Final answer:
The sensitivity of tumors to inhibition of activated oncogenes, termed 'oncogene addiction', is true. Oncogenes that are mutated and activated drive the growth and survival of cancer cells, making them targets for treatments like Herceptin, which inhibits the oncogene HER2 in breast cancers.
Step-by-step explanation:
The sensitivity of tumors to the inhibition of activated oncogenes is indeed known as oncogene addiction. This concept suggests that despite the complexity of the genetic alterations in cancer cells, their growth and survival may be heavily reliant on one or a few genes, such as mutated oncogenes. These oncogenes drive the cancerous phenotype and when targeted, can result in the regression of the tumor. Normally, oncogenes are dominant alleles containing gain-of-function mutations, and they promote cell growth through various mechanisms including production of growth factors, protein kinases, GTPases, and transcription factors.
Herceptin (trastuzumab) is an example of a therapeutic agent that targets the oncogene HER2, which is overexpressed in a significant fraction of breast cancers due to gene duplication. Herceptin functions as a monoclonal antibody, marking HER2 for removal by the immune system to control signaling and thereby exhibiting the principle of oncogene addiction. The consequent decrease in oncogenic activity can significantly improve patient survival rates when used in combination with chemotherapy.
Tumor suppressor genes function in contrast to oncogenes; they serve to inhibit cell division and promote appropriate programmed cell death. Mutations or inactivation of tumor suppressor genes, along with the constitutive activation of oncogenes, are necessary steps in the transformation of normal cells into cancer cells, resulting in the disruption of the cell's "cruise control" for growth.