Russell C. Cattley

Works (7)

Updated: February 10th, 2025 16:10

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.

By: S. Anderson*, C. Dunn, R. Cattley* & J. Corton

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)
UN Sustainable Development Goals Color Wheel
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.

By: R. Miller n, S. Anderson n, J. Corton n & R. Cattley n

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 Goals Color Wheel
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

Alteration of protein kinase C isoform-specific expression during rat hepatocarcinogenesis after exposure to the peroxisome proliferator WY-14,643

Corton, J. C., Swanson, C., Miller, R. T., & Cattley, R. C. (1999, March 1). Cancer Letters.

By: J. Corton *, C. Swanson*, R. Miller n & R. Cattley*

author keywords: protein kinase C; peroxisome proliferators; hepatocarcinogenesis; rat
MeSH headings : Adenoma / chemically induced; Adenoma / enzymology; Animals; Carcinogens; Chloroform / toxicity; Liver Neoplasms, Experimental / chemically induced; Liver Neoplasms, Experimental / enzymology; Male; Neoplasm Proteins / metabolism; Protein Isoforms / metabolism; Protein Kinase C / metabolism; Pyrimidines; Rats; Rats, Inbred F344; Rats, Sprague-Dawley
topics (OpenAlex): Peroxisome Proliferator-Activated Receptors; Protein Kinase Regulation and GTPase Signaling; Metabolism, Diabetes, and Cancer
TL;DR: Results indicate that alterations in PKCalpha, beta and delta isoforms, which regulate mitogenesis, could play important roles in perpetuating the high cell proliferative rate in PPC-induced hepatocellular adenomas. (via Semantic Scholar)
UN Sustainable Development Goals Color Wheel
UN Sustainable Development Goal Categories
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.

By: J. Christensen n

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 Goals Color Wheel
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

1999 journal article

Dysregulation of apoptosis by c-myc in transgenic hepatocytes and effects of growth factors and nongenotoxic carcinogens

Molecular Carcinogenesis, 25(4), 273–284.

By: J. Christensen, T. Goldsworthy & R. Cattley

Source: NC State University Libraries
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.

By: S. Anderson n, R. Cattley* & J. Corton *

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 Goals Color Wheel
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

1998 journal article

Regulation of apoptosis in mouse hepatocytes and alteration of apoptosis by nongenotoxic carcinogens

Cell Growth & Differentiation, 9(9), 815–825.

By: J. Christensen, A. Gonzales, R. Cattley & T. Goldsworthy

Source: NC State University Libraries
Added: August 6, 2018

Citation Index includes data from a number of different sources. If you have questions about the sources of data in the Citation Index or need a set of data which is free to re-distribute, please contact us.

Certain data included herein are derived from the Web of Science© and InCites© (2026) of Clarivate Analytics. All rights reserved. You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.