DNA Repair

Definition

DNA repair refers to the cellular mechanisms that detect and correct various types of damage to the DNA molecule, ensuring the integrity and proper functioning of the genetic material. This process is crucial in the context of cancer and cancer therapy, as defects in DNA repair pathways can lead to the accumulation of genetic mutations and the development of cancerous cells.

5 Must Know Facts For Your Next Test

1. Defects in DNA repair pathways can lead to the accumulation of genetic mutations, which is a hallmark of cancer development.
2. Certain cancer therapies, such as radiation and chemotherapy, work by inducing DNA damage in cancer cells, which they are less able to repair compared to healthy cells.
3. The efficiency of DNA repair mechanisms can influence the sensitivity of cancer cells to various treatments, as cells with impaired DNA repair are more susceptible to DNA-damaging agents.
4. Specific DNA repair pathways, such as nucleotide excision repair and mismatch repair, are often dysregulated in different types of cancer, contributing to the genetic instability of cancer cells.
5. Understanding the DNA repair mechanisms and their role in cancer development and treatment response is crucial for the development of targeted cancer therapies and personalized medicine approaches.

Review Questions

• Explain how defects in DNA repair pathways contribute to the development of cancer.
  • Defects in DNA repair pathways can lead to the accumulation of genetic mutations, a hallmark of cancer development. When DNA damage is not properly repaired, it can result in the activation of oncogenes or the inactivation of tumor suppressor genes, driving the transformation of normal cells into cancerous ones. The inability to maintain genomic integrity due to impaired DNA repair mechanisms is a key factor in the genetic instability and uncontrolled cell growth observed in many types of cancer.
• Describe how certain cancer therapies exploit the DNA repair deficiencies of cancer cells.
  • Many cancer treatments, such as radiation therapy and certain chemotherapeutic agents, work by inducing DNA damage in cancer cells. Cancer cells, which often have impaired DNA repair mechanisms compared to healthy cells, are less able to effectively repair this DNA damage. As a result, the DNA-damaging agents used in cancer therapy preferentially kill or inhibit the growth of cancer cells, while healthy cells with intact DNA repair pathways are better able to recover from the treatment-induced DNA damage. This selective targeting of cancer cells' DNA repair deficiencies is a key principle in the design of effective cancer therapies.
• Analyze how the understanding of DNA repair mechanisms can inform the development of personalized cancer treatment approaches.
  • The understanding of DNA repair mechanisms and their dysregulation in different types of cancer has significant implications for the development of personalized cancer treatment approaches. By assessing the specific DNA repair deficiencies present in a patient's cancer cells, healthcare providers can select therapies that are most likely to be effective. For example, cancers with impaired homologous recombination DNA repair may be more sensitive to PARP inhibitor drugs, while those with defects in mismatch repair may respond better to immunotherapies. This personalized approach, which takes into account the unique DNA repair profile of a patient's cancer, allows for more targeted and effective treatment strategies, ultimately improving patient outcomes.

Related terms

Nucleotide Excision Repair: A DNA repair mechanism that removes and replaces damaged DNA segments, particularly those caused by ultraviolet radiation or bulky chemical adducts.

Mismatch Repair: A DNA repair process that corrects errors made during DNA replication, such as the insertion, deletion, or misincorporation of nucleotides.

Double-Strand Break Repair: A DNA repair mechanism that addresses the most severe type of DNA damage, where both strands of the DNA double helix are broken, using either homologous recombination or non-homologous end joining.