Loading
EGFR-mutated lung cancer is driven by a single faulty growth receptor and is treated first with a pill rather than chemotherapy. Osimertinib keeps the disease under control for about a year and a half on average, adding chemotherapy or the antibody amivantamab extends that further, and three years of osimertinib after surgery roughly halves the risk of death in early-stage disease.
EGFR mutations were discovered in 2004 when three Boston groups worked out why a minority of lung cancers, mostly in never-smoking women and East Asian patients, melted away on gefitinib. The IPASS trial (2009) then showed that in mutation carriers gefitinib beat chemotherapy and in non-carriers it was worse, which made EGFR testing mandatory before first-line treatment and established the model of a driver mutation matched to a pill. Exon 19 deletions and L858R are the classical sensitising mutations; exon 20 insertions are resistant to the classical inhibitors; and uncommon mutations (G719X, L861Q, S768I) respond best to afatinib or osimertinib.
Osimertinib, designed against the T790M resistance mutation, beat gefitinib and erlotinib first line in FLAURA (2018): median progression-free survival 18.9 versus 10.2 months and overall survival 38.6 versus 31.8 months, with far less brain progression. Two trials then built on it: FLAURA2 (2023) added platinum-pemetrexed to osimertinib (progression-free survival 25.5 versus 16.7 months, hazard ratio 0.62, with the 2025 survival analysis also in favour), and MARIPOSA (2024) combined the EGFR-MET bispecific antibody amivantamab with lazertinib (23.7 versus 16.6 months, hazard ratio 0.70, and longer overall survival), at the cost of rash, nail changes and venous thrombosis. For exon 20 insertions, PAPILLON (2023) showed amivantamab plus chemotherapy beat chemotherapy (11.4 versus 6.7 months, hazard ratio 0.40) and sunvozertinib was approved in 2025 after platinum chemotherapy. After osimertinib the escape routes are MET amplification (osimertinib plus savolitinib), C797S, small-cell transformation and, most often, no identifiable mechanism, where amivantamab plus chemotherapy (MARIPOSA-2) and the TROP2 antibody-drug conjugate datopotamab deruxtecan are the options.
In early disease ADAURA (2020) showed that three years of adjuvant osimertinib after resection cut recurrence by 83 percent in stage II to IIIA (hazard ratio 0.17) and improved five-year overall survival from 78 to 88 percent, and LAURA (2024) showed that osimertinib after chemoradiation for unresectable stage III disease extended progression-free survival from 5.6 to 39.1 months. Checkpoint inhibitors work poorly in EGFR-mutated disease and are held back until targeted options are exhausted. Open questions are how to choose between the three first-line strategies, whether circulating tumour DNA clearance can guide escalation, and how to prevent rather than treat resistance.
Averages across everyone diagnosed, often years ago. A median is the middle of a group: half the people counted lived longer than the figure shown, and some lived far longer. Your stage, subtype, age, fitness and the treatment you receive matter more than the average, and the numbers are improving quickly.
About 15 percent of lung adenocarcinomas in Europe and North America and 40 to 50 percent in East Asia carry an activating EGFR mutation; it is the commonest driver in never-smokers and in women. Exon 19 deletions and L858R make up about 85 percent of cases, exon 20 insertions about 10 percent.
Central tumours arise in the large airways, peripheral ones in the alveoli; both drain to hilar then mediastinal nodes, and the pleural lining is a separate cancer site.
Same organ: Mediastinal germ cell tumour, Pleuropulmonary blastoma (types I, Ir, II and III), Type A and type AB thymoma, Type B1 and type B2 thymoma, Type B3 thymoma, Micronodular thymoma with lymphoid stroma, Adenocarcinoma of the lung, Squamous cell carcinoma of the lung, Large cell carcinoma of the lung, Sarcomatoid carcinoma of the lung, Adenosquamous carcinoma of the lung, Invasive mucinous adenocarcinoma of the lung, Adenocarcinoma in situ and minimally invasive adenocarcinoma of the lung, Basaloid squamous cell carcinoma of the lung, Lymphoepithelial carcinoma of the lung, Pulmonary blastoma (adult), Non-small-cell lung cancer, Lung cancer (all types), Small-cell lung cancer, Mesothelioma, Pleural mesothelioma, Thymoma and thymic carcinoma, Childhood lung and airway tumours (pleuropulmonary blastoma, tracheobronchial tumours), Inflammatory myofibroblastic tumour (IMT), ALK-positive non-small-cell lung cancer, KRAS G12C-mutant non-small-cell lung cancer, ROS1-positive non-small-cell lung cancer, MET exon 14 and MET-amplified non-small-cell lung cancer, RET fusion-positive non-small-cell lung cancer, BRAF V600E-mutant non-small-cell lung cancer, HER2-mutant non-small-cell lung cancer, NTRK fusion-positive non-small-cell lung cancer, PD-L1-high non-small-cell lung cancer without a driver mutation, Resectable stage I to III non-small-cell lung cancer, Unresectable stage III non-small-cell lung cancer, Limited-stage small-cell lung cancer, Extensive-stage small-cell lung cancer, Lung neuroendocrine tumours (typical and atypical carcinoid), Large cell neuroendocrine carcinoma of the lung, Thymoma (WHO types A, AB, B1, B2 and B3), Thymic carcinoma
Nothing recorded yet.
Also on OnCo: Symptoms and red flags · Early detection roadmap.
Osimertinib alone (FLAURA), osimertinib plus platinum-pemetrexed (FLAURA2) for patients with high burden or brain metastases who can take chemotherapy, or amivantamab plus lazertinib (MARIPOSA) with prophylaxis against rash and clots.
Amivantamab plus carboplatin-pemetrexed first line (PAPILLON); sunvozertinib after platinum chemotherapy.
Biopsy or plasma test for the mechanism: osimertinib plus savolitinib for MET amplification; otherwise amivantamab plus platinum chemotherapy (MARIPOSA-2), platinum-pemetrexed, or datopotamab deruxtecan after chemotherapy; platinum-etoposide for small-cell transformation.
Surgery, adjuvant platinum chemotherapy where indicated, then three years of osimertinib (ADAURA).
Concurrent platinum chemoradiation followed by osimertinib until progression (LAURA) rather than durvalumab.
Osimertinib has high brain penetration and is preferred; stereotactic radiosurgery for symptomatic or large lesions; high-dose osimertinib for leptomeningeal disease.
Trials recruiting now, the landmark trials, the trials held by this cancer's subtypes, the key papers and what they mean, the latest literature, and the milestones year by year.
The targets of this cancer's medicines and the ones linked to it directly.
Cases by country, the UK and NHS pathway and other country lenses, the expert centres with trials on record, and the centres named on this cancer's subtypes.
One section per setting: the options named, what each is for, the trials behind them, the recorded trade-offs and the questions to ask.
Fainting, near-fainting, or an irregular or racing heartbeat; several kinase inhibitors prolong the QT interval and the labels require ECG and electrolyte monitoring.
Bleeding that does not stop by itself, bleeding from more than one site, or new bruising in several places or one large area.
Any new or worsening cough, breathlessness or fever. The label says to interrupt treatment for any suspected ILD and to permanently discontinue for grade 2 or higher.
Temperature of 38 C or higher, or feeling shivery and unwell even without a fever. Antibody-drug conjugates suppress the bone marrow, and several carry a boxed warning for severe neutropenia.
No food effect (intravenous or subcutaneous antibody).
Known QT prolongation. Avoid other QT-prolonging drugs where possible; check ECG and correct potassium and magnesium before and during treatment.
See all on the product pages:AmivantamabCarboplatinDatopotamab deruxtecanLazertinibOsimertinibPemetrexedPlatinum + etoposide (EP / CE)SavolitinibSunvozertinib·Printable cards in the navigator
Newly diagnosed? Read the first 60 days with EGFR-mutated non-small-cell lung cancer, then print the one-page appointment sheet with room for the answers.
Print this page for your appointment (your browser's print command). These prompts are for discussion; your clinical team knows your case.
Everything in development, the medicines held by this cancer's subtypes, the open problems and what is being done about them, the roadmaps, and what changed on this record.
Every connected record, the notes, the JSON, Markdown and RDF twins, and where the record came from and when it was checked.