The visitor returns walkthrough mutation6/10/2023 These drugs are specifically used to treat the EGFR exon 20 insertion mutation: These EGFR inhibitors can treat the EGFR exon 19 deletion and EGFR exon 21 L858R point mutations: EGFR inhibitors block signals from the EGFR protein. The EGFR protein helps cancers with the EGFR mutation grow. In 2021, the Food and Drug Administration (FDA) approved sotorasib (Lumakras), the first KRAS inhibitor for lung cancer. Getting into a trial could give you access to a new drug for your NSCLC type before it’s available to everyone else. These studies test new targeted therapies. If no drug is currently available for your specific mutation, you may qualify for a clinical trial. They can also be paired with another targeted therapy, chemotherapy, or other lung cancer treatments.Īt the moment, there are no targeted therapies for cancers involving TP53, NRAS, or PIK3CA gene mutations. The treatment your doctor recommends will be based on the results of your genetic test as well as your type and stage of cancer.Ī few targeted drugs treat NSCLC gene mutations. neurotrophic tyrosine receptor kinase (NTRK)Įach of these mutations affects less than 2% of NSCLC cases, according to research such as a 2017 study and a 2021 literature review.Some of the less common mutations linked to NSCLC include: It’s most common in people with adenocarcinomas and people who’ve never smoked. Human epidermal growth factor receptor 2 (HER2)īetween 1% and 4% of NSCLCs involve the human epidermal growth factor receptor 2 gene mutation, more commonly known as HER2. It accounts for half of all BRAF mutations. One subtype is known as the BRAF V600E mutation. These mutations are also more common in female patients than in male patients. Most people who have these mutations are current or former smokers. Up to 3.5%–4% of NSCLCs test positive for BRAF mutations. adenocarcinoma, which is the most common form of lung cancer overall.The three main types of non-small cell lung cancer (NSCLC) are: It’s more common in squamous cell lung carcinomas than in adenocarcinomas. The phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha ( PIK3CA) gene mutation is present in up to 5% of NSCLCs, according to research. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha ( PIK3CA) MET exon 14 deletion (METex14) is a type of MET mutation that’s been linked to around 3% of NSCLCs. MET-positive lung cancers tend to be more aggressive than lung cancers without the mutation. The MET gene is changed in up to 5% of all NSCLCs. Mesenchymal–epithelial transition (MET) and METex14 It’s also more common in people who’ve never smoked. The EML4-ALK mutation occurs when the ALK gene fuses with the echinoderm microtubule-associated protein-like 4 ( EML4) gene. The ALK mutation is common in younger people and nonsmokers. It allows cancer cells to grow and spread. Anaplastic lymphoma kinase (ALK)Ībout 5% of NSCLC cases have the anaplastic lymphoma kinase (ALK) gene mutation, according to research published in 2017. Less common EGFR mutations don’t typically respond to these targeted therapies. They respond to targeted therapies known as EGFR inhibitors. The EGFR exon 19 deletion mutation and EGFR exon 21 L858R point mutation are the most common. These mutations are more common in certain groups, including women and nonsmokers. EGFR-positive cancers account for around 10% to 15% of all lung cancers in the United States, according to the American Lung Association. Some NSCLC cells have too much of this protein, which makes them grow faster than usual. Epidermal growth factor receptor (EGFR)Įpidermal growth factor receptor (EGFR) is a protein on the surface of cells. Experts aren’t sure of the significance of the STK11 mutation or what effect it has on treatment options. The STK11 mutation often appears alongside the KRAS mutation. The outlook for people with this type of mutation isn’t as good as it is for those without it. The KRAS mutation is found in about 30% of all NSCLCs. Research into targeted TP53 therapies is ongoing. Research like a 2018 study suggests that TP53 mutations combined with EGFR, ALK, or ROS1 mutations are linked to a shorter survival time for people with NSCLC.īecause there’s not yet an established targeted therapy for TP53 mutations, there’s debate about whether doctors should always test for them in people with cancer. They’re usually acquired and happen in both smokers and people who’ve never smoked. TP53 mutations are common in cancers and are found in about 50% of all cases of NSCLC, according to research. This means it keeps damaged cells from growing out of control or growing too fast. This protein monitors cells for DNA damage and acts as a tumor suppressor. The TP53 gene is responsible for the production of tumor protein p53. Some of the most common gene mutations are described below. A few different gene mutations help NSCLCs spread and grow.
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