Final answer:
Cancer cells exhibit unchecked division due to failures in cell cycle control mechanisms, characterized by a lack of contact inhibition, reduced cell adhesion, and mutations in cell cycle regulatory genes. Unlike normal cells, they continue to grow and form masses, often leading to metastasis and tissue damage.
Step-by-step explanation:
The cell cycle of cancer cells differs from that of normal cells in several key aspects. Unlike normal cells, which only divide to a confluent layer and exhibit contact inhibition, cancer cells lack this regulatory mechanism and can continue to divide uncontrollably, leading to tumor formation. This is partly because cancer cells generally have changes in their DNA that disrupt the normal regulation of the cell cycle caused by genetic abnormalities or environmental damage, allowing them to divide at a much faster rate, consume more nutrients, and expand beyond the space of normal cells.
Additionally, cancer cells often lose the ability to stick to each other and to the extracellular matrix due to reduced expression of cell adhesion molecules like cadherens and integrins. This contributes to a failure in stopping division even when they come in contact with other cells, a phenomenon known as loss of contact inhibition. This loss may explain why cancer can metastasize and spread throughout the body.
Finally, the cell cycle disruption in cancer cells results from mutations in genes that encode regulatory proteins. These mutations can arise from genetic predisposition or environmental factors such as radiation. Continual divisions without proper checkpoints can lead to more mutations, worsening the condition.