Final answer:
In cancer cells, the DNA undergoes mutations that disrupt normal cell cycle regulation, leading to uncontrolled cell division. These mutations can affect crucial genes, such as tumor-suppressor genes or proto-oncogenes, causing a failure in cell-cycle checkpoints and an accumulation of further genetic errors, ultimately resulting in tumor formation or leukemia.
Step-by-step explanation:
What Happens to the DNA in a Cancer Cell?
Cancer occurs when there is a breakdown in the mechanisms that regulate the cell cycle, leading to unchecked cell division. This loss of control often starts with alterations in the DNA—specifically, mutations in genes that code for proteins involved in cell regulation. When these genes are mutated, they may produce proteins that do not function properly, disrupting the normal monitoring of cell division and allowing errors to accumulate. As a result, we see a cell cycle that proceeds without the necessary checkpoints, leading to the production of more cells that carry these mutations.
Two significant types of genes that, when mutated, contribute to cancerous growths are tumor-suppressor genes and proto-oncogenes. Tumor-suppressor genes normally work to prevent division of cells with DNA damage. Should these genes become inoperative due to mutations, cells with damaged DNA are permitted to divide. Proto-oncogenes control cell division as well, but their mutation leads to the transformation into oncogenes that promote the division of the impaired cells.
Mutations that compromise the DNA repair functions of these genes lead to a cascading effect, with damaged, cancerous cells beginning to replicate uncontrollably. This can result in the formation of tumors, mass growths of abnormal cells, or in blood cancers like leukemia, where abnormal cells crowd out healthy blood cells. Over time, this unregulated division and mutation accumulation can lead to a tumor, which, if unchecked, can grow, spread, or metastasize to different body parts.