Weight-loss drug could fight resistant lung cancer

In In The News by Barbara Jacoby

From: futurity.org

New research could pave the way for using versions of an existing drug to keep lung cancer cells from becoming drug-resistant.

Researchers have discovered that a key enzyme in lipid metabolism controls the response to a class of targeted drugs called tyrosine kinase inhibitors (TKIs) in lung cancer.

Cells use nutrients such as glucose, amino acids, and lipids to produce the energy to support the essential processes that keep them alive and functioning. Cancer cells, those ultimate survivors, have figured out a way to tweak their own metabolism to increase the supply of energy, allowing them to multiply uncontrollably. These altered metabolic pathways can serve as targets for new cancer therapies, according to the new research.

Lung cancer is the most common cancer in the world and the top cause of cancer deaths, accounting for one in five deaths from cancer. A large majority of lung cancers (85 percent) are known as non-small cell lung cancers (NSCLC). A significant proportion of NSCLC patients (10-15 percent in Europe and the US, and more than 40 percent in Asia) have gene alterations (or mutations) in the epidermal growth factor receptor (EGFR) gene.

Currently, the most effective treatment for this type of NSCLC are TKIs that specifically target the altered EGFR, with an overall survival of two to four years. However, over time, resistance to TKIs develops. At that point, patients have very few treatment options and a very poor prognosis.

Understanding how this inevitable resistance to TKIs develops is crucial to tackling the problem. Several different mechanisms for TKI resistance in this type of lung cancer have already been described.

Taking this understanding further, Ali Azhar, senior research scientist at Cancer Science Institute of Singapore (CSI) at the National University of Singapore, and colleagues discovered a completely new mechanism involving fatty acid synthase (FASN), a key enzyme in lipid synthesis that facilitates the production of the saturated fatty acid palmitate.