Certain gene mutations are linked to non-small cell lung cancer (NSCLC). Having one of these mutations could affect the type of treatment your doctor recommends.

Genes are the instructions that make our bodies run. They tell our cells which proteins to make. Proteins control how quickly cells grow, divide, and survive.

Sometimes genes change. This may happen before a person is born or later in life. These changes are called mutations. These changes can affect certain functions in our bodies.

Gene mutations can prevent DNA from repairing itself. They can also enable cells to grow uncontrollably or to live for too long. Eventually, those extra cells can form tumors, which is how cancer starts.

The gene mutations that cause lung cancer can happen in one of two different ways.

Somatic mutations are acquired mutations. They’re the most common cause of cancer.

They happen when you’re exposed to chemicals, tobacco, UV radiation, viruses, and other damaging substances over the course of your lifetime.

Germline mutations are hereditary mutations. They’re passed from a mother or father to their baby through an egg or sperm. About 5 to 10 percent of all cancers are inherited.

A few different gene mutations help non-small cell lung cancers (NSCLCs) spread and grow. These are some of the most common gene mutations:

TP53

The TP53 gene is responsible for the production of the tumor protein p53. This protein monitors cells for DNA damage and acts as a tumor suppressor. That means it keeps damaged cells from growing too fast or uncontrollably.

TP53 mutations are common in cancers and found in about 50 percent of all NSCLC. They’re usually acquired and happen in both smokers and people who have never smoked.

Research suggests that TP53 mutations combined with EGFR, ALK, or ROS1 gene mutations is linked with a shorter survival time.

There’s debate about whether people with cancer should always be tested for TP53 genetic mutations because there’s no targeted therapy yet to treat this mutation.

Research for targeted TP53 therapies is ongoing.

KRAS

The KRAS gene mutation is found in about 30 percent of all NSCLCs. It’s more common in people who smoke. The outlook for people with this type of genetic change isn’t as good as it is for those without it.

EGFR

Epidermal growth factor receptor (EGFR) is a protein on the surface of cells that helps them grow and divide. Some NSCLC cells have too much of this protein, which makes them grow faster than usual.

Up to 23 percent of NSCLC tumors contain the EGFR mutation. These mutations are more common in certain groups of people, including women and nonsmokers.

ALK

About 5 percent of NSCLC tumors have the anaplastic lymphoma kinase (ALK) gene mutation. This change is common in younger people and nonsmokers. It allows cancer cells to grow and spread.

MET and METex14

The MET gene is changed in up to 5 percent of all NSCLCs. MET-positive lung cancers tend to be more aggressive than those without this mutation.

MET exon 14 deletion (METex14) is a type of MET mutation that’s been linked to about 3 to 4 percent of NSCLCs.

BRAF

About 3 to 4 percent of NSCLCs test positive for BRAF mutations. Most people who have these mutations are current or former smokers. These mutations are also more common in women than men.

ROS1

This mutation affects between 1 and 2 percent of NSCLC tumors. It’s often found in people who are younger and haven’t smoked.

ROS1-positive cancers may be more aggressive and can spread to areas like the brain and bones.

Some of the less common mutations linked to NSCLC include:

  • NRAS
  • PIK3CA
  • RET
  • NTRK
  • HER2

When you’re first diagnosed with NSCLC, your doctor may test you for certain genetic mutations.

These tests are called molecular analysis, biomarker, or genomic tests. They give your doctor a genomic profile of your tumor.

Knowing whether you have one of these mutations helps your doctor figure out which treatment might work best for you. Targeted treatments work on cancers with EGFR, KRAS, ALK, and other gene mutations.

Genetic tests use a sample of tissue from your tumor that your doctor removes during a biopsy. The tissue sample goes out to a lab for testing. A blood test can also detect the EGFR gene mutation.

It may take 1 to 2 weeks to get your results.

The treatment your doctor recommends is based on your genetic test results, as well as your type and stage of cancer.

A few targeted drugs treat NSCLC gene mutations. You may get these as a solo treatment. They’re also paired with chemotherapy, another targeted therapy, or other lung cancer treatments.

EGFR inhibitors block signals from the EGFR protein, which helps cancers with this type of mutation grow. This group of drugs includes:

  • afatinib (Gilotrif)
  • dacomitinib (Vizimpro)
  • erlotinib (Tarceva)
  • gefitinib (Iressa)
  • Necitumumab (Portrazza)
  • osimertinib (Tagrisso)

Drugs that target ALK gene mutations include:

  • alectinib (Alecensa)
  • brigatinib (Alunbrig)
  • ceritinib (Zykadia)
  • crizotinib (Xalkori)
  • lorlatinib (Lorbrena)

Targeted therapies for ROS-1 positive lung cancers include:

  • ceritinib (Zykadia)
  • crizotinib (Xalkori)
  • entrectinib (Rozlytrek)
  • lorlatinib (Lorbrena)

Drugs that target BRAF mutations include:

  • dabrafenib (Tafinlar)
  • trametinib (Mekinist)

The drug capmatinib (Tabrecta) treats lung cancers with the METex14 mutation.

If no drug is currently available for your specific mutation, you may qualify for a clinical trial. These studies test new targeted therapies.

Getting into a trial could give you access to a new drug for your type of NSCLC before it’s available to everyone else.

NSCLC treatment used to be one-size-fits-all. Everyone received the same regimen, which often involved chemotherapy.

Today, a number of treatments target specific gene mutations. Your doctor should test your tumor when you’re diagnosed and let you know if you’re a good candidate for a targeted drug.

You may qualify for a clinical trial if no drug is currently available for your mutation.