The Experts below are selected from a list of 93 Experts worldwide ranked by ideXlab platform
N. Beck - One of the best experts on this subject based on the ideXlab platform.
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Influence of suture material on experimental colonic carcinogenesis in rats
1992Co-Authors: T. Hupp, Heinz J. Buhr, S. Ivancovic, N. BeckAbstract:To assess the possible risk of cancer in the operated colon after stapling compared with vicryl sutures, the influence of the nickel-containing staples was tested in caecum-resected and carcinogen-treated rats. The nickel-containing staples were seen as a Cocarcinogen. The aim of the study was to determine whether a higher incidence of cancer occurs at the anastomotic suture line depending on stapler vs. vicryl sutures after subcutaneous application of carcinogens (dimethylhydrazine). The results show that there is no increased risk of cancer following mechanical stapling.
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Tierexperimentelle untersuchungen zur karzinogeninduzierten tumorbildung an kolotomien in abhängigkeit von nahtmaterialien
Langenbeck's Archives of Surgery, 1992Co-Authors: T. Hupp, Heinz J. Buhr, S. Ivancovic, N. BeckAbstract:To assess the possible risk of cancer in the operated colon after stapling compared with vicryl sutures, the influence of the nickel-containing staples was tested in caecum-resected and carcinogen-treated rats. The nickel-containing staples were seen as a Cocarcinogen. The aim of the study was to determine whether a higher incidence of cancer occurs at the anastomotic suture line depending on stapler vs. vicryl sutures after subcutaneous application of carcinogens (dimethylhydrazine). The results show that there is no increased risk of cancer following mechanical stapling.
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Tierexperimentelle untersuchungen zur karzinogeninduzierten tumorbildung an kolotomien in abhängigkeit von nahtmaterialien
Langenbecks Archiv für Chirurgie, 1992Co-Authors: T. Hupp, Heinz J. Buhr, S. Ivancovic, N. BeckAbstract:Der Einfluß nickelhaltiger Klammerndhte im Vergleich zu resorbierbaren Vicrylnähten auf eine mögliche Karzinomgefährdung des Kolons nach Zökalpolresektion wurde tierexperimentell an BD IX-Ratten untersucht. Die nickelhaltigen Klammerndhte wurden als Kokarzinogen angesehen. Das Ziel der Untersuchung war zu überprtifen, inwieweit im Vergleich zur Vicrylnaht an den maschinellen Klammernähten bei gleichzeitiger Applikation des Karzinogens 1,2Dimethylhydrazin (DMH) häufiger Karzinome an der Nahtlinie entstehen. Die Ergebnisse der Untersuchungen zeigen, daß die Karzinominduktion an der Nahtlinie durch Verwendung von KlammernLähten nicht begünstigt wird. To assess the possible risk of cancer in the operated colon after stapling compared with vicryl sutures, the influence of the nickel-containing staples was tested in caecum-resected and carcinogen-treated rats. The nickel-containing staples were seen as a Cocarcinogen. The aim of the study was to determine whether a higher incidence of cancer occurs at the anastomotic suture line depending on stapler vs. vicryl sutures after subcutaneous application of carcinogens (dimethylhydrazine). The results show that there is no increased risk of cancer following mechanical stapling.
Fredric J Burns - One of the best experts on this subject based on the ideXlab platform.
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evidence that arsenite acts as a Cocarcinogen in skin cancer
Toxicology and Applied Pharmacology, 2004Co-Authors: Toby G Rossman, Ahmed N Uddin, Fredric J BurnsAbstract:Inorganic arsenic (arsenite and arsenate) in drinking water has been associated with skin cancers in several countries such as Taiwan, Chile, Argentina, Bangladesh, and Mexico. This association has not been established in the United States. In addition, inorganic arsenic alone in drinking water does not cause skin cancers in animals. We recently showed that concentrations as low as 1.25 mg/l sodium arsenite were able to enhance the tumorigenicity of solar UV irradiation in mice. The tumors were almost all squamous cell carcinomas (SCCs). These data suggest that arsenic in drinking water may need a carcinogenic partner, such as sunlight, in the induction of skin cancers. Arsenite may enhance tumorigenicity via effects on DNA repair and DNA damage-induced cell cycle effects, leading to genomic instability. Others have found that dimethlyarsinic acid (DMA), a metabolite of arsenite, can induce bladder cancers at high concentrations in drinking water. In those experiments, skin cancers were not produced. Taken together, these data suggest that arsenite (or possibly an earlier metabolite), and not DMA, is responsible for the skin cancers, but a second genotoxic agent may be a requirement. The differences between the US and the other arsenic-exposed populations with regard to skin cancers might be explained by the lower levels of arsenic in the US, less sun exposure, better nutrition, or perhaps genetic susceptibility differences.
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arsenite is a Cocarcinogen with solar ultraviolet radiation for mouse skin an animal model for arsenic carcinogenesis
Toxicology and Applied Pharmacology, 2001Co-Authors: Toby G Rossman, Ahmed N Uddin, Fredric J Burns, Maarten C BoslandAbstract:Although epidemiological evidence shows an association between arsenic in drinking water and increased risk of skin, lung, and bladder cancers, arsenic compounds are not animal carcinogens. The lack of animal models has hindered mechanistic studies of arsenic carcinogenesis. Previously, this laboratory found that low concentrations of arsenite (the likely environmental carcinogen) which are not mutagenic can enhance the mutagenicity of other agents, including ultraviolet radiation (UVR). This enhancing effect appears to result from inhibition of DNA repair by arsenite. Recently we found that low concentrations of arsenite disrupted p53 function and upregulated cyclin D1. These results suggest that the failure to find an animal model for arsenic carcinogenesis is because arsenite is not a carcinogen per se, but rather acts as an enhancing agent (Cocarcinogen) with a genotoxic partner. We tested this hypothesis with solar UVR as carcinogenic stimulus in hairless Skh1 mice. Mice given 10 mg/l sodium arsenite in drinking water for 26 weeks had a 2.4-fold increase in yield of tumors after 1.7 KJ/m2 UVR three times weekly compared with mice given UVR alone. No tumors appeared in mice given arsenite alone. The tumors were mostly squamous cell carcinomas, and those occurring in mice given UVR plus arsenite appeared earlier and were much larger and more invasive than in mice given UVR alone. These results are consistent with the hypothesis that arsenic acts as a Cocarcinogen with a second (genotoxic) agent by inhibiting DNA repair and/or enhancing positive growth signaling.
Toby G Rossman - One of the best experts on this subject based on the ideXlab platform.
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evidence that arsenite acts as a Cocarcinogen in skin cancer
Toxicology and Applied Pharmacology, 2004Co-Authors: Toby G Rossman, Ahmed N Uddin, Fredric J BurnsAbstract:Inorganic arsenic (arsenite and arsenate) in drinking water has been associated with skin cancers in several countries such as Taiwan, Chile, Argentina, Bangladesh, and Mexico. This association has not been established in the United States. In addition, inorganic arsenic alone in drinking water does not cause skin cancers in animals. We recently showed that concentrations as low as 1.25 mg/l sodium arsenite were able to enhance the tumorigenicity of solar UV irradiation in mice. The tumors were almost all squamous cell carcinomas (SCCs). These data suggest that arsenic in drinking water may need a carcinogenic partner, such as sunlight, in the induction of skin cancers. Arsenite may enhance tumorigenicity via effects on DNA repair and DNA damage-induced cell cycle effects, leading to genomic instability. Others have found that dimethlyarsinic acid (DMA), a metabolite of arsenite, can induce bladder cancers at high concentrations in drinking water. In those experiments, skin cancers were not produced. Taken together, these data suggest that arsenite (or possibly an earlier metabolite), and not DMA, is responsible for the skin cancers, but a second genotoxic agent may be a requirement. The differences between the US and the other arsenic-exposed populations with regard to skin cancers might be explained by the lower levels of arsenic in the US, less sun exposure, better nutrition, or perhaps genetic susceptibility differences.
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arsenite is a Cocarcinogen with solar ultraviolet radiation for mouse skin an animal model for arsenic carcinogenesis
Toxicology and Applied Pharmacology, 2001Co-Authors: Toby G Rossman, Ahmed N Uddin, Fredric J Burns, Maarten C BoslandAbstract:Although epidemiological evidence shows an association between arsenic in drinking water and increased risk of skin, lung, and bladder cancers, arsenic compounds are not animal carcinogens. The lack of animal models has hindered mechanistic studies of arsenic carcinogenesis. Previously, this laboratory found that low concentrations of arsenite (the likely environmental carcinogen) which are not mutagenic can enhance the mutagenicity of other agents, including ultraviolet radiation (UVR). This enhancing effect appears to result from inhibition of DNA repair by arsenite. Recently we found that low concentrations of arsenite disrupted p53 function and upregulated cyclin D1. These results suggest that the failure to find an animal model for arsenic carcinogenesis is because arsenite is not a carcinogen per se, but rather acts as an enhancing agent (Cocarcinogen) with a genotoxic partner. We tested this hypothesis with solar UVR as carcinogenic stimulus in hairless Skh1 mice. Mice given 10 mg/l sodium arsenite in drinking water for 26 weeks had a 2.4-fold increase in yield of tumors after 1.7 KJ/m2 UVR three times weekly compared with mice given UVR alone. No tumors appeared in mice given arsenite alone. The tumors were mostly squamous cell carcinomas, and those occurring in mice given UVR plus arsenite appeared earlier and were much larger and more invasive than in mice given UVR alone. These results are consistent with the hypothesis that arsenic acts as a Cocarcinogen with a second (genotoxic) agent by inhibiting DNA repair and/or enhancing positive growth signaling.
Michele Carbone - One of the best experts on this subject based on the ideXlab platform.
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crocidolite asbestos and sv40 are Cocarcinogens in human mesothelial cells and in causing mesothelioma in hamsters
Proceedings of the National Academy of Sciences of the United States of America, 2006Co-Authors: Barbara Kroczynska, Rochelle Cutrone, Maurizio Bocchetta, Haining Yang, Amira G Elmishad, Pamela M Vacek, Maria E Ramosnino, Brooke T Mossman, Harvey I Pass, Michele CarboneAbstract:Only a fraction of subjects exposed to asbestos develop malignant mesothelioma (MM), suggesting that additional factors may render some individuals more susceptible. We tested the hypothesis that asbestos and Simian virus (SV40) are Cocarcinogens. Asbestos and SV40 in combination had a costimulatory effect in inducing ERK1/2 phosphorylation and activator protein-1 (AP-1) activity in both primary Syrian hamster mesothelial cells (SHM) and primary human mesothelial cells (HM). Ap-1 activity caused the expression and activation of matrix metalloprotease (MMP)-1 and MMP-9, which in turn led to cell invasion. Experiments using siRNA and chemical inhibitors confirmed the specificity of these results. The same effects were observed in HM and SHM. Experiments in hamsters showed strong Cocarcinogenesis between asbestos and SV40: SV40 did not cause MM, asbestos caused MM in 20% of hamsters, and asbestos and SV40 together caused MM in 90% of hamsters. Significantly lower amounts of asbestos were sufficient to cause MM in animals infected with SV40. Our results indicate that mineral fibers and viruses can be Cocarcinogens and suggest that lower amounts of asbestos may be sufficient to cause MM in individuals infected with SV40.
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Human mesothelial cells are unusually susceptible to simian virus 40-mediated transformation and asbestos Cocarcinogenicity
Proceedings of the National Academy of Sciences of the United States of America, 2000Co-Authors: Maurizio Bocchetta, Harvey I Pass, Ilaria Di Resta, Amy Powers, Raoul Fresco, Alessandra Tosolini, Joseph R. Testa, Paola Rizzo, Michele CarboneAbstract:Mesothelioma, a malignancy associated with asbestos, has been recently linked to simian virus 40 (SV40). We found that infection of human mesothelial cells by SV40 is very different from the semipermissive infection thought to be characteristic of human cells. Mesothelial cells are uniformly infected but not lysed by SV40, a mechanism related to p53, and undergo cell transformation at an extremely high rate. Exposure of mesothelial cells to asbestos complemented SV40 mutants in transformation. Our data provide a mechanistic explanation for the ability of SV40 to transform mesothelial cells preferentially and indicate that asbestos and SV40 may be Cocarcinogens.
T. Hupp - One of the best experts on this subject based on the ideXlab platform.
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Influence of suture material on experimental colonic carcinogenesis in rats
1992Co-Authors: T. Hupp, Heinz J. Buhr, S. Ivancovic, N. BeckAbstract:To assess the possible risk of cancer in the operated colon after stapling compared with vicryl sutures, the influence of the nickel-containing staples was tested in caecum-resected and carcinogen-treated rats. The nickel-containing staples were seen as a Cocarcinogen. The aim of the study was to determine whether a higher incidence of cancer occurs at the anastomotic suture line depending on stapler vs. vicryl sutures after subcutaneous application of carcinogens (dimethylhydrazine). The results show that there is no increased risk of cancer following mechanical stapling.
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Tierexperimentelle untersuchungen zur karzinogeninduzierten tumorbildung an kolotomien in abhängigkeit von nahtmaterialien
Langenbeck's Archives of Surgery, 1992Co-Authors: T. Hupp, Heinz J. Buhr, S. Ivancovic, N. BeckAbstract:To assess the possible risk of cancer in the operated colon after stapling compared with vicryl sutures, the influence of the nickel-containing staples was tested in caecum-resected and carcinogen-treated rats. The nickel-containing staples were seen as a Cocarcinogen. The aim of the study was to determine whether a higher incidence of cancer occurs at the anastomotic suture line depending on stapler vs. vicryl sutures after subcutaneous application of carcinogens (dimethylhydrazine). The results show that there is no increased risk of cancer following mechanical stapling.
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Tierexperimentelle untersuchungen zur karzinogeninduzierten tumorbildung an kolotomien in abhängigkeit von nahtmaterialien
Langenbecks Archiv für Chirurgie, 1992Co-Authors: T. Hupp, Heinz J. Buhr, S. Ivancovic, N. BeckAbstract:Der Einfluß nickelhaltiger Klammerndhte im Vergleich zu resorbierbaren Vicrylnähten auf eine mögliche Karzinomgefährdung des Kolons nach Zökalpolresektion wurde tierexperimentell an BD IX-Ratten untersucht. Die nickelhaltigen Klammerndhte wurden als Kokarzinogen angesehen. Das Ziel der Untersuchung war zu überprtifen, inwieweit im Vergleich zur Vicrylnaht an den maschinellen Klammernähten bei gleichzeitiger Applikation des Karzinogens 1,2Dimethylhydrazin (DMH) häufiger Karzinome an der Nahtlinie entstehen. Die Ergebnisse der Untersuchungen zeigen, daß die Karzinominduktion an der Nahtlinie durch Verwendung von KlammernLähten nicht begünstigt wird. To assess the possible risk of cancer in the operated colon after stapling compared with vicryl sutures, the influence of the nickel-containing staples was tested in caecum-resected and carcinogen-treated rats. The nickel-containing staples were seen as a Cocarcinogen. The aim of the study was to determine whether a higher incidence of cancer occurs at the anastomotic suture line depending on stapler vs. vicryl sutures after subcutaneous application of carcinogens (dimethylhydrazine). The results show that there is no increased risk of cancer following mechanical stapling.