Tumor suppressor genes

Definition

Tumor suppressor genes are segments of DNA that produce proteins responsible for regulating cell growth and division, acting as a brake on cell proliferation. When these genes are mutated or inactivated, they lose their ability to control the cell cycle, leading to uncontrolled cell growth and potentially resulting in cancer. They play a critical role in maintaining genomic stability and preventing tumor formation by encoding proteins that can repair DNA damage, induce apoptosis, or inhibit cell cycle progression.

5 Must Know Facts For Your Next Test

1. Common examples of tumor suppressor genes include TP53, BRCA1, and RB1, which are associated with various cancers when mutated.
2. Tumor suppressor genes are typically involved in repairing DNA damage, controlling the cell cycle, and initiating apoptosis in response to cellular stress.
3. Both alleles of a tumor suppressor gene must be inactivated for cancer to develop, which is known as the 'two-hit hypothesis.'
4. Mutations in tumor suppressor genes can arise from environmental factors, such as radiation or carcinogens, or can be inherited through familial cancer syndromes.
5. The loss of function of tumor suppressor genes is a critical event in the progression of many types of cancer, making them key targets for cancer therapy and research.

Review Questions

• How do tumor suppressor genes interact with the cell cycle to prevent cancer development?
  • Tumor suppressor genes play a crucial role in regulating the cell cycle by controlling key checkpoints that monitor for DNA damage and other cellular stresses. For example, when DNA damage is detected, tumor suppressor proteins like p53 can activate repair mechanisms or trigger apoptosis to prevent damaged cells from dividing. This regulation helps maintain genomic stability and prevents the accumulation of mutations that could lead to cancer.
• Discuss the significance of the 'two-hit hypothesis' in relation to tumor suppressor gene function and cancer susceptibility.
  • The 'two-hit hypothesis' suggests that both alleles of a tumor suppressor gene must be mutated or inactivated for cancer to occur. This is significant because it highlights the need for both genetic changes to compromise the gene's protective functions. In familial cases of cancer, individuals may inherit one mutated allele and only require a second hit (such as a mutation from environmental exposure) to lose tumor suppression entirely, thus increasing their susceptibility to cancer.
• Evaluate the impact of mutations in tumor suppressor genes on cancer treatment strategies and research directions.
  • Mutations in tumor suppressor genes significantly influence cancer treatment strategies by identifying potential targets for therapy. Understanding how these mutations disrupt normal cellular processes allows researchers to develop targeted therapies that restore function or mimic tumor suppressor activity. Additionally, studying these mutations aids in the design of personalized medicine approaches, where treatment regimens can be tailored based on an individual's genetic profile, ultimately improving patient outcomes and advancing cancer research.

Related terms

Oncogenes: Oncogenes are mutated forms of proto-oncogenes that promote cell division and survival, leading to cancer when activated.

Cell Cycle Checkpoints: Cell cycle checkpoints are control mechanisms that ensure the proper progression of the cell cycle, allowing for repair of damaged DNA before cell division.

Apoptosis: Apoptosis is a programmed cell death process that helps eliminate damaged or unwanted cells, a mechanism often regulated by tumor suppressor genes.