Works (4)
Updated: July 5th, 2023 16:02
2001 article
Hepatocellular proliferation in response to a peroxisome proliferator does not require TNFα signaling
Anderson, S. P., Dunn, C. S., Cattley, R. C., & Corton, J. C. (2001, November 1). Carcinogenesis.
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
topics (OpenAlex): Peroxisome Proliferator-Activated Receptors; Drug Transport and Resistance Mechanisms
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)
open access via academic.oup.com (publisher PDF)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018
2000 article
Apoptosis, mitosis and cyclophilin-40 expression in regressing peroxisome proliferator-induced adenomas
Miller, R. T., Anderson, S. P., Corton, J. C., & Cattley, R. C. (2000, April 1). Carcinogenesis.
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
topics (OpenAlex): Peroxisome Proliferator-Activated Receptors; Signaling Pathways in Disease; Metabolism, Diabetes, and Cancer
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018
1999 article
Altered bcl-2 family expression during non-genotoxic hepatocarcinogenesis in mice
Christensen, J. G. (1999, August 1). Carcinogenesis.
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
topics (OpenAlex): Cell death mechanisms and regulation; Drug Transport and Resistance Mechanisms; Drug-Induced Hepatotoxicity and Protection
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science; OpenAlex)
11. Sustainable Cities and Communities
(Web of Science)
Source: Web Of Science
Added: August 6, 2018
1999 article
Hepatic expression of acute-phase protein genes during carcinogenesis induced by peroxisome proliferators
Anderson, S. P., Cattley, R. C., & Corton, J. C. (1999, December 1). Molecular Carcinogenesis.
author keywords: hepatocarcinogenesis; gene expression; differential display; acute-phase proteins
topics (OpenAlex): Peroxisome Proliferator-Activated Receptors; Metabolism, Diabetes, and Cancer; Cancer, Hypoxia, and Metabolism
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018