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10 slides generated from the cancer page, with a quiz from the open benchmark and speaker notes that cite the sources. Arrow keys move between slides; Print gives one slide per page.
Lung cancer splits into non-small-cell disease, about 85 percent of it, and small-cell disease, which was 6.6 percent of English cases in 2024 and 9.1 percent of Welsh ones (National Lung Cancer Audit, State of the Nation 2026); the two behave and are treated very differently. Screening, staging and the things both types share are common ground; the rest belongs to each subtype.
Lung cancer is divided by histology into non-small-cell lung cancer, itself split into adenocarcinoma, squamous and large-cell carcinoma, and small-cell lung cancer, a fast-growing neuroendocrine tumour almost always linked to smoking. Non-small-cell disease has more than a dozen targetable driver mutations and is treated with surgery, radiotherapy, targeted drugs and immunotherapy by stage and biology; small-cell disease is treated with chemotherapy, immunotherapy and radiotherapy and relapses quickly. Low-dose CT screening of heavy smokers cuts lung cancer deaths by about a fifth, and tobacco control remains the largest lever. Mesothelioma and thymic tumours are separate thoracic cancers.
How the family is organised. Four classifications of lung cancer are in daily use at once and they do not nest. The World Health Organization's Classification of Thoracic Tumours, fifth edition (2021), names the tumour types: adenocarcinoma and its patterns, squamous cell carcinoma, large cell carcinoma, the sarcomatoid carcinomas, adenosquamous carcinoma, the salivary-gland-type tumours, and a separate chapter of neuroendocrine neoplasms holding typical carcinoid, atypical carcinoid, large cell neuroendocrine carcinoma and small cell carcinoma. The NCI's PDQ summaries use the clinical split instead, one summary for non-small-cell lung cancer and one for small-cell lung cancer, because that split decides the first fork of treatment. The molecular subsets (EGFR-mutant, ALK-rearranged, ROS1, KRAS G12C, MET exon 14, RET, BRAF, HER2, NTRK, NRG1) decide the second fork but are states a tumour is in rather than types of tumour, and no classification lists them as entities. On this site the family reads: lung cancer, then non-small-cell and small-cell, then the histologies under non-small-cell, with large cell neuroendocrine carcinoma sitting beside the clinical split rather than inside it because it belongs to neither. Mesothelioma arises from the pleura and is not a lung cancer, however close it sits in the chest.
| Setting | Approach | Guideline |
|---|---|---|
| Referral when symptoms suggest lung cancer (UK) | Refer on the suspected cancer pathway for chest X-ray findings that suggest lung cancer, or for unexplained haemoptysis at 40 and over. Offer an urgent direct access chest X-ray at 40 and over for two or more of cough, fatigue, shortness of breath, chest pain, weight loss and appetite loss, or for one of them in anyone who has ever smoked. Consider one for persistent or recurrent chest infection, finger clubbing, supraclavicular or persistent cervical lymphadenopathy, chest signs consistent with lung cancer, or thrombocytosis. Mesothelioma has its own rules in the same section, with asbestos exposure lowering the threshold. | not mapped |
| Prevention and stopping smoking | Tobacco control and stopping smoking, which is the only lever that reaches the 72 percent of UK cases caused by smoking. NICE NG209 covers preventing uptake in people aged 24 and under and treating dependence in everyone aged 12 and over, and was updated in February 2025 to add cytisinicline. Screening services carry smoking cessation with them, as the UK National Screening Committee required. Radon can be measured in a home and reduced; workplace exposures are regulated. | not mapped |
| Early lung cancer: surgery, radiotherapy or both, and what your lung function means for the choice | For lung cancer that has not spread, the first question is not which treatment is strongest but which treatment your lungs can afford. NICE NG122 (1.5.1) says that for people who are well enough and for whom treatment with curative intent is suitable, offer lobectomy, either open or thoracoscopic, and (1.5.2) offer more extensive surgery only where it is needed to get clear margins. NICE's own explanation is that lobectomy gives better survival than stereotactic ablative radiotherapy and is a good compromise between preserving lung function and removing the cancer. The fitness assessment runs on numbers rather than on impressions: spirometry and transfer factor before any treatment with curative intent (1.4.9), a functional segment count to predict lung function after the operation (1.4.11), a shuttle walk test with 400 m as the cut-off for good function or an exercise test with 15 ml/kg/minute where the risk of breathlessness afterwards is moderate to high (1.4.13 and 1.4.14), and a global risk score such as Thoracoscore with the person told the risk before they consent (1.4.1). Where predicted lung function after surgery is low, the guideline does not close the door: it says to offer people with a predicted postoperative FEV1 or transfer factor below 30 percent the option of treatment with curative intent if they accept the risks of breathlessness and associated complications (1.4.12). Two branches follow. If you decline a lobectomy or it is contraindicated, NICE offers stereotactic ablative radiotherapy or a sublobar resection (1.5.5), and says the evidence does not establish which of those two is better. If you decline any surgery or none is possible, it offers stereotactic ablative radiotherapy, and conventional or hyperfractionated radiotherapy if that is contraindicated (1.5.8). Stereotactic radiotherapy is outpatient treatment over a handful of visits, which is why people often prefer it. Smoking sits inside this row rather than beside it: NICE says to explain that smoking increases the risk of lung complications after surgery and to advise stopping as soon as the diagnosis is suspected, and in the same section says not to postpone surgery to allow people to stop (1.3.1 to 1.3.3). | not mapped |
| Treatment before or after surgery, and which results have to come back first | An operation is rarely the whole of the treatment for anything above the smallest tumours, and the order matters. Before surgery, NICE NG122 (1.6.8) recommends nivolumab with chemotherapy for neoadjuvant treatment of resectable disease at least 4 cm or node positive, and (1.6.9 and 1.6.10) durvalumab or pembrolizumab with platinum chemotherapy given before and then continued after the operation, durvalumab restricted to disease without EGFR mutations or ALK rearrangements. That restriction is why the molecular result has to be back before this decision is made rather than after it. After surgery, NICE (1.6.11) says to offer systemic anticancer therapy to people with good performance status and T1a to 4, N1 to 2, M0 disease, (1.6.12) to consider it for T2b to 4, N0, M0 tumours larger than 4 cm, and (1.6.13) to use a platinum-based combination. Where a targetable change is present the adjuvant treatment is a tablet instead: osimertinib after complete resection of stage 1b to 3a EGFR exon 19 deletion or L858R disease, stopped at 3 years or earlier on recurrence or unacceptable toxicity (1.6.14), and alectinib after complete resection of stage 1b (at least 4 cm) to 3a ALK-positive disease (1.6.15). For operable stage 3a N2 disease NICE (1.6.3 to 1.6.6) says to consider chemoradiotherapy with surgery, to discuss the benefits and risks first including that it improves progression-free survival and may improve overall survival, to schedule the operation 3 to 5 weeks after the chemoradiotherapy finishes so there is time to recover, and to do it only in teams with expertise in the combined treatment and in each of its parts. The practical questions this row generates are about sequence and waiting: what has to come back before we decide, how long the treatment before surgery adds, and what the pathology report will change afterwards. | not mapped |
| Locally advanced lung cancer that cannot be removed: chemoradiotherapy, then a year of immunotherapy | Locally advanced lung cancer is the stage where the treatment is hardest and the intent is still cure. NICE NG122 (1.6.17) says to consider chemoradiotherapy for people with stage 2 or 3 disease whose condition is not suitable for surgery or who decline it, and to balance the potential survival benefit against the risk of additional toxicities, which is an unusually honest sentence for a guideline and worth quoting back in clinic. What follows the chemoradiotherapy is now part of the plan rather than an afterthought: NICE (1.6.18) recommends durvalumab for locally advanced unresectable disease with PD-L1 expression on 1 percent or more of tumour cells where the disease has not progressed after concurrent platinum-based chemoradiation; the schedule this came from, PACIFIC, gave it for a year. For people whose tumour carries an EGFR change, the corpus records LAURA, which tested osimertinib in the same position after chemoradiotherapy, so what is offered depends on both the PD-L1 result and the gene result and is worth asking about by name. Where chemoradiotherapy is too much, NICE (1.5.9 and 1.5.10) says to consider radical radiotherapy, conventional or hyperfractionated, for people with stage 3a or 3b disease who are eligible, while saying plainly that some people who cannot tolerate chemoradiotherapy will not manage radical radiotherapy either. The side effect that defines this row is inflammation of the lung: both the radiotherapy and the immunotherapy can cause it, the symptoms are identical (breathlessness, a cough that does not go away, wheezing, a fever over 37.5 C), and Macmillan's instruction for all of them is the same, which is to ring the 24-hour number straight away rather than wait for the next clinic. | not mapped |
| What a biomarker result changes once the cancer has spread, and why waiting for it is usually right | Once lung cancer has spread, the tumour's genes decide the first treatment more completely than in almost any other cancer, and the honest advice is usually to wait for the result. NICE NG122 (1.2.12) says to see the National Genomics Test Directory for guidance on next-generation sequencing panels to guide treatment, and (1.2.11) that samples must be adequate, without unacceptable risk to the person, to permit subtyping and assessment of molecular markers. The genes with a treatment attached that the record carries are EGFR, ALK, ROS1, KRAS G12C, BRAF V600, MET exon 14 skipping, RET fusions, HER2 mutations and NTRK fusions, and for most of them the matched tablet does better than what would otherwise be given first. The case for waiting is not only that a targeted drug might be missed. Some of the immunotherapy recommendations are written to exclude EGFR and ALK disease (NICE 1.6.9 does so explicitly for durvalumab around surgery), and a treatment started in the wrong lane is harder to undo than a fortnight of waiting. The case against waiting is real too, and belongs in the conversation: if someone is unwell, losing weight quickly or in pain, a team may sensibly start something now and change when the result lands. That is a judgement about the person, not a failure of the system, and the question to ask is what would be started and how fast the switch could happen. Where tissue is short, a blood test for circulating tumour DNA can sometimes answer sooner; it cannot show a change in how the cancer looks under the microscope, so it complements a biopsy rather than replacing it. | not mapped |
| Which immunotherapy, and whether with chemotherapy, by the PD-L1 score | Where no targetable change is found, the first treatment for advanced lung cancer is immunotherapy, and the PD-L1 score decides whether it is given alone or with chemotherapy. NICE NG122 organises its published treatment pathways for advanced disease around exactly this split, separately for squamous and non-squamous cancer: no targetable mutations with PD-L1 below 50 percent, and no targetable mutations with PD-L1 at 50 percent or higher, with further pathways for RET fusion, KRAS G12C, MET exon 14 skipping and BRAF V600 disease at each PD-L1 level. In practice a high score opens the option of a checkpoint antibody on its own, which is a gentler treatment with fewer visits and no hair loss; adding chemotherapy works faster and is usually preferred when there is a lot of disease, when symptoms are pressing, or when the score is low. Neither is a better treatment in the abstract, and the question worth asking is which of those considerations is driving the recommendation for you. The trade-off in side effects is different in kind rather than in degree. Chemotherapy's effects are mostly predictable and temporary; immune effects are less predictable, can affect any organ, and Macmillan says they can begin during treatment or after it ends, which is why the alert card is issued and why the same short list is repeated at every visit: breathlessness, a new cough, wheezing or a fever over 37.5 C; more stools than is normal for you or stools at night; a spreading, blistering or peeling rash with flu-like symptoms; and feeling unwell even with a normal temperature. | not mapped |
| When a targeted drug stops working (resistance): the second biopsy and what comes next | Targeted tablets work until the cancer finds a way round them, and planning for that in advance makes the day it happens less frightening. The first thing to establish is the pattern. One growing area with everything else stable is often treated locally, with stereotactic radiotherapy to that spot and the tablet continued; growth in several places usually means changing treatment. The second is whether to look at the cancer again. NICE NG122 (1.2.11) asks for samples adequate to permit pathological diagnosis including subtyping and assessment of molecular markers, and (1.2.13) to choose investigations that give the most information with the least risk to the person, thinking carefully before performing a test that gives only diagnostic pathology when other information is needed too. Applied at resistance, that is the argument for and against a repeat biopsy: it can show a new resistance mutation, an amplified second gene, or that the cancer has transformed into a different type entirely, and each of those points somewhere different. A blood test for tumour DNA is quicker and can find a new mutation, but it cannot see a transformation, so where that is the question tissue is still needed. What follows depends on what is found: a next-generation inhibitor of the same target, chemotherapy with or without an antibody, an antibody drug conjugate such as patritumab deruxtecan in the HERTHENA-Lung02 setting, or a trial. Trials usually require you to be well enough to take part, so this is the point at which to ask for the referral rather than several months later. | not mapped |