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Role of active cell death (apoptosis) in multi-stage carcinogenesis
R Schulte-Hermann1, W Bursch, B Grasl-Kraupp
1Institut für Tumorbiologie-Krebsforschung, Wien, Austria.
Abstract:
Active cell death is a genetically encoded self-destruction of a cell. There occur morphologically different types of active cell death, e.g. apoptosis in the liver or autophagic cell death in human mammary carcinoma cells after tamoxifen treatment (Pre)neoplastic lesions in rat liver exhibit enhanced rates of apoptosis, which tend to increase with increasing malignancy. Tumor promoters and non-genotoxic carcinogens inhibit active cell death, thereby increasing the accumulation of (pre)neoplastic cells and accelerating the development of cancer. On the other hand promoter withdrawal, fasting or application of negative growth signals such as transforming growth factor beta 1 (TGF beta 1) enhance apoptosis and can lead to selective regression of preneoplastic lesions or tumors.
Insights
Active cell death, including apoptosis, is crucial for preventing cancer. Inhibiting this process accelerates tumor development, while promoting it can lead to lesion regression.
Area of Science:
- Cell biology
- Cancer research
- Biochemistry
Background:
- Active cell death is a genetically controlled cellular self-destruction process.
- Morphologically distinct forms of active cell death exist, such as apoptosis and autophagic cell death.
- Enhanced apoptosis rates are observed in preneoplastic lesions, correlating with increased malignancy.
Purpose of the Study:
- To investigate the role of active cell death in cancer development and regression.
- To explore how tumor promoters and inhibitors of active cell death influence cancer progression.
- To examine the potential of enhancing apoptosis for therapeutic benefit in preneoplastic lesions and tumors.
Main Methods:
- Literature review on active cell death mechanisms.
- Analysis of apoptosis rates in preneoplastic liver lesions.
- Investigation of the effects of tumor promoters and growth factors on cell death.
Main Results:
- Tumor promoters and non-genotoxic carcinogens inhibit active cell death, promoting cell accumulation and cancer development.
- Withdrawal of promoters, fasting, or TGF-β1 application enhances apoptosis.
- Enhanced apoptosis can induce selective regression of preneoplastic lesions and tumors.
Conclusions:
- Active cell death is a critical mechanism in preventing and potentially reversing cancer.
- Modulating active cell death pathways presents a potential therapeutic strategy for cancer treatment.
- Understanding the regulation of apoptosis is key to developing novel cancer therapies.