• STK11 / KEAP1 co-mutations: Two genes whose loss, often alongside a KRAS mutation, makes lung cancer 'cold' to immunotherapy and shortens survival on standard treatment.
• Immune surveillance and cancer immunoediting: The immune system patrols for cells that have turned malignant and destroys most of them; the tumours we see are the ones that learned to hide.
• Histology: The study of tissue under the microscope.
• Biopsy: Taking a small piece of the suspicious tissue so a pathologist can examine it under the microscope.
• EGFR C797S: A mutation that stops osimertinib from binding to EGFR; the main on-target way lung cancers escape it.
• Lung-RADS and nodule reporting: The scoring systems that turn a screening CT into an action.
• Amplification: When a cell carries extra copies of a gene, sometimes 50 or more instead of the normal two, so it makes far too much of that protein.
• Pleura: The two-layered lining around each lung.
• EGFR mutation subtypes (exon 19 deletion, L858R, exon 20 insertion, T790M): Lung cancers with a mutated EGFR gene are treated with EGFR pills, but which pill and how well it works depends on exactly where the mutation is.
• Lung cancer drugs in England: what NICE has recommended: Which lung cancer drugs the NHS in England funds, and which it does not.

Biomarker results to ask for: EGFR, ALK, ROS1, BRAF V600E, MET ex14 / amplification / c-MET IHC, RET, NTRK, KRAS G12C, HER2 mutation, PD-L1 TPS, ctDNA, PD-L1 TPS (22C3), EGFR (exon 19 del, L858R, exon 20 ins, T790M, C797S), ALK fusion, ROS1 fusion, KRAS G12C (and G12D/V), MET exon 14 skipping, MET amplification, c-Met IHC, RET fusion, HER2 (ERBB2) mutation, NTRK fusion, STK11 / KEAP1 (prognostic, IO resistance), TP53 / RB1 (transformation risk), ctDNA (genotyping, MRD, resistance tracking), TMB (limited use), TTF-1 and p40 immunohistochemistry to assign histology on a small biopsy before molecular testing, Spread through air spaces, recorded on resection specimens since the 2021 WHO classification, Pathological stage by TNM 9, including the N2a and N2b split, KRAS G12C: 41-51%, EGFR: 12-47%, EGFR exon 19 deletion: 13-19%, EGFR L858R: 9-21%, EGFR exon 20 insertion: 1-3%, STK11 (LKB1): 13-18%, KEAP1: 11-18%, MET exon 14 skipping: 2-4%, MET amplification: 2-3%, ERBB2 (HER2) mutation: 2-4%, BRAF V600E: 1-2%, ALK fusion: 3-6%, ROS1 fusion: 1-3%, RET fusion: 1-2%, NTRK fusion: 0.2%, NRG1 fusion: 0.3%.

Scans and tests linked to this cancer: Companion diagnostics, Comprehensive genomic profiling, CT (computed tomography), Cytogenetics and FISH, Endoscopic ultrasound and EBUS systems, Germline (hereditary) testing.

Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.

• Screening (age 50-80, ≥20 pack-years): Annual low-dose CT with Lung-RADS reporting; AI nodule scoring emerging; robotic bronchoscopy for peripheral nodule biopsy. (Low-dose CT lung screening, NLST & NELSON (low-dose CT screening), Robotic and navigational bronchoscopy, AI in radiology)
• Stage I-II resectable: Lobectomy or segmentectomy (small peripheral) with nodal staging; SBRT if inoperable. Stage IB-IIIA: neoadjuvant chemo-IO (CheckMate 816) or perioperative chemo-IO (KEYNOTE-671); adjuvant osimertinib if EGFR-mutant (ADAURA), alectinib if ALK-positive (ALINA); adjuvant chemotherapy otherwise for stage II+. (Robotic & minimally invasive surgery, SBRT / SABR (stereotactic radiotherapy), CheckMate 816, KEYNOTE-671, ADAURA, ALINA, Osimertinib, Alectinib)
• Stage III unresectable: Concurrent platinum chemoradiation → durvalumab 1 year (PACIFIC), or osimertinib until progression if EGFR-mutant (LAURA). Proton therapy in selected cases. (IMRT / IGRT (modern external beam), PACIFIC, LAURA, Durvalumab, Osimertinib, Proton therapy)
• Metastatic, EGFR exon 19 del / L858R: First line: osimertinib ± platinum-pemetrexed (FLAURA2) or amivantamab + lazertinib (MARIPOSA, OS benefit). Progression: re-biopsy/ctDNA; amivantamab + chemotherapy (MARIPOSA-2), Dato-DXd (TROPION-Lung05), platinum doublet; MET TKI add-on if MET-amplified; platinum-etoposide if small-cell transformation. (Osimertinib, FLAURA2, Amivantamab, Lazertinib, MARIPOSA, Amivantamab + lazertinib (first-line EGFR NSCLC), Datopotamab deruxtecan, TROPION-Lung05, EGFR exon 19 deletion & L858R, EGFR C797S, MET amplification (bypass resistance), Histologic transformation)
• Metastatic, EGFR exon 20 insertion: Amivantamab + platinum-pemetrexed (PAPILLON); sunvozertinib later line. (Amivantamab, EGFR exon 20 insertion)
• Metastatic, ALK-rearranged: Lorlatinib (CROWN; 5-year PFS 60%) or alectinib first line; on progression, neladalkib (under review) or lorlatinib if not used; local therapy for oligoprogression; chemotherapy. (Lorlatinib, CROWN, Alectinib, Neladalkib, ALKOVE-1, Oligoprogression)
• Metastatic, ROS1-rearranged: Repotrectinib or zidesamtinib (2026) first line; entrectinib/crizotinib alternatives. (Repotrectinib, Zidesamtinib, ROS1)
• Metastatic, KRAS G12C: First line: PD-(L)1 ± chemotherapy by PD-L1 (G12C inhibitor + IO combinations in phase 3: olomorasib SUNRAY-01, divarasib Krascendo 2). Second line: sotorasib or adagrasib (CodeBreaK 200, KRYSTAL-12); divarasib superior head-to-head (Krascendo 1, 2026). (Sotorasib, Adagrasib, Divarasib, Olomorasib, CodeBreaK 200, KRYSTAL-12, Krascendo 1, KRAS & RAS inhibitors)
• Metastatic, BRAF V600E: Dabrafenib + trametinib or encorafenib + binimetinib first line; chemo-IO as alternative. (Dabrafenib + trametinib, Encorafenib, BRAF)
• Metastatic, MET exon 14 skipping: Capmatinib or tepotinib first line; telisotuzumab vedotin for c-Met-overexpressing EGFR-wild-type disease after chemotherapy (accelerated 2025). (Capmatinib & tepotinib, Telisotuzumab vedotin, TeliMET NSCLC-01, MET)
• Metastatic, RET-fusion: Selpercatinib first line (LIBRETTO-431); pralsetinib alternative. (Selpercatinib, LIBRETTO-431, Pralsetinib, RET)
• Metastatic, HER2-mutant: First line: zongertinib (2026) or chemo-IO; sevabertinib (Nov 2025) or T-DXd after prior therapy. (Zongertinib, Sevabertinib, SOHO-01, Trastuzumab deruxtecan, HER2)
• Metastatic, NTRK-fusion: Larotrectinib, entrectinib, or repotrectinib (tumour-agnostic). (Repotrectinib, NTRK, Tumour-agnostic (tissue-agnostic) approval)
• Metastatic, driver-negative, PD-L1 TPS ≥50%: Pembrolizumab (KEYNOTE-024) or cemiplimab monotherapy; add chemotherapy for high burden or rapid progression. Ivonescimab beat pembrolizumab in China (HARMONi-2); not approved in the US. (Pembrolizumab, Cemiplimab, KEYNOTE-024 & KEYNOTE-189, Ivonescimab, HARMONi-2, Tumour proportion score (TPS))
• Metastatic, driver-negative, PD-L1 TPS <50%: Pembrolizumab + platinum doublet (KEYNOTE-189 non-squamous; KEYNOTE-407 squamous); nivolumab + ipilimumab ± chemotherapy; tremelimumab + durvalumab + chemotherapy for PD-L1-negative or STK11/KEAP1-altered disease. Second line: docetaxel ± ramucirumab, TTFields, or trials of ADCs. (Pembrolizumab, Nivolumab, Ipilimumab, Tremelimumab, Durvalumab, PD-1 blockade + chemotherapy in PD-L1-low NSCLC, Optune / Optune Pax (TTFields))
• Metastatic, squamous: Pembrolizumab + carboplatin + (nab-)paclitaxel (KEYNOTE-407); no ADC approved (TROPION-Lung01 showed no benefit in squamous); ivonescimab + chemotherapy under study (HARMONi-3). (Pembrolizumab, Paclitaxel / nab-paclitaxel, Carboplatin, TROPION-Lung01, HARMONi-3)

From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.