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Mollecularly, cancer is typically associated with gain of function mutations in oncogenes as well as loss of function mutations in tumor-suppressor genes. One gene in particular has been associated with a wide variety of cancers, PIK3CA. PIK3CA is a gene responsible for PI3K, a downstream protein in RTK signaling that converts PIP2 to PIP3, thus continuing the signal transduction pathway. However, in double PIK3CA mutants, PI3K acts independently of RTK signaling, converting PIP2 to PIP3 leading to hyperactive downstream AKT, activating the signal pathway with no ligand present in the RTK. This hyperactivation leads to increased and unregulated cell proliferation and survival¹. This double mutant PIK3CA is a common mutations in many cancers, especially breast cancer.