Precision medicine offers hope after a life-changing cancer diagnosis. But some cancers that initially respond to targeted chemotherapy become treatment-resistant — and the tumor itself is the culprit.
Now, new research from UC Merced and UC Irvine is helping explain how therapy-resistant cancers arise — findings with important implications for the future of cancer therapy. The results are reported in a study published today in the journal BMC Systems Biology.
To understand how cancer becomes treatment resistant, a research team at the Systems Biology and Cancer Metabolism Lab, led by UC Merced Professor Fabian V. Filipp of the School of Natural Sciences, compared genetic and metabolic pathways in treatment-responsive and treatment-resistant melanomas.
Melanoma is a cancer that originates in melanocytes, the cells that produce the skin pigment melanin. Though not the most common form of skin cancer, it is the most aggressive. And if it’s not caught and treated early, it’s also among the deadliest.
“Melanoma is usually induced by the sun — by UV damage,” Filipp said. “In the majority of cases, that UV damage changes a single target by causing point mutations.”
UV damage gives rise to point mutations — changes in a single letter of the 3 billion letter human genome. These mutations can interfere with signals that tell cells when to grow and divide and when to stop. Mutations in a protein called BRAF, the main focus of the new study, cause growth signals to be stuck in the “on” position and drive cancer development.
