Thwarting Drug Resistance in Lung Cancer

[D.ap]

May 16, 2014
Written by Emma Shtivelman, PhD

If you’ve read up on lung cancer research in the last few years, you probably know that large strides have been made in targeted therapies for non-small cell lung cancer (NSCLC). Targeted therapies are drugs that identify and attack specific mutated proteins that are detected in tumors. Because noncancerous cells do not have these specific mutations, targeted therapies can make a beeline for cancer, while leaving healthy tissue unharmed.

But targeted therapies are by no means a perfect solution. During treatment with a targeted therapy, a patient’s tumors can develop new mutations that make them resistant to the drug. Oncologists are working out how to treat patients who have developed resistance to targeted therapies—and how to prevent resistance in the first place.

A substantial percentage of NSCLC tumors harbor mutations in genes (DNA) that encode proteins called receptor tyrosine kinases (RTKs). Recurrent mutations make RTKs abnormally active, unleashing a cascade of cellular signaling events that culminate in runaway cancer cell multiplication and tumor growth. Four RTKs—EGFR, ALK, ROS, and RET—are targets of drugs that inhibit their function and slow down or even stop tumor growth. The U.S Food and Drug Administration (FDA) has approved drugs that target mutant EGFR (erlotinib [Tarceva], gefitinib [Iressa], and afatinib [Gilotrif]) and mutant ALK (crizotinib [Xalkori] and ceritinib [Zykadia], which was approved just last week).


https://www.cancercommons.org/knowledge ... more-30625