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Soft tissues case studies

Oliveira AM, Dei Tos AP, Fletcher CD, et al. Primary giant cell tumor of soft tissues A study of 22 cases. Am J Surg Pathol. 2000 24 248-256. [Pg.136]

Meis-Kindblom JM, KindblomLG. Angiosarcoma of soft tissue a study of 80 cases. Am J Surg Pathol. 1998 22 683-697. [Pg.248]

Hardell L, Eriksson M The association between soft-tissue sarcomas and exposure to phenoxyacetic acids. A new case-referent study. Cancer 61-.652-656, 1988... [Pg.235]

Case reports and case control studies in humans have suggested a possible association between cancer, including soft tissue sarcoma, acute leukemia, Hodgkin disease, and non-Hodgkin lymphoma, and occupational exposure to pentachlorophenol. However, in all cases concomitant exposure to other toxic substances may have contributed to the effects seen. "... [Pg.560]

When these three cancers (soft-tissue sarcoma, non-Hodgkin s leukemia, and Hodgkin s disease) are considered as a whole, it is noteworthy that the strongest evidence for an association with exposure to phenoxy herbicides is the series of case-control studies conducted by Hardell [Lennart Harden, a Swedish physician] and colleagues and the cohort studies of herbicide applicators and agricultural workers.25 26... [Pg.218]

J.D., Neuberg, M., Benn, T, Fannett, B., Pearce, N. Saracci, R. (1995) Soft tissue sarcoma and non-Hodgkin s lymphoma in workers exposed to phenoxy herbicides, chlorophenols, and dioxins two nested case-control studies. Epidemiology, 6, 396-402... [Pg.379]

Associations with chlorophenols were, however, analysed in two case-control studies nested within 24 of the 36 cohorts of the lARC study. These compared 11 cases of soft-tissue sarcoma and 32 cases of non-Hodgkin lymphoma with 55 and 158 controls, respectively (Kogevinas et al., 1995). Exposure to chlorophenols, phenoxy acid herbicides, dibenzodioxins and -furans and other agents was assessed by a team of industrial hygienists (Kauppinen et al., 1994). Odds ratios for non-Hodgkin lymphoma, not adjusted for exposure to other agents, were 1.3 (95% CI, 0.5-3.1) for any chlorophenol, 2.8 (0.5-17.0) for pentachlorophenol and 1.0 (0.3-3.1) for 2,4-dichlorophenol. No excess risk was found in relation to other chlorophenols, but the munber of exposed cases was small. The odds... [Pg.776]

These investigations have shown significant associations with several types of cancer, but the most consistent findings have been for soft-tissue sarcoma and non-Hodgkin lymphoma. Although the odds ratios in some case-control studies may have been inflated by recall bias, this cannot explain all of the findings. Nor are they likely to have arisen by chance. It is not possible, however, to exclude a confounding effect of polychlorinated dibenzo-para-dioxins which occur as contaminants in chlorophenols. [Pg.805]

Eriksson, M., Hardell, L., Berg, N.O., Mdller, T. Axelson, 0. (1981) Soft-tissue sarcoma and exposure to chemical substances a case-referent study. Br. J. ind. Med, 38, 27-33... [Pg.808]

Eriksson, M., Hardell, L. Adami, H.-O. (1990) Exposure to dioxins as a risk factor for soft tissue sarcoma a population-based case-control study. J. natl Cancer Inst., 82, 486-490 Exon, J.H. Koller, L.D. (1982) Effects of transplacental exposure to chlorinated phenols. Envi-... [Pg.808]

Harden, L. Sandstrom, A. (1979) Case-control study soft-tissue sarcomas and exposure to phenoxyacetic acids or chlorophenols. Br. J. Cancer, 39, 711-717... [Pg.809]

Harden, L., Eriksson, M. Dcgcrmann, A. (1995) Meta-analysis of four Swedish case-control studies on exposure to pesticides as risk-factor for soft-tissue sarcoma including the relation to tumour localization and histopathological type. Int. J. Oncol., 6, 847-851... [Pg.809]

Humans occupationally exposed to phosphorus probably ingested some airborne white phosphorus. In a study of 71 humans occupationally exposed to fumes/vapors and paste containing white phosphorus, oral exposure to phosphorus passed from hand to mouth was likely, because the workers constantly handled a paste containing 4-6% white phosphorus, and washroom facilities at the plants were inadequate (Ward 1928). White phosphorus-related deaths occurred in 0 of 44 and 2 of 27 of the workers exposed for intermediate and chronic durations, respectively. In the two cases of death, the workers died from complications related to phossy jaw, a degenerative condition affecting the soft tissue, bones, and teeth of the oral cavity. In this condition, the toxic effects of white phosphorus probably result from the local irritant action of white phosphorus on tissues in the mouth. Thus, white phosphorus paste passed from hand to mouth and the local action of airborne white phosphorus on the oral cavity may have contributed to the development of phossy jaw, and subsequent death, of these two workers. It is not known whether white phosphorus ingested and absorbed into the systemic circulation contributed to the development of phossy jaw in the two workers that died (Ward 1928). Details of this study are provided in Section 2.2.2.2. [Pg.50]

Longer term occupational exposure to white phosphorus can result in a condition (phossy jaw) that is potentially life-threatening. Two white phosphorus-related deaths were reported in a study of 71 workers from three plants involved in the production of fireworks (Ward 1928). Both workers developed phossy jaw, a degenerative condition affecting the soft tissue, bones, and teeth of the oral cavity, after chronic exposure to the atmosphere at the factory. It is likely that white phosphorus-related necrosis results from a direct local effect following contact of phosphorus with tissues in the oral cavity. The cause of death in both cases was listed as septicemia, with abscess of a tooth and necrosis of the jaw listed as contributory causes. Thus, death in both cases resulted from infections, probably secondary to the degenerative effects of white phosphorus on the oral cavity (Ward 1928). [Pg.121]

Case-control studies have been designed to determine if 2,3,7,8-TCDD exposure results in increased risks for site-specific cancers. Case-control studies have found significant increases in the risk of soft-tissue sarcomas in Swedish agricultural, forestry, and horticultural workers (Eriksson et al. 1981, 1990 Hardell and Eriksson 1988 Hardell and Sandstrom 1979), workers involved in manufacturing and application of phenoxy herbicides (Kogevinas et al. 1995), and New Zealand farmers (Smith et al. 1984a). In the Eriksson et al. (1990) study, the risk ratio of soft-tissue sarcoma was 1.80 (95% 0=1.02-3.18) in subjects exposed to phenoxyacetic acid herbicides and/or chlorophenols. In subjects exposed to phenoxyacetic acid herbicides only or chlorophenols only, the risk ratios were 1.34 (95% 0=0.7-2.56) and 5.25 (95%... [Pg.86]

Eriksson M, Hardell L, Berg NO, et al. 1979. Case-control study on malignant mesenchymal tumors of the soft tissue and exposure to chemical substances. Lakartidningen 76 3872-3875. [Pg.616]

Several case-control studies examined the association between phenoxy herbicide exposure and non-Hodgkin s lymphoma and soft tissue sarcoma.46-60... [Pg.78]

The polymerase chain reaction (PCR) is an ideal tool for the study of ancient DNA because it has the ability to amplify a small number of intact DNA molecules that exist in a complex mixture of large amounts of partially degraded and modified templates. Of crucial importance for the use of ancient DNA extracts is the extent to which the damage limits or inhibits the enzymatic reaction. An observation often made is that the maximum sizes of amplifiable products are reduced in old, damaged DNA compared to modem DNA extracts.14 This is also true for DNA from ancient bones, which seem in many cases to allow for longer amplifications than soft tissues. For example, we have determined the maximum size of amplifiable DNA from 3500-year-old moas found at a dry cave site in New Zealand and found that, whereas soft tissues allowed the amplification of pieces only up to 120 bp, bone extracts from the same individual yielded products of up to 380 bp. However, DNA extracted from a modem ratite bird easily allowed the amplification of pieces of over 1000 bp.15... [Pg.409]

Carcinoma of the prostate is today one of the three most frequent causes of death from neoplastic disease in men in the United States (G4). The early studies of Gutman and his associates (Gil, G12, R6, S30) established that serum acid phosphatase activity was elevated very frequently in patients with metastatic carcinoma of the prostate. It is of interest to consider briefly the uncertainties inherent in the development of this relationship. Skeletal metastases, if sufficiently large, are of course detectable by roentgenographic examination, but smaller ones may not be, and metastases to soft tissues may likewise be undetectable. For example, in 15 cases of metastazing carcinoma reported by Gutman... [Pg.101]


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