Oncogenes and Tumor Suppressors: Videos & Practice Problems

Cancer cells exhibit unique properties such as uncontrolled growth, insensitivity to anti-growth signals, evasion of apoptosis, and genetic instability. These characteristics arise from mutations in oncogenes and tumor suppressor genes. Oncogenes, like RAS, promote cell proliferation when overexpressed, while tumor suppressors, such as p53, prevent tumor formation by regulating cell cycle and DNA repair. Loss of tumor suppressor function leads to increased mutations and tumor development, highlighting the critical balance between these gene types in cancer progression.

Oncogenes and Tumor Suppressors

Cancer is characterized by cells that exhibit several distinct properties due to various mutations. These properties include the ability to grow without external growth signals, insensitivity to anti-growth signals, evasion of apoptosis (programmed cell death), unlimited replication, angiogenesis (formation of new blood vessels), invasion and metastasis (spreading to other tissues), and genetic instability, which leads to rapid accumulation of mutations. Each of these characteristics contributes to the uncontrolled growth and spread of cancer cells.

At the genetic level, two main types of genes are involved in cancer development: oncogenes and tumor suppressor genes. Oncogenes are mutated forms of normal genes (proto-oncogenes) that become overexpressed, leading to increased cell proliferation, survival, and tumor development. This overexpression can occur through mutations or gene amplification, resulting in excessive activity that drives cancerous behavior. Common examples of oncogenes include growth factors, growth factor receptors, GTP-binding proteins, and transcription factors. A notable oncogene is RAS, which is mutated in approximately 20% of human cancers, highlighting its significant role in tumorigenesis.

In contrast, tumor suppressor genes function to inhibit cell growth and promote apoptosis. When these genes are mutated, their activity is lost, which can lead to unchecked cell proliferation and survival. A well-known tumor suppressor is p53, a transcription factor that responds to DNA damage by initiating repair processes or triggering apoptosis. When p53 is mutated, cancer cells can accumulate further mutations without the necessary checks, facilitating tumor growth. Another example is the retinoblastoma gene, which regulates the cell cycle and can be inherited in its mutated form, leading to increased cancer risk.

Understanding the roles of oncogenes and tumor suppressors is crucial in cancer biology, as these genes are central to the mechanisms that allow cancer cells to thrive and proliferate despite the body's regulatory systems. The interplay between these two types of genes underscores the complexity of cancer development and the importance of targeted therapies that can address these genetic alterations.

Tumor suppressors are mutated genes that results in higher amounts of gene activity.

• A. True
• B. False

Answer: (B)

Which of the following properties is not one given to cancer by gene mutations?

• A. Ability to evade apoptosis
• B. Unlimited replication
• C. Self-sufficiency from growth signals
• D. Genetic Stability

Answer: (D)

Here’s what students ask on this topic:

What are oncogenes and how do they contribute to cancer development?

Oncogenes are mutated genes that become overexpressed and support cancer development. They originate from normal genes called proto-oncogenes, which regulate cell growth and division. When proto-oncogenes mutate, they become oncogenes, leading to uncontrolled cell proliferation. This overexpression can occur through mutations or gene amplification. Oncogenes contribute to cancer by promoting cell survival, proliferation, and tumor development. For example, the RAS gene, when mutated, is involved in 20% of human cancers. It leads to the activation of multiple signaling pathways that drive cancerous growth. Thus, oncogenes play a crucial role in the transformation of normal cells into cancerous ones.

What is the role of tumor suppressor genes in preventing cancer?

Tumor suppressor genes are crucial in preventing cancer by regulating cell cycle progression, promoting DNA repair, and inducing apoptosis in damaged cells. When these genes are functional, they act as a safeguard against uncontrolled cell growth. A well-known example is the p53 gene, which responds to DNA damage by halting the cell cycle and initiating repair mechanisms. If the damage is irreparable, p53 can trigger apoptosis to prevent the propagation of mutated cells. However, when tumor suppressor genes like p53 are mutated and lose their function, cells can proliferate uncontrollably, leading to tumor development. Thus, the loss of tumor suppressor activity is a significant factor in cancer progression.

How do cancer cells evade apoptosis?

Cancer cells evade apoptosis through several mechanisms, often involving mutations in genes that regulate cell death. One common way is by mutating tumor suppressor genes like p53, which normally induce apoptosis in response to DNA damage. Without functional p53, cells with damaged DNA can continue to divide. Additionally, cancer cells may overexpress anti-apoptotic proteins or downregulate pro-apoptotic proteins, tipping the balance in favor of survival. These alterations allow cancer cells to ignore signals that would typically trigger cell death, contributing to their unchecked growth and the formation of tumors.

What is the significance of the RAS gene in cancer?

The RAS gene is highly significant in cancer because it is involved in about 20% of all human cancers. RAS is a GTPase that plays a critical role in cell signaling pathways that control growth and differentiation. When mutated, RAS becomes constitutively active, continuously sending growth signals to the cell even in the absence of external stimuli. This leads to uncontrolled cell proliferation and contributes to tumor development. The persistent activation of RAS can also activate other downstream signaling pathways, further promoting cancerous behaviors. Therefore, mutations in the RAS gene are a major driver of cancer progression.

How do mutations in tumor suppressor genes lead to cancer?

Mutations in tumor suppressor genes lead to cancer by eliminating the cell's ability to regulate growth and repair DNA damage. Tumor suppressor genes, such as p53 and retinoblastoma (RB), normally function to control cell cycle checkpoints, repair DNA, and induce apoptosis in damaged cells. When these genes are mutated, their protective functions are lost. For instance, a mutated p53 gene cannot halt the cell cycle or initiate DNA repair, allowing cells with genetic damage to continue dividing. This accumulation of mutations and unchecked cell proliferation ultimately leads to tumor development. Thus, the loss of tumor suppressor gene function is a critical step in cancer progression.