Thomas L. Goldsworthy

Works (4)

Updated: July 5th, 2023 16:03

1999 journal article

Altered bcl-2 family expression during non-genotoxic hepatocarcinogenesis in mice

CARCINOGENESIS, 20(8), 1583–1590.

By: J. Christensen n, E. Romach, L. Healy, A. Gonzales, S. Anderson, D. Malarkey, J. Corton, T. Fox, R. Cattley, T. Goldsworthy

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)
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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

1998 journal article

Attenuation of G(1) checkpoint function by the non-genotoxic carcinogen phenobarbital

CARCINOGENESIS, 19(7), 1173–1183.

By: A. Gonzales *, J. Christensen, R. Preston, T. Goldsworthy, T. Tlsty & T. Fox

MeSH headings : Animals; Bleomycin / pharmacology; Carcinogens / toxicity; Cell Cycle / drug effects; Cell Cycle / physiology; Cells, Cultured; DNA / drug effects; DNA / metabolism; DNA Damage; G1 Phase / drug effects; G1 Phase / physiology; Liver / cytology; Liver / drug effects; Liver / metabolism; Liver Neoplasms, Experimental / chemically induced; Liver Neoplasms, Experimental / genetics; Male; Mice; Mice, Inbred C57BL; Phenobarbital / toxicity; S Phase / drug effects; S Phase / physiology; Tumor Suppressor Protein p53 / biosynthesis; Tumor Suppressor Protein p53 / metabolism
TL;DR: Altered G1 checkpoint function represents an epigenetic mechanism by which phenobarbital may prevent the detection and repair of DNA damage and indirectly increase the frequency of genotoxic events above that occurring spontaneously. (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

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