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Apoptosis and cancer mechanisms
H Pan1, C Yin, T Van Dyke
1Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, USA.
Cancer Surveys
|January 1, 1997
Summary
Cancer research now recognizes apoptosis regulation as key to tumorigenesis. Animal models studying BCL2 and TP53 genes reveal how apoptosis dysregulation drives cancer growth.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cancer research initially focused on cell growth regulators.
- The role of apoptosis (programmed cell death) in tumorigenesis is a more recent focus.
- Genes like BCL2 and TP53 are implicated in both cancer and apoptosis regulation.
Purpose of the Study:
- To explore the contribution of apoptosis dysregulation to cancer development.
- To discuss animal models investigating the role of apoptosis in tumorigenesis.
- To specifically examine the roles of bcl-2 family genes and p53 in cancer.
Main Methods:
- Review of cell culture studies demonstrating TP53-induced and BCL2-suppressed apoptosis.
- Analysis of findings from mammalian virus studies on apoptosis induction and evasion.
- Discussion of various animal models developed to study apoptosis regulation in tumorigenesis.
Main Results:
- TP53 can induce apoptosis, while BCL2 can suppress it.
- Dysregulation of apoptosis is linked to neoplastic transformation and malignant growth.
- Animal models provide insights into the in vivo roles of apoptosis regulators.
Conclusions:
- Apoptosis regulation is a critical factor in cancer development.
- Understanding the interplay between genes like BCL2, TP53, and apoptosis is vital for cancer research.
- Animal models are valuable tools for dissecting the complex mechanisms of apoptosis in tumorigenesis.