Final answer:
Cancer is the result of mutations in proto-oncogenes and tumor suppressor genes that disrupt cell cycle regulation. Proto-oncogenes can become oncogenes that drive cell division, while tumor suppressor genes, when inactivated, fail to restrict abnormal growth. Additionally, viruses can contribute to cancer by introducing oncogenes or activating proto-oncogenes.
Step-by-step explanation:
Viruses, proto-oncogenes, and tumor suppressor genes play critical roles in the development of cancer by disrupting the normal regulation of cell growth and division. Oncogenes are mutated forms of proto-oncogenes and actively promote cell proliferation, acting like an overactive accelerator in a car. These oncoproteins push the cell forward in its cycle, stimulating cell division even when not needed. On the other hand, tumor suppressor genes act as brakes, normally inhibiting uncontrollable cell division. When these genes are inactivated through mutations, they lose their ability to suppress abnormal cell growth, resulting in cancer.
Cancer-causing viruses can contribute to this process in different ways. Acutely transforming viruses introduce a viral-oncogene directly into cells, immediately changing the normal cell cycle control. Slowly-transforming viruses insert viral DNA near proto-oncogenes in the host genome, which can lead to overexpression of these genes and subsequent uncontrolled cell proliferation. As a result, the balance between cell growth signals (from oncogenes) and growth inhibitory signals (from tumor suppressor genes) is disturbed, tipping the scale towards uncontrollable cell division and tumor formation.