Lung adenocarcinoma is the most common type of lung cancer and arises from glandular cells in the lung, often in the peripheral regions of the lungs. It is strongly associated with smoking but also occurs frequently in never smokers, particularly women and younger patients. Risk factors include tobacco smoke, air pollution, radon exposure and some inherited genetic susceptibilities.

Diagnosis relies on imaging, typically CT scans, followed by tissue sampling with bronchoscopy or needle biopsy. Under the microscope, pathologists distinguish subtypes such as lepidic, acinar, papillary, micropapillary and solid patterns. These patterns correlate with prognosis, with lepidic growth generally more favorable and solid or micropapillary patterns associated with higher risk of recurrence and metastasis.

Molecular profiling has transformed understanding and treatment. Frequent driver mutations include changes in EGFR, KRAS, ALK, ROS1, BRAF, MET, RET and others. Identifying these alterations guides the use of targeted therapies that can shrink tumors and prolong survival, often with fewer side effects than traditional chemotherapy. Resistance to targeted drugs is common, and ongoing research explores second and third generation inhibitors and combination strategies.

Immunotherapy, especially immune checkpoint inhibitors directed at PD 1 or PD L1, has become a key component of treatment, particularly for tumors with high PD L1 expression or high tumor mutational burden. Research continues into optimal sequencing and combinations of immunotherapy, targeted drugs, chemotherapy and radiation. Early detection with low dose CT screening in high risk populations improves outcomes by finding tumors at earlier, more curable stages.