Oncogenetics - Mechanism of Cancer (tumor suppressor genes and oncogenes)

Summary

This video explores the genetic mechanisms behind cancer, focusing on how mutations in the cell cycle lead to uncontrolled cell growth. It explains the phases of the cell cycle, including G1, S, G2, and M, and the role of checkpoints in regulating cell progression. The activation of oncogenes like Ras and Myc promotes excessive cell division, while the inactivation of tumor suppressor genes such as p53 prevents DNA repair and apoptosis. These genetic changes cause cells to bypass normal regulatory processes, resulting in cancerous growth. Understanding these mechanisms sheds light on the development and potential treatment of cancer.

Takeaways

• 😀 The cell cycle consists of distinct phases: G0 (quiescent phase), G1 (growth phase), S (synthesis phase), G2 (growth phase), and M (mitosis).
• 😀 The cell cycle is controlled by checkpoints at the end of the G1, G2, and M phases to ensure no errors in the DNA or cell processes.
• 😀 Cyclins and CDKs are key proteins that drive the progression of the cell cycle. Their levels must be tightly regulated for normal cell growth.
• 😀 Mutations in cyclins or CDKs can cause uncontrolled cell division, leading to cancer development.
• 😀 Genetic mutations, such as point mutations, DNA amplification, chromosomal rearrangements, and epigenetic modifications, can trigger cancer.
• 😀 Cancerous cells often bypass the regular checkpoints in the cell cycle, leading to unchecked growth and proliferation.
• 😀 Oncogenes, like the Ras and Myc genes, can become activated through mutations, leading to excessive cell growth and cancer development.
• 😀 Tumor suppressor genes, such as p53, APC, and BRCA1/2, normally prevent cells with damaged DNA from proliferating by inducing arrest, repair, or apoptosis.
• 😀 Mutations in tumor suppressor genes, particularly p53, can prevent the cell from arresting, repairing, or undergoing apoptosis, resulting in uncontrolled growth.
• 😀 In summary, cancer is often caused by the activation of oncogenes and the inactivation of tumor suppressor genes, disrupting normal cell cycle regulation.

Q & A

What is the role of cyclins and CDKs in the cell cycle?

Cyclins and cyclin-dependent kinases (CDKs) are key regulators that drive the progression of the cell cycle. Cyclins activate CDKs, which then phosphorylate target proteins to allow the cell to progress through different phases of the cell cycle, such as from G1 to S phase and from G2 to M phase.

What happens when there is an overproduction of cyclins and CDKs?

Overproduction of cyclins and CDKs can lead to uncontrolled cell cycle progression, where cells continuously divide without proper regulation. This uncontrolled growth is one of the main mechanisms that contribute to cancer development.

What are the checkpoints in the cell cycle, and why are they important?

The cell cycle has several checkpoints, such as at the G1, G2, and M phases, to ensure that the cell has no DNA damage or errors before proceeding. These checkpoints prevent the division of damaged cells, thus protecting the organism from uncontrolled cell growth and cancer.

How do mutations in the Ras gene contribute to cancer?

Mutations in the Ras gene lead to the production of continuously active Ras proteins, which bypass normal regulatory controls in the cell. This causes an overactivation of signaling pathways that drive cell growth and division, contributing to uncontrolled cell proliferation typical of cancer.

What role does the MYC gene play in cancer development?

The MYC gene produces proteins that regulate cell growth, survival, and activity. Mutations in MYC can cause overproduction of these proteins, leading to excessive cell growth, increased survival of abnormal cells, and resistance to cell death, all of which contribute to cancer.

What are tumor suppressor genes, and how do they prevent cancer?

Tumor suppressor genes, such as p53, APC, and BRCA1/2, act as safety mechanisms in the cell cycle. They either halt the cell cycle to allow for DNA repair or induce apoptosis (programmed cell death) if the damage is irreparable. Inactivation of these genes can prevent these protective responses, allowing damaged cells to survive and proliferate, leading to cancer.

How does the p53 protein help prevent cancer?

The p53 protein plays a crucial role in responding to DNA damage. When DNA is damaged, p53 activates genes that halt the cell cycle (like p21) to allow for repair, and if the damage cannot be fixed, p53 can trigger apoptosis to prevent the damaged cell from proliferating.

What is the difference between oncogenes and tumor suppressor genes?

Oncogenes are mutated genes that promote uncontrolled cell growth, while tumor suppressor genes normally inhibit cell cycle progression or promote cell death to prevent cancer. In cancer, oncogenes are often overactive, and tumor suppressor genes are inactivated, leading to unchecked cell division.

What is the G0 phase, and why is it important for the cell cycle?

The G0 phase is a resting phase where cells are not actively dividing. It is important because it represents a state of dormancy or quiescence, where cells are not at risk of uncontrolled division. Cells can re-enter the cycle from G0 when stimulated by certain signals.

How do mutations in tumor suppressor genes lead to cancer?

Mutations in tumor suppressor genes, like p53, prevent the normal checkpoints in the cell cycle from functioning. This means that cells with DNA damage or other abnormalities can continue dividing without repair or being eliminated, leading to cancerous growth.