Mutations that turn proto-oncogenes into oncogenes can take different forms. Some change the amino acid sequence of the protein, altering its shape and trapping it in an “always on” state. Others involve amplification, in which a cell gains extra copies of a gene and then starts making too much protein. In still other cases, an error in DNA repair may attach a proto-oncogene to part of a different gene, producing a “combo” protein with unregulated activity. When oncogenes arise in normal cells, they can contribute to the development of cancer by telling cells to make proteins that stimulate excessive cell growth and division. an example of this is the HER-2/neu gene which encodes for a cell surface receptor that can stimulate cell division. The HER-2/neu gene is amplified in up to 30% of human breast cancers. Also, Ras mutations are found in about 90% of pancreatic cancers. Ras is a proto-oncogene, meaning that it switches back and forth between an inactive form and an active form. Cancer-causing mutations often change Ras’s structure so that it can no longer switch to its inactive form, or can do so only very slowly, leaving the protein stuck in the “on”