If a cell suffers damage to its DNA while in S phase, how can this damage be repaired before the cell enters mitosis?
Table of contents
- 1. Introduction to Genetics51m
- 2. Mendel's Laws of Inheritance3h 37m
- 3. Extensions to Mendelian Inheritance2h 41m
- 4. Genetic Mapping and Linkage2h 28m
- 5. Genetics of Bacteria and Viruses1h 21m
- 6. Chromosomal Variation1h 48m
- 7. DNA and Chromosome Structure56m
- 8. DNA Replication1h 10m
- 9. Mitosis and Meiosis1h 34m
- 10. Transcription1h 0m
- 11. Translation58m
- 12. Gene Regulation in Prokaryotes1h 19m
- 13. Gene Regulation in Eukaryotes44m
- 14. Genetic Control of Development44m
- 15. Genomes and Genomics1h 50m
- 16. Transposable Elements47m
- 17. Mutation, Repair, and Recombination1h 6m
- 18. Molecular Genetic Tools19m
- 19. Cancer Genetics29m
- 20. Quantitative Genetics1h 26m
- 21. Population Genetics50m
- 22. Evolutionary Genetics29m
19. Cancer Genetics
Overview of Cancer
Problem 18
Textbook Question
How do normal cells protect themselves from accumulating mutations in genes that could lead to cancer? How do cancer cells differ from normal cells in these processes?

1
Normal cells protect themselves from accumulating mutations through several mechanisms: DNA repair systems, cell cycle checkpoints, and apoptosis. DNA repair systems identify and correct errors in the DNA sequence, ensuring genetic stability.
Cell cycle checkpoints, such as the G1/S and G2/M checkpoints, monitor the integrity of the DNA before allowing the cell to proceed to the next phase of the cell cycle. If damage is detected, the cell cycle is paused to allow for repair.
Apoptosis, or programmed cell death, is another protective mechanism. If the damage to the DNA is irreparable, the cell undergoes apoptosis to prevent the propagation of mutations.
Cancer cells differ from normal cells in these processes because they often have mutations in genes that regulate DNA repair, cell cycle checkpoints, and apoptosis. For example, mutations in tumor suppressor genes like TP53 can disable these protective mechanisms.
As a result, cancer cells accumulate mutations more readily, leading to uncontrolled cell division and the potential for tumor formation and progression.

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Key Concepts
Here are the essential concepts you must grasp in order to answer the question correctly.
DNA Repair Mechanisms
Normal cells possess various DNA repair mechanisms, such as nucleotide excision repair and mismatch repair, which identify and correct errors in the DNA sequence. These processes are crucial for maintaining genomic stability and preventing the accumulation of mutations that could lead to cancer. When these repair systems are functioning properly, they help to ensure that any damage caused by environmental factors or replication errors is effectively repaired.
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Cell Cycle Regulation
Cell cycle regulation involves a series of checkpoints that monitor and control the progression of the cell cycle. Proteins such as cyclins and cyclin-dependent kinases (CDKs) play essential roles in ensuring that cells only divide when they are ready and that any DNA damage is repaired before replication. In cancer cells, these regulatory mechanisms are often disrupted, allowing for uncontrolled cell division and the accumulation of mutations.
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Apoptosis
Apoptosis, or programmed cell death, is a critical process that allows cells to eliminate themselves when they are damaged or no longer needed. Normal cells can undergo apoptosis in response to severe DNA damage or other stress signals, preventing the propagation of potentially cancerous cells. In contrast, cancer cells often evade apoptosis, allowing them to survive despite having accumulated harmful mutations that contribute to tumorigenesis.
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