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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Cancer-Critical Genes I: Proto-oncogenes01:33

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Mutagenicity and Carcinogenicity01:25

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Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Spontaneous and Induced Mutations01:30

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Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Pathological markers for non-genotoxic agent-associated carcinogenesis.

N Ito1, R Hasegawa, K Imaida

  • 1First Department of Pathology, Nagoya City University Medical School, Japan.

Toxicology Letters
|December 1, 1992
PubMed
Summary

Glutathione S-transferase placental form (GST-P) positive foci are effective preneoplastic markers in rat liver bioassays. This method simplifies quantitative analysis and improves carcinogen detection for risk assessment.

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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
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Published on: December 19, 2019

Area of Science:

  • Toxicology
  • Biomarker Discovery
  • Carcinogenesis Research

Background:

  • Preneoplastic lesions in rat liver are crucial for carcinogenicity risk assessment.
  • Enzyme-altered foci have been proposed as markers, but practical limitations exist.

Purpose of the Study:

  • To compare the suitability of various histochemical and immunohistochemical markers for preneoplastic lesions in rat liver.
  • To establish and validate a liver medium-term bioassay using glutathione S-transferase placental form (GST-P) positive foci as endpoint lesions.

Main Methods:

  • Comparison of histochemical and immunohistochemical staining techniques for enzyme-altered foci.
  • Development of an 8-week rat liver bioassay model using diethylnitrosamine initiation.
  • Quantification of GST-P positive foci in fixed paraffin-embedded liver tissues.

Main Results:

  • Immunohistochemically stained GST-P positive foci offer practical advantages for risk assessment due to ease of analysis and clear visualization.
  • The established bioassay model successfully detected carcinogenic potential for many agents, primarily liver carcinogens.
  • Two peroxisome proliferators, clofibrate and DEHP, were identified as exceptions requiring specific peroxisomal enzyme markers.

Conclusions:

  • GST-P positive foci are highly suitable preneoplastic markers for rat liver risk assessment, facilitating quantitative analysis.
  • The developed medium-term bioassay model is effective for detecting the carcinogenic potential of various chemicals.
  • Further investigation into specific markers like peroxisomal enzymes is necessary for certain chemical classes.