Mouse skin application in chemical carcinogenesis.
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BACKGROUND: Certain types of potassium channels (known as Eag1, KCNH1, Kv10.1) are associated with the production of tumours in patients and in animals. We have now studied the expression pattern of the Eag1 channel in a large range of normal and tumour tissues from different collections utilising molecular biological and immunohistochemical techniques. RESULTS: The use of reverse transcription real-time PCR and specifically generated monoclonal anti-Eag1 antibodies showed that expression of the channel is normally limited to specific areas of the brain and to restricted cell populations throughout the body. Tumour samples, however, showed a significant overexpression of the channel with high frequency (up to 80% depending on the tissue source) regardless of the detection method (staining with either one of the antibodies, or detection of Eag1 RNA). CONCLUSION: Inhibition of Eag1 expression in tumour cell lines reduced cell proliferation. Eag1 may therefore represent a promising target for the tailored treatment of human tumours. Furthermore, as normal cells expressing Eag1 are either protected by the blood-brain barrier or represent the terminal stage of normal differentiation, Eag1 based therapies could produce only minor side effects.
After a brief survey of the factors of clinical tumor radioresistance the available data on the growth rate and on the kinetics of cell proliferation of U.R.D.T. tumors are reviewed. The growth fraction and the cell turnover rate appear to be similar in U.R.D.T. tumors and in other squamous cell carcinomas. These two parameters are correlated with clinical tumor radiosensitivity and chemosensitivity. The possible value of tailoring fractionation and drug administration to the biological characteristics of the tumor is discussed.
In order to analyze the pattern in the geographical distribution of cancer death in 24 countries of the world, correlation coefficients were calculated between pairs of mortality rates of different cancer sites, using the data for 13 sites in males and 14 sites in females over 18 years from 1950 to 1967. Then factor analysis by means of varimax method was performed on 13 x 13 correlation matrix for males, 14 x 14 correlation matrix for females and 27 x 27 correlation matrix for males and females combined. As a result of factor analysis, three factors are extracted, which are commonly recognized in both males and females. The first factor has high positive factor loadings on pancreas, prostate (for males), skin, and intestine cancers, and negative loadings on stomach and liver cancers. The second factor has high positive factor loading on rectum, intestine, and lung cancers, and the third factor on larynx, oral, and esophagus cancers. Factor analysis based on 27 x 27 correlation matrix revealed that the third factor of both sexes are heterogeneous with regards to the distributions of the factor score. In order that we may find some clues to develop an etiological hypothesis for each site of cancer, we obtained the correlation coefficient between the scores of the extracted factors and the variables on food and environmental agent, and performed stepwise regression methods as well. One of the most striking results we obtained was that excessive drinking of alcohol and the lack of appropriate intake of fruit are suspected as etiological promoters in the pathogenesis of oral, esophagus, and larynx cancers in males.
The OSHA standard for coke oven emissions, which went into effect in January 1977, sets a permissible exposure limit to coke oven emissions of 150 micrograms/m3 benzene-soluble fraction of total particulate matter (BSFTPM). Review of the epidemiologic evidence for the standard indicates an excess relative risk for lung cancer as high as 16-fold in topside coke oven workers with 15 years of exposure or more. There is also evidence for a consistent dose-response relationship in lung cancer mortality when duration and location of employment at the coke ovens are considered. Dose-response models fitted to these same data indicate that, while excess risks may still occur under the OSHA standard, the predicted levels of increased relative risk would be about 30-50% if a linear dose-response model is assumed and 3-7% if a quadratic model is assumed. Lung cancer mortality data for other steelworkers suggest the predicted excess risk has probably been somewhat overestimated, but lack of information on important confounding factors limits further dose-response analysis.
The study describes the mortality of 5 017 men known to have been employed in the boot and shoe manufacturing industry in three towns in Great Britain in 1939. At the end of 1982, 97.5% of the men were traced, and 3 434 (68.4%) were known to be dead. Expected numbers were calculated according to the person-years method and were adjusted according to the standardized mortality ratios of the counties in which the towns were situated. The mortality experience of the men for all causes, all cancers combined, and all other causes was favorable. The anticipated excess of deaths from nasal cancer (10 observed, 1.87 expected) was found, and the excess was significant for workers in the finishing room. Deficits were found for other types of respiratory cancer. An excess mortality from leukemia was found for workers in one town (7 observed, 3.0 expected), and the excess was significant for workers in the lasting and making room, where glues and solvents, including benzene, were known to have been used. An excess mortality from rectal cancer was found for workers in two towns (61 observed, 47.6 expected), and it was significant for workers in the lasting and making rooms (25 observed, 12.4 expected). Some supporting evidence for a risk of rectal cancer in this industry was found in the literature.
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This study compares cancer incidence in the United States National Survey areas and Puerto Rico for the period of 1969 to 1974. There are several differences between the 2 areas. Puerto Rico has a higher incidence of cancer of the mouth, pharynx, esophagus, stomach, cervix uteri, vulva, and penis. The Survey areas have higher incidences of cancer of the colon, rectum, lung, corpus uteri, female breast, and ovary. The differences between sexes are more or less the same as in other countries.
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OBJECTIVE: To determine there was excessive risk of malignant tumors or not among workers exposure to chrysotile fiber alone by applying a meta-analysis technique. METHODS: All data meeting the criteria of cohort studies on cancer mortality among workers exposed only to chrysotile would incorporate into the meta-analysis. The pooled standardized mortality ratios (SMR) and their corresponding 95% confidence intervals (95% CI) for main cancer sites were calculated using two approaches of unweighted ratio and random effects model. The heterogeneity and its sources of the results were examined with a Q-statistic and Z-score test. RESULTS: 26 chrysotile-exposed alone cohorts were summarized. The significantly elevated meta-SMRs for all deaths (1.28), all cancers (1.26), cancers of respiratory organs (2.24), cancer of lung (2.29) and cancer of stomach (1.27) were observed. The significantly elevated meta-SMRs for lung cancer within occupational strata were observed among textile workers (3.64), asbestos products manufacturers (3.07), miners and millers (2.24), cement products workers (1.22), and for stomach cancer among asbestos products manufacturers (1.48). Meta-SMRs for cancers at other sites were not significant. CONCLUSION: There were excessive risks of lung cancer and mesothelioma among workers exposure to chrysotile fiber alone, and likely no convincing indication of an etiological association between chrysotile exposure and cancers at other sites.
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Hilar and mediastinal lymphadenopathy are sometimes the only radiological manifestation of metastatic disease from extrathoracic neoplasms. This association has not been previously described with carcinoma of the cervix. We report two patients in whom hilar and mediastinal lymph node enlargement represented the first evidence of tumor recurrence.
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