Genetic changes that help lung cancer thrive also make it vulnerable to a promising experimental drug, according to a study led by researchers from Perlmutter Cancer Center at NYU Langone Health, and published online October 2 in Nature Medicine.
Genetic changes that help lung cancer thrive also make it vulnerable to a promising experimental drug, according to a study led by researchers from Perlmutter Cancer Center at NYU Langone Health, and published online October 2 in Nature Medicine.
Specifically, the study found that mutations in the DNA code for the gene KEAP1 help lung adenocarcinoma cells counter a process called oxidative stress, in which molecules known as reactive oxygen species (ROS) are created as a side effect of “burning” fuel to make energy. Cancer cells need extra fuel to support abnormal growth, produce more ROS, and depend more for survival on naturally occurring antioxidants that keep ROS from damaging cell parts.
The new study confirmed that mutations that weaken KEAP1 function lead to greater production of antioxidants that cancer cells need to thrive. It also found that KEAP1 mutations create vulnerability in cancer cells when combined with mutations in the gene KRAS, which cause cancer cells to multiply aggressively.
The vulnerability found by the new study reflects the ability of lung adenocarcinoma cells to use extra fuel sources in support of abnormal growth. Along with the blood sugar that most cells use, cancer cells also break down a compound called glutamate to make energy. At the same time, such cells also expel glutamate as part of a process that supports the building of antioxidants. Importantly, cancer cells cannot both break down for energy, and expel, the same molecule of glutamate, say the study authors.
Read more at NYU Langone Health / NYU School of Medicine
Photo credit: Nephron via Wikimedia Commons
