The research team has pinpointed the cancer abnormality to a mutation in a gene called PIK3CA that results in a mutant protein, which may be an early cancer switch. By disrupting the mutated signaling pathway, the Case Western Reserve team, led by John Wang, PhD, inhibited the growth of cancer cells, opening the possibility to new cancer therapies.
Cancer arises from a single cell, which has mutated in a small number of genes because of random errors in the DNA replication process. These mutations play key roles in carcinogenesis.
"This discovery has a broad impact on the treatment of human cancer patients because so many cancers are affected by this particular mutation in the p110a protein, which is encoded by the PIK3CA gene," said Wang, an associate professor in the Department of Genetics and Case Comprehensive Cancer Center.
"This is a significant advance because we can now disrupt this misdirected signaling pathway in cancer cells," the researcher added.
"If you turn on a light, you have to turn on a switch. But in the case of the mutation of this protein, p110a turns on by itself," Wang explained.
"The mutation rewires the circuit and is uncontrolled. This implies that if you break these wires, you can control the growth of cancer. Our current discovery may lead to finding less toxic drugs that can be used for personalized treatment for cancer patients in the future," he added.
This research will impact the field by focusing us on new targets for treating and preventing metastasis in patients in a many different types of human cancers, noted Stanton Gerson, MD, Asa and Patricia Shiverick-Jane Shiverick (Tripp) Professor of Hematological Oncology, and director of Case Comprehensive Cancer Center and of Seidman Cancer Center at University Hospitals Case Medical Center.
Their findings were published in the journal Cancer Cell.