Final answer:
The Philadelphia chromosome activates an oncogene by fusing a protooncogene with another protein, specifically by creating the BCR-ABL fusion gene that leads to increased tyrosine kinase activity and uncontrolled cell division.
Step-by-step explanation:
The Philadelphia chromosome is the result of a translocation, specifically between chromosomes 9 and 22. This translocation fuses part of the BCR gene from chromosome 22 with part of the ABL gene from chromosome 9. This creates the BCR-ABL fusion gene on the abnormally shortened chromosome 22, which then functions as an oncogene because it codes for a tyrosine kinase that is always active, rather than being regulated by cellular signals.
The correct answer to the question is that the Philadelphia chromosome activates an oncogene by fusing a protooncogene with another protein (ABL with parts of BCR), which results in an altered activity of this protein. The resulting BCR-ABL protein has increased tyrosine kinase activity, which then increases cell division and can lead to chronic myelogenous leukemia.
Oncogenes are mutated forms of proto-oncogenes. They promote cell division in an uncontrolled manner when they are overexpressed or their product protein's activity is altered. This is in contrast to tumor suppressor genes, which normally inhibit uncontrolled cell growth. If these are mutated, they can lose their ability to control the cell cycle, also contributing to cancer development.