Environmental chemical carcinogens and liver cancer

Ca, Linsell

doi:10.1080/15287397909529742

Cited by 7 publications

(3 citation statements)

References 11 publications

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“…A large variety of hepatic carcinogens have been intensively investigated, e.g. food contamination with aflatoxins (4); anabolic steroids, oestrogens (5); and last but not least the association with liver cirrhosis (6). The latter causes trouble in interpreting both radiological and scintigraphic findings.…”

Section: Differential Diagnostic Aspects Of Common Focal Liver Lesionsmentioning

confidence: 99%

Focal Liver Lesions: Receptor Scintigraphy for Differential Diagnosis

Kienast

Kurtaran

2003

Imaging Decisions

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Section: Differential Diagnostic Aspects Of Common Focal Liver Lesionsmentioning

confidence: 99%

Focal Liver Lesions: Receptor Scintigraphy for Differential Diagnosis

Kienast

Kurtaran

2003

Imaging Decisions

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“…Aflatoxins have been isolated from Aspergillusflavus. Aflatoxin B~ has been shown to be a potent hepatocarcinogen and a mutagen (Wogan, 1973(Wogan, , 1976Linsell, 1979;Hayes, 1981), but requires metabolic activation in order to be genotoxic (Lin et al, 1977). Aflatoxin Bz, however, has been found to be much less active than aflatoxin B~ (Wong et al, 1976).…”

Section: Introductionmentioning

confidence: 99%

Effect of biological toxins on gap-junctionai intercellular communication in Chinese hamster V79 cells

et al. 1987

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Since chemical modulation of gap-junctional intercellular communication has been implicated in several toxicological endpoints, a study to examine the ability of several biological toxins to inhibit this process was undertaken. Eight biological toxins were tested for their ability to inhibit metabolic cooperation, a measure of gap-junctional intercellular communication, in the Chinese V79 cell system. Aplysiatoxin, anhydrodebromoaplysiatoxin and debromoaplysiatoxin showed the strongest ability to inhibit metabolic cooperation while T2-toxin and vomitoxin inhibited metabolic cooperation to a lesser degree. Aflatoxin B1, aflatoxin B2 and palytoxin were inactive in the Chinese V79 system. Palytoxin, which was extremely cytotoxic, might act as a tumor promoter if it induces compensatory hyperplasia in vivo.

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“…It has long been recognized that exposure to certain toxins and chronic inflammatory states are known mechanisms of cancer development in several different organs such as the lung, liver and bladder [37][38][39][40][41][42][43]. These toxins are thought to cause specific mutations that lead to uncontrolled growth of tissues.…”

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confidence: 99%

Repair and regeneration: opportunities for carcinogenesis from tissue stem cells

Perryman

Sylvester

2006

Journal of Cellular and Molecular Medicine

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This review will discuss the mechanisms of repair and regeneration in various tissue types and how dysregulation of these mechaisms may lead to cancer. Normal homeostasis involves a careful balance between cell loss and cell renewal. Stem and progenitor cells perform these biologic processes as the functional units of regeneration during both tissue homeostasis and repair. The concept of tissue stem cells capable of giving rise to all differentiated cells within a given tissue led to the concept of a cellulr hierarchy in tissues and in tumors. Thus, only a few cells may be necessary and sufficient for tissue repair or tumor regeneration. This is known as the hierarchical model of tumorigenesis. This report will compare this model with the stochastic model of tumorigenesis. Under normal circumstances, the processes of tissue regeneration or homeostasis are tightly regulated by several morphogen pathways to prevent excessive or inappropriate cell growth. This review presents the recent evidence that dysregulation of these processes may provide opportunities for carcinogenesis for the long-lived, highly proliferative tissue stem cell population. New findings of cancer initiating tissue stem cells identified in several solid and circulating cancers including breast, brain hematopoietic tumors will also be reviewed. Finally, this report reviews the cellular biology of cancer and its relevance to the development of more effective cancer treatment protocols.

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Environmental chemical carcinogens and liver cancer

Cited by 7 publications

References 11 publications

Focal Liver Lesions: Receptor Scintigraphy for Differential Diagnosis

Focal Liver Lesions: Receptor Scintigraphy for Differential Diagnosis

Effect of biological toxins on gap-junctionai intercellular communication in Chinese hamster V79 cells

Repair and regeneration: opportunities for carcinogenesis from tissue stem cells

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