A mutation that results in a single amino acid substitution in Ras abolishes its ability to hydrolyze GTP, even when GTPase-activating proteins (GAPs) are present. Approximately 30% of human cancers have this mutation in Ras. The pharmaceutical company AztraZeneca, which markets popular breast cancer drugs like Iressa® (generic: Gefitinib) has recently developed a new drug that prevents the dimerization of a receptor tyrosine kinase expressed in lung cancer cells, which signals via Ras. Would you expect this new drug to be effective for the treatment of cancers that express the mutant form of Ras?

The new drug will not be effective against the treatment of cancer.

Explanation:

The drug will not be effective against the cancer treatment because the drug will inhibit the dimerization of receptor tyrosine kinase (RTK) but as the Ras has undergone mutation due to replacement of one amino acid, it will be constitutively expressed and the drug is not effective in stopping the Ras functioning.

Thus, Gefitinib cannot work against the cancerous cell as it is not potent to stop the functioning of mutant Ras protein.

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