Cancer screening uses medical tests to detect disease in large groups of people who have no symptoms. For individuals with high risk of developing lung cancer, computed tomography (CT) screening can detect cancer and give a person options to respond to it in a way that prolongs life. This form of screening reduces the chance of death from lung cancer by an absolute amount of 0.3% (relative amount of 20%). High risk people are those age 55–74 who have smoked equivalent amount of a pack of cigarettes daily for 30 years including time within the past 15 years.

CT screening is associated with a high rate of falsely positive tests which may result in unneeded treatment. For each true positive scan there are about 19 falsely positives scans. Other concerns include radiation exposure and the cost of testing along with follow up. Research has not found two other available tests—sputum cytology or chest radiograph (CXR) screening tests—to have any benefit.

The United States Preventive Services Task Force (USPSTF) recommends yearly screening using low-dose computed tomography in those who have a total smoking history of 30 pack-years and are between 55 and 80 years old until a person has not been smoking for more than 15 years. Screening should not be done in those with other health problems that would make treatment of lung cancer if found not an option. The English National Health Service was in 2014 re-examining the evidence for screening.

Performing a chest radiograph is one of the first investigative steps if a person reports symptoms that may suggest lung cancer. This may reveal an obvious mass, widening of the mediastinum (suggestive of spread to lymph nodes there), atelectasis (collapse), consolidation (pneumonia) or pleural effusion. CT imaging is typically used to provide more information about the type and extent of disease. Bronchoscopy or CT-guided biopsy is often used to sample the tumor for histopathology.

Lung cancer often appears as a solitary pulmonary nodule on a chest radiograph. However, the differential diagnosis is wide. Many other diseases can also give this appearance, including metastatic cancer, hamartomas, and infectious granulomas such as tuberculosis, histoplasmosis and coccidioidomycosis. Lung cancer can also be an incidental finding, as a solitary pulmonary nodule on a chest radiograph or CT scan done for an unrelated reason. The definitive diagnosis of lung cancer is based on histological examination of the suspicious tissue in the context of the clinical and radiological features.

Clinical practice guidelines recommend frequencies for pulmonary nodule surveillance. CT imaging should not be used for longer or more frequently than indicated as extended surveillance exposes people to increased radiation.

The prognosis of patients with FA as a whole is considered to be better than that of most other forms of non-small cell carcinoma, including biphasic pulmonary blastoma.

Staging is a formal procedure to determine how developed the cancer is. This determines treatment options.

The American Joint Committee on Cancer (AJCC) and the International Union Against Cancer (UICC) recommend TNM staging, using a uniform scheme for non-small cell lung carcinoma, small-cell lung carcinoma and broncho-pulmonary carcinoid tumors. With TNM staging, the cancer is classified based on the size of the tumor and spread to lymph nodes and other organs. As the tumor grows in size and the areas affected become larger, the staging of the cancer becomes more advanced as well.

There are several components of NSCLC staging which then influence physicians' treatment strategies. The lung tumor itself is typically assessed both radiographically for overall size as well as by a pathologist under the microscope to identify specific genetic markers or to see if there has been invasion into important structures within the chest (e.g., bronchus or pleural cavity). Next, the patient's nearby lymph nodes within the chest cavity known as the mediastinum will be checked for disease involvement. Finally, the patient will be evaluated for more distant sites of metastatic disease, most typically with brain imaging and or scans of the bones.

The survival rates for stages I through IV decrease significantly due to the advancement of the disease. For stage I, the five-year survival rate is 47%, stage II is 30%, stage III is 10%, and stage IV is 1%.

The major criterion for diagnosis is typically a confirmed surgical biopsy. Minor diagnostic criteria have been proposed for DIPNECH.

- Clinical presentation: woman, between the age of 45 and 67 with cough and/or shortness of breath for 5–10 years

- Pulmonary function: increased residual volume, increased total lung capacity, fixed obstruction, low diffusing capacity of the lung for carbon monoxide that corrects with alveolar volume

- High-resolution CT scan: diffuse pulmonary nodules 4–10 mm, greater than 20 nodules, mosaic attenuation or air trapping in greater than 50% of the lung

- Transbronchial biopsy: proliferation of pulmonary neuroendocrine cells

- Serum markers: elevated serum chromogranin A levels

Asbestos can cause lung cancer that is identical to lung cancer from other causes. Exposure to asbestos is associated with all major histological types of lung carcinoma (adenocarcinoma, squamous cell carcinoma, large-cell carcinoma and small-cell carcinoma). The latency period between exposure and development of lung cancer is 20 to 30 years. It is estimated that 3%-8% of all lung cancers are related to asbestos. The risk of developing lung cancer depends on the level, duration, and frequency of asbestos exposure (cumulative exposure). Smoking and individual susceptibility are other contributing factors towards lung cancer. Smokers who have been exposed to asbestos are at far greater risk of lung cancer. Smoking and asbestos exposure have a multiplicative (synergistic) effect on the risk of lung cancer. Symptoms include chronic cough, chest pain, breathlessness, haemoptysis (coughing up blood), wheezing or hoarseness of the voice, weight loss and fatigue. Treatment involves surgical removal of the cancer, chemotherapy, radiotherapy, or a combination of these (multimodality treatment). Prognosis is generally poor unless the cancer is detected in its early stages. Out of all patients diagnosed with lung cancer, only 15% survive for five years after diagnosis.

All in all, small-cell carcinoma is very responsive to chemotherapy and radiotherapy, and in particular, regimens based on platinum-containing agents. However, most people with the disease relapse, and median survival remains low.

In "limited-stage" disease, median survival with treatment is 14–20 months, and about 20% of patients with limited-stage small-cell lung carcinoma live 5 years or longer. Because of its predisposition for early metastasis, the prognosis of SCLC is poor, with only 10% to 15% of patients surviving 3 years.

The prognosis is far more grim in "extensive-stage" small-cell lung carcinoma; with treatment, median survival is 8–13 months; only 1–5% of patients with extensive-stage small-cell lung carcinoma treated with chemotherapy live 5 years or longer.

Adenocarcinoma of the lung tends to stain mucin positive as it is derived from the mucus-producing glands of the lungs. Similar to other adenocarcinoma, if this tumor is well differentiated (low grade) it will resemble the normal glandular structure. Poorly differentiated adenocarcinoma will not resemble the normal glands (high grade) and will be detected by seeing that they stain positive for mucin (which the glands produce). Adenocarcinoma can also be distinguished by staining for TTF-1, a cell marker for adenocarcinoma.

To reveal the adenocarcinomatous lineage of the solid variant, demonstration of intracellular mucin production may be performed. Foci of squamous metaplasia and dysplasia may be present in the epithelium proximal to adenocarcinomas, but these are not the precursor lesions for this tumor. Rather, the precursor of peripheral adenocarcinomas has been termed "atypical adenomatous hyperplasia" (AAH). Microscopically, AAH is a well-demarcated focus of epithelial proliferation, containing cuboidal to low-columnar cells resembling club cells or type II pneumocytes. These demonstrate various degrees of cytologic atypia, including hyperchromasia, pleomorphism, prominent nucleoli. However, the atypia is not to the extent as seen in frank adenocarcinomas. Lesions of AAH are monoclonal, and they share many of the molecular aberrations (like KRAS mutations) that are associated with adenocarcinomas.

Giant-cell lung cancers have long been considered to be exceptionally aggressive malignancies that grow very rapidly and have a very poor prognosis.

Many small series have suggested that the prognosis of lung tumors with giant cells is worse than that of most other forms of non-small-cell lung cancer (NSCLC), including squamous cell carcinoma, and spindle cell carcinoma.

The overall five-year survival rate in GCCL varies between studies but is generally considered to be very low. The (US) Armed Forces Institute of Pathology has reported a figure of 10%, and in a study examining over 150,000 lung cancer cases, a figure of 11.8% was given. However, in the latter report the 11.8% figure was based on data that included spindle cell carcinoma, a variant which is generally considered to have a less dismal prognosis than GCCL. Therefore, the likely survival of "pure" GCCL is probably lower than the stated figure.

In the large 1995 database review by Travis and colleagues, giant-cell carcinoma has the third-worst prognosis among 18 histological forms of lung cancer. (Only small-cell carcinoma and large-cell carcinoma had shorter average survival.)

Most GCCL have already grown and invaded locally and/or regionally, and/or have already metastasized distantly, and are inoperable, at the time of diagnosis.

Because of its rarity, there have been no randomized clinical trials of treatment of GCCL, and all information available derives from small retrospective institutional series or multicenter metadata.

The findings on chest imaging in DIPNECH patients are bilateral and diffuse. The most frequent findings on a computed tomography (CT) of the chest are multiple primary nodules and/or masses, on a background of mosaic attenuation and airway wall thickening.

The nodules have an indolent pattern of growth and are found throughout the lungs. The nodules are typically rounded and well-defined. Upon surgical resection, histologically the nodules are found to be typical carcinoids or carcinoid tumorlets depending on size.

15% of lung cancers in the US are of this type. Small cell lung cancer occurs almost exclusively in smokers; most commonly in heavy smokers and rarely in non-smokers.

Because of its extreme rarity, there have been no controlled clinical trials of treatment regimens for FA and, as a result, there are no evidence-based treatment guidelines. Complete surgical resection is the treatment of choice in FA, as it is in nearly all forms of lung cancer.

Anecdotal reports suggest that FA is rarely highly sensitive to cytotoxic drugs or radiation. Case reports suggest that chemotherapy with UFT may be useful in FA.

The prognosis of EMECL is relatively good, and considerably better than most other forms of NSCLC. The skull and dura are possible sites for metastasis from pulmonary EMC. The MIB-1 index is a predictive marker of malignant potential.

Early stage disease is treated surgically. Targeted therapy is available for lung adenocarcinomas with certain mutations. Crizotinib is effective in tumors with fusions involving ALK or ROS1, whereas gefitinib, erlotinib, and afatinib are used in patients whose tumors have mutations in EGFR.

The definitive diagnosis is rendered by a microscopic examination, after excision. Typical carcinoids have cells with stippled chromatin and a moderate quantity of cytoplasm. They typically have few mitoses and lack necrosis. By definition, they are greater than 4 mm in largest dimension; smaller lesions are referred to as "pulmonary carcinoid tumourlets".

The differential diagnosis of typical pulmonary carcinoid tumour includes: "atypical pulmonary carcinoid tumour", "pulmonary carcinoid tumourlet" and "lung adenocarcinoma".

EMECL is staged in the same manner as other non-small cell lung carcinomas, based on the TNM (Tumor-Node-Metastasis) staging system.

Malignant mesothelioma is an aggressive and incurable tumour caused by asbestos arising from mesothelial cells of the pleura, peritoneum (the lining of the abdominal cavity) and rarely elsewhere. Pleural mesothelioma is the most common type of mesothelioma, representing about 75 percent of cases. Peritoneal mesothelioma is the second most common type, consisting of about 10 to 20 percent of cases. Mesothelioma appears from 20 to 50 years after the initial exposure to asbestos. The symptoms include shortness of breath, chronic chest pain, cough, and weight loss. Diagnosing mesothelioma is often difficult and can include physical examination, chest X-ray and lung function tests, followed by CT scan and MRI. A biopsy is needed to confirm a diagnosis of malignant mesothelioma. Mesothelioma has a poor prognosis, with most patients dying within 1 year of diagnosis. The treatment strategies include surgery, radiotherapy, chemotherapy or multimodality treatment. Several tumour biomarkers (soluble mesothelin-related protein (SMRP), osteopontin and fibulin3) have been evaluated for diagnostic purposes to allow early detection of this disease. Novel biomarkers such as volatile organic compounds measured in exhaled breath are also promising.

Staging of c-SCLC patients is usually performed in an analogous fashion to patients with "pure" small cell lung carcinoma.

For several decades, SCLC has been staged according to a dichotomous distinction of "limited disease" (LD) "vs." "extensive disease" (ED) tumor burdens. Nearly all clinical trials have been conducted on SCLC patients staged dichotomously in this fashion. LD is roughly defined as a locoregional tumor burden confined to one hemithorax that can be encompassed within a single, tolerable radiation field, and without detectable distant metastases beyond the chest or supraclavicular lymph nodes. A patient is assigned an ED stage when the tumor burden is greater than that defined under LD criteria — either far advanced locoregional disease, malignant effusions from the pleura or pericardium, or distant metastases.

However, more recent data reviewing outcomes in very large numbers of SCLC patients suggests that the TNM staging system used for NSCLC is also reliable and valid when applied to SCLC patients, and that more current versions may allow better treatment decisionmaking and prognostication in SCLC than with the old dichotomous staging protocol.

Lung carcinoids typically present with a cough or hemoptysis. Findings may closely mimic malignant tumours of the lung, i.e. lung cancer.

Respiratory diseases may be investigated by performing one or more of the following tests

- Biopsy of the lung or pleura

- Blood test

- Bronchoscopy

- Chest x-ray

- Computed tomography scan, including high-resolution computed tomography

- Culture of microorganisms from secretions such as sputum

- Ultrasound scanning can be useful to detect fluid such as pleural effusion

- Pulmonary function test

- Ventilation—perfusion scan

Flavorings-related lung disease can be prevented with the use of engineering controls (e.g. exhaust hoods or closed systems), personal protective equipment, monitoring of potentially affected workers, worker education, and by not using lung-disease-causing flavorings.

Multiple abnormal laboratory findings have been noted in indium lung. High levels of serum indium have been found in all cases of indium lung. Other abnormal laboratory values that have been found include elevated alanine aminotransferase, elevated aspartate aminotransferase, elevated C-reactive protein, elevated interstitial lung disease markers, and elevated GM-CSF autoantibodies.

Current consensus is that the long-term prognosis of c-SCLC patients is determined by the SCLC component of their tumor, given that "pure" SCLC seems to have the worst long-term prognosis of all forms of lung cancer. Although data on c-SCLC is very sparse, some studies suggest that survival rates in c-SCLC may be even worse than that of pure SCLC, likely due to the lower rate of complete response to chemoradiation in c-SCLC, although not all studies have shown a significant difference in survival.

Untreated "pure" SCLC patients have a median survival time of between 4 weeks and 4 months, depending on stage and performance status at the time of diagnosis.

Given proper multimodality treatment, SCLC patients with limited disease have median survival rates of between 16 and 24 months, and about 20% will be cured. In patients with extensive disease SCLC, although 60% to 70% will have good-to-complete responses to treatment, very few will be cured, with a median survival of only 6 to 10 months.

Some evidence suggests that c-SCLC patients who continue to smoke may have much worse outcomes after treatment than those who quit.