Final answer:
Cancer involves the accumulation of DNA mutations leading to uncontrolled cell growth and tumor development. Such mutations can affect cell-cycle control proteins like p53, resulting in faulty repair mechanisms and tumor growth. Cancer is characterized by its ability to metastasize and its development is often influenced by the malfunction of genes that regulate the cell cycle.
Step-by-step explanation:
Cancer is a complex group of diseases characterized primarily by unchecked cell division. This usually starts with a mutation in the DNA sequence of a gene that codes for regulatory molecules in the cell cycle. One key protein involved in this process is the p53 protein, which plays a major role at the G₁ checkpoint. Mutations in the p53 gene can result in a loss of function, leading to an inability to repair damaged DNA or to trigger cell death. Without this checkpoint, cells with damaged DNA continue to proliferate, leading to further mutations and the potential development of tumors.
Mutations can also result in the increased phosphorylation of cyclin B, altering the cell growth rate and compromising the cell cycle's regulation. Over time, the accumulation of genetic mutations may result in the inactivation of DNA repair genes or the activation of oncogenes from proto-oncogenes, contributing further to cancer progression. A critical aspect of cancer development is the alteration of normal cell division processes, whereby tumor suppressor genes may be inactivated, leading to the formation and growth of tumors.
The result of these cumulative genetic errors can manifest in forms such as pancreatic cancer, colon cancer, and colorectal cancer. In some instances, these mutations are somatic and affect only the individual, while others can occur in germ cells and have the potential to be passed on to the next generation.