Which of the following genetic changes would not convert a proto-oncogene into an oncogene?

The genetic change that would not convert a proto-oncogene into an oncogene is one that introduces a stop codon immediately after the codon for the initiator methionine. This scenario would likely result in a truncated protein that cannot function properly, thereby eliminating its activity altogether. Proto-oncogenes typically code for proteins that are involved in the regulation of cell growth and division. When functioning normally, they contribute positively to cell cycle regulation and cellular proliferation.

Introducing a stop codon very early in the coding sequence would disrupt the synthesis of a complete, functional protein. Since an oncogene is defined by its ability to drive uncontrolled cell proliferation, a complete loss of function due to a premature stop codon would clearly not result in oncogenic activity. Consequently, the proto-oncogene would retain its non-cancerous, regulatory role, rather than transitioning to an oncogenic state.

In contrast, mutations that lead to hyperactive proteins, amplifications that cause overproduction, or alterations that result in the promoter driving overexpression all contribute to the aberrant signaling or excessive production of proteins that promote malignancy. These changes reflect mechanisms by which proto-oncogenes become oncogenes, fostering tumorigenesis.