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?

Mutations are changes in the DNA sequence that can result from various factors such as exposure to radiation, chemicals, or errors during DNA replication. Some mutations can lead to the development of cancer, which is characterized by uncontrolled cell growth and the ability to invade other tissues. Normal cells have mechanisms in place to prevent the accumulation of these mutations and protect themselves from developing into cancer cells.

There are several mechanisms that normal cells use to protect themselves from accumulating mutations that could lead to cancer: a. DNA repair mechanisms: Cells have specific repair systems that can detect and repair DNA damage or errors. Examples include base excision repair, nucleotide excision repair, and mismatch repair. b. Cell cycle checkpoints: The cell cycle is controlled by a series of checkpoints that ensure proper progression through the phases and prevent cells with DNA damage from dividing. Checkpoints exist at the G1/S transition, intra-S phase, and G2/M transition. c. Apoptosis: Also known as programmed cell death, apoptosis is a process that leads to the controlled elimination of cells with severe DNA damage or errors, preventing them from forming cancer cells. d. Tumor suppressor genes: These are genes that help control cell division, preventing the formation of cancer cells. When these genes are functional, they can suppress the development of tumors. Examples include the p53 and BRCA1/2 genes.

Cancer cells differ from normal cells in the following aspects of these protective mechanisms: a. Impaired DNA repair: Cancer cells often have defects in their DNA repair systems, leading to the accumulation of mutations that can promote cancer development further. b. Dysregulation of cell cycle checkpoints: Many cancer cells have alterations in their cell cycle control mechanisms, allowing them to bypass critical checkpoints that would otherwise prevent them from dividing with damaged DNA. c. Resistance to apoptosis: Cancer cells can develop resistance to apoptotic signals, enabling them to survive and proliferate despite having DNA damage or errors. d. Inactivation of tumor suppressor genes: In many cases, cancer cells have mutations that inactivate tumor suppressor genes, relieving the constraints on cell division and promoting uncontrolled proliferation. In conclusion, normal cells have multiple protective mechanisms in place to prevent the accumulation of mutations that could lead to cancer. Cancer cells, on the other hand, often have defects or alterations in these mechanisms that facilitate their uncontrolled growth and ability to invade other tissues.