Steven Paul Anderson

MeSH headings : Animals; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; Cell Division / drug effects; DNA / metabolism; DNA Primers / chemistry; DNA-Binding Proteins; Hepatocyte Nuclear Factor 4; Interleukin-1 / metabolism; Interleukin-6 / metabolism; Liver / drug effects; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Peroxisome Proliferators / pharmacology; Peroxisomes / drug effects; Peroxisomes / ultrastructure; Phosphoproteins / metabolism; Pyrimidines / pharmacology; RNA / metabolism; Receptors, Cytoplasmic and Nuclear / metabolism; Receptors, Tumor Necrosis Factor / genetics; Receptors, Tumor Necrosis Factor / metabolism; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Transcription Factors / metabolism; Tumor Necrosis Factor-alpha / metabolism

TL;DR: The data suggest that the hepatic mitogenesis and carcinogenesis associated with peroxisome proliferator exposure is not mediated via TNFalpha but instead may involve an alternative pathway requiring IL1beta and IL6. (via Semantic Scholar)

MeSH headings : Adenoma / chemically induced; Adenoma / metabolism; Adenoma / pathology; Animals; Apoptosis / drug effects; Carrier Proteins / analysis; Carrier Proteins / physiology; Cyclophilin D; Cyclophilins; Liver / drug effects; Liver Neoplasms, Experimental / chemically induced; Liver Neoplasms, Experimental / metabolism; Liver Neoplasms, Experimental / pathology; Male; Mitosis / drug effects; Peptidylprolyl Isomerase / analysis; Peptidylprolyl Isomerase / physiology; Peroxisome Proliferators / toxicity; Pyrimidines / metabolism; Rats; Rats, Inbred F344; Receptors, Cytoplasmic and Nuclear / physiology; Transcription Factors / physiology

TL;DR: Results indicate that WY, 643-induced adenomas regress rapidly following withdrawal of the PP in association with declining liver WY-14,643 levels, suggesting that peroxisome proliferator-activated receptor alpha may mediate PP-induced alterations in mitogenic and/or apoptotic regulation in growing tumors, in conjunction with alterations in Cyp-40 signal transduction. (via Semantic Scholar)

MeSH headings : Adenoma / chemically induced; Adenoma / metabolism; Adenoma / pathology; Animals; Apoptosis; Carcinogens; Carcinoma / chemically induced; Carcinoma / metabolism; Carcinoma / pathology; Carrier Proteins / metabolism; Chlordan; DNA-Binding Proteins; Liver Neoplasms, Experimental / chemically induced; Liver Neoplasms, Experimental / metabolism; Liver Neoplasms, Experimental / pathology; Male; Mice; Neoplasm Proteins / metabolism; Phenobarbital; Phenotype; Polychlorinated Dibenzodioxins; Proto-Oncogene Proteins / metabolism; Proto-Oncogene Proteins c-bcl-2 / metabolism; Pyrimidines; Transcription Factors; bcl-2-Associated X Protein; bcl-X Protein

TL;DR: The results suggest that regulation of apoptotic proteins is altered during non-genotoxic carcinogenesis in mouse liver and there were both chemical- and lesion-specific aspects of expression of apoptosis proteins during hepatocarcinogenesis in mice. (via Semantic Scholar)

author keywords: hepatocarcinogenesis; gene expression; differential display; acute-phase proteins

TL;DR: It is concluded that PPARα activation by several different PPs leads to dysregulation of hepatic APP gene expression in rats and mice, which may indicate alterations in cytokine signaling networks regulating both APP geneexpression and hepatocellular proliferation. (via Semantic Scholar)