• Many receptor tyrosine kinases have stimulatory effects on cell growth, and increased receptor activity occurs with a variety of cancers.  For example, overexpression of EGFR and MET are associated with non–small cell lung cancer, and HER2 is associated with breast cancer.
• Abnormal K-Ras GTPase function due to a KRAS mutation prevents the conversion of GTP to GDP, which results in constant activation of the MAPK pathway and uncontrolled cellular proliferation.  KRAS mutations are associated with lung and colorectal cancers.
• Tumor suppressor protein p53 arrests the cell cycle at the G1/S checkpoint if DNA damage is detected and initiates cell apoptosis if DNA repair fails.  Mutations of p53 are associated with most cancers, particularly Li-Fraumeni syndrome (sarcoma, breast, leukemia, and adrenal cancers).  Rb and p53 proteins are both critical components of tumor suppression pathways, and their normal function complements one another to prevent cancer progression.
• Retinoblastoma is associated with inactivating mutations of the RB1 tumor suppressor gene, which normally restricts cells from passing the G1/S checkpoint until the cell is ready to divide.  Impaired function of the Rb protein allows unrestricted progression through the G1/S checkpoint, leading to uncontrolled cell division.
• BRCA1 and BRCA2 are two of many DNA repair genes that have been identified.  When mutated, these genes are associated with an increased risk of breast and ovarian cancer.