothelioma.” By Bajorin, D, Kelsen, D, Mintzer, DM – CANCER TREAT. REP. Vol. 71, no. 9, pp. 857-858. 1987.  Here is an excerpt: “Malignant mesothelioma is a highly lethal neoplasm. Recent data noted in vivo antineoplastic effects of a combination of mitomycin and cisplatin (DDP) greater than either agent alone in human tumor xenograft mesothelioma. While DDP singly has some efficacy, mitomycin has not been systematically evaluated in this disease. A phase II trial was therefore conducted to determine the activity of mitomycin in malignant mesothelioma. Pulmonary toxicity was substantial. Two responding patients developed dyspnea and hypoxemia occurring at cumulative doses of 40 and 50 mg/m super(2), respectively. One patient had a transbronchial biopsy consistent with drug-induced pulmonary fibrosis and never achieved resolution of hypoxemia with corticosteroid therapy prior to death from progressive mesothelioma. The second patient responded to corticosteroid therapy with resolution of dyspnea and hypoxemia but relapsed after discontinuing mitomycin.”

Another interesting study is called, “Immunohistological staining of reactive mesothelium, mesothelioma, and lung carcinoma with a panel of monoclonal antibodies.” – J Clin Pathol 1987;40:19-25 by A K Ghosh, K C Gatter, M S Dunnill, D Y Mason.  Here is an excerpt: “Abstract – A panel of seven monoclonal antiepithelial antibodies of different specificities, including anticytokeratin, human milk fat globule membrane, C, and carcinoembryonic antigen (CEA) were used with the alkaline phosphatase-antialkaline phosphatase (APAAP) immunostaining technique to determine their value in the differentiation between benign and malignant mesothelial cells and lung carcinoma in histological preparations. The anticytokeratin antibody reacted strongly with all cases of reactive mesothelium, mesothelioma, and lung carcinoma. Antibodies to human milk fat globule membrane and the Ca antigen stained mesothelioma and carcinoma and 43% of cases of reactive mesothelium. Staining for carcinoembryonic antigen was not detected in reactive mesothelium or mesothelioma, but was present in most of the lung carcinomas. CEA seemed to be the single most useful marker in distinguishing carcinoma from mesothelioma in that a positive reaction for CEA would indicate carcinoma rather than mesothelioma.”

Another interesting study is called, “Podoplanin as a marker for Mesothelioma” by Noriko Kimura, Itaru Kimura – Pathology International – Volume 55, Issue 2, pages 83–86, February 2005.  Here is an excerpt: “Podoplanin is a specific marker for lymph vessel endothelial cells. It was noted that podoplanin is expressed in reactive mesothelial cells. The utility of podoplanin for the histological diagnosis of tumors was then investigated, especially for mesothelioma. Immunohistochemical study of podoplanin was carried out in five malignant mesotheliomas and 118 other tumors including 93 adenocarcinomas, four squamous cell carcinomas, six gastrointestinal stromal tumors and five endocrine tumors. Immunoreactivity for podoplanin was demonstrated on the cell membrane of tumor cells for all mesotheliomas. All other tumors were negative for podoplanin. Among the many antibodies used for differential diagnosis of malignant mesothelioma, podoplanin has the potential to be an excellent tumor marker in both specificity and sensitivity. The utility of podoplanin as a marker for mesothelioma will be confirmed by further studies.”

We all owe a debt of gratitude to these fine researchers.  If you found any of these excerpts interesting, please read the studies in their entirety.

Monty Wrobleski is the author of this article.  For more information please click on the following links

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Pseudomesotheliomatous Pulmonary Adenocarcinoma

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