Question

Oncogenes can be produced by a. missense mutations. b. gene amplification. c. chromosomal translocation. d. retroviral insertion. e. all of the above.

Short answer

All the mentioned mechanisms (missense mutations, gene amplification, chromosomal translocation, and retroviral insertion) can potentially lead to the production of oncogenes, hence the answer is (e) all of the above.

Step-by-step solution

Understanding the Terms

Missense mutations are the genetic changes that result in a codon that codes for a different amino acid. Gene amplification is an increase in the number of copies of a particular gene. Chromosomal translocation is a chromosome abnormality caused by rearrangement of parts between nonhomologous chromosomes. Retroviral insertion implies that a virus inserts its own genetic material into the DNA of the host cell.

Connecting the Terms with Oncogenes

All these mutations and changes have a potential to result in an altered protein or an increase in protein production that can cause a normal cell to become cancerous. Therefore, any of these can potentially lead to the production of oncogenes.

Answer Determination

Given the understanding of each term and how each can lead to the production of oncogenes, the correct answer would be (e) all of the above.

Key concepts

Missense Mutations

Missense mutations are a type of genetic mutation where a single nucleotide change results in the substitution of one amino acid for another in the protein produced. These mutations can affect protein function in various ways:

• If the new amino acid has similar properties to the original, the protein may still function properly.
• If the new amino acid has different properties, it could alter the protein's structure or function, potentially causing disease.

In the context of oncogenes, missense mutations may activate a normally harmless gene, leading to uncontrolled cell growth and cancer. The change in protein function could disrupt normal signaling pathways, ultimately contributing to tumor development.

Gene Amplification

Gene amplification involves the increase of the number of copies of a particular gene. This means more messenger RNA (mRNA) is transcribed, leading to higher amounts of the corresponding protein. A significant increase in protein production can have several effects on a cell:

• The cell might grow faster than normal.
• It might gain a new ability, such as resistance to a drug.
• It could become less responsive to normal regulatory mechanisms.

When it comes to oncogenes, gene amplification can cause an overproduction of proteins that control cell division and survival. Too many copies of an oncogene may lead to excessive cellular proliferation, contributing to the development of cancer.

Chromosomal Translocation

Chromosomal translocation is a genetic event where a section of one chromosome is transferred to another, nonhomologous chromosome. This rearrangement can result in one of several outcomes:

• The creation of a new fusion gene that may have oncogenic properties.
• Misdirected gene regulation, where a gene's expression is increased or decreased abnormally.

A classic example in cancer is the translocation between chromosomes 9 and 22, resulting in the Philadelphia chromosome, which is associated with chronic myelogenous leukemia (CML). Such translocations can produce proteins that drive the cell cycle or evade apoptosis, leading to the transformation of normal cells into cancerous ones.

Retroviral Insertion

Retroviral insertion occurs when a retrovirus integrates its genetic material into the host's genome. This random insertion can disrupt normal genes and influence oncogene activation in a few ways:

• Integration near an oncogene might enhance its expression – this is called insertional mutagenesis.
• It might introduce viral genes that interfere with the cell's normal regulatory mechanisms.

In some instances, the viral insertion can activate oncogenes or inactivate tumor suppressor genes, promoting oncogenesis. Retroviruses, like the Human T-cell Leukemia Virus (HTLV), demonstrate this potential by increasing the risk of leukemia in infected individuals.