If you have non-small-cell lung cancer, some of the most powerful information you can have is about gene mutations and their role in lung cancer treatment. With an up-to-date knowledge of gene mutations, you and your doctors may be able to manage a great quality of life for a substantial period of time, even if your cancer is advanced and incurable.

Basically, cancer happens when something in the genes or DNA of your cells goes haywire. The mechanisms that control the division and multiplication of cells get fouled up, resulting in an uncontrolled proliferation of cells. Unlike an infection, which is a foreign organism invading your body, cancer is your own body – your own cells – gone wrong.

Scientists are now able to look at the genes of cancer cells and, in more and more cases, see exactly what has gone wrong. They can see where the molecules have been rearranged so that the genes can’t do their job anymore. It’s almost like computer programmers finding the tiny bug – the line of scrambled code – that causes a whole system to crash.

Some genetic mutations (the lines of scrambled code) have a physical shape that makes it possible to target them with medicine. Some of the newest cancer drugs are designed to shut down particular genetic mutations by binding to them. Imagine a unique key sliding into a keyhole and turning a lock, only at a microscopic level.

Lung cancer is caused by different genetic mutations. You and I may have the same symptoms, but precisely what is out of kilter in your DNA may be different from what is out of kilter in mine. There are many microscopic locks, and not all of them have been discovered yet. To some of the locks, however, oncology now has keys.

The three most common known gene mutations in non-small-cell lung cancer are EFGR (epidermal growth factor receptor), ALK (anaplastic lymphoma kinase), and KRAS (Kirsten RNA Associated Rat Sarcoma 2 Virus Gene). There are other less common ones, such as ROS1, which I have. Many remain unknown.

For EFGR and ALK, there are targeted medicines on the market now, and they are more effective against cancer with those mutations than standard chemotherapy. They are oral medicines (no being hooked up to a chemotherapy pump all day). You may hear about Tarceva (generic name erlotinib), which targets the EFGR mutation, or Xalkori (generic name crizotinib) which targets ALK. ROS1 is a rare mutation and does not yet have medicines specifically developed for it, but we are fortunate that ROS1 cancer can also respond well to Xalkori/crizotinib. This is why I’m doing so well right now: we finally figured out that I have the ROS1 mutation, and I am thriving on crizotinib.

Unfortunately, these medicines do not work forever. Eventually the cancer mutates again and figures out how to outsmart them. I am told that the average patient who responds well to crizotinib gets a little less than a year of great health from it, and then it stops working. I’ve already had four months of great health. However, scientists and doctors are already working on ways to get around this resistance, and they are making progress.

This is why you need to see a specialized thoracic oncologist, especially if your cancer is advanced. It’s also why you may want to ask your doctors to take extra tissue for testing, even if you are having a biopsy at a community hospital. This aspect of lung cancer treatment is very new, and not all oncologists are even up to speed. I’ve read stories of lung cancer patients being sent to hospice because their doctors thought there was nothing else they could do, and then recovering dramatically, though not permanently, on genetically targeted medicine. If you have advanced non-small-cell lung cancer and your doctors have not discussed genetic testing with you at all, find new doctors.