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Chapter 3: Respiratory oncology 135

Table 3.21 Risks of cigarette smoking types:
1 Squamous cell carcinoma, 50%.
Cigarettes per Never Ex- 1–14 15–24 >25
day 2 Small/oat cell carcinoma, 20%.
Male deaths per 0.1 0.4 0.78 1.27 2.51 3 Adenocarcinoma, 20%.
1000 per year 4 Large cell anaplastic carcinoma, 10%.
Afew show a mixed pattern: 70% of all tumours arise
in relation to the main bronchus (central or hilar) and
Ittakesanex-smokerof ≤20perday13yearstoreturn

30% arise in the peripheral airways or alveoli.
to just above the risk of a non-smoker. Pipe smokers
1 Squamous cell carcinoma: Usually located centrally
have about 40% the risk of cigarette smokers.
close to the carina and so presents with the sequelae
Occupational and environmental factors include ex-

of bronchial obstruction and local invasion. Lesions
posure to radioactive material (including radon), as-
may cavitate. Histologically squamous cell carcinoma
bestos, nickel, chromium, iron oxides and coal gas
shows a variety of patterns from well-differentiated le-
plants.
sionsproducinglotsof keratintopoorlydifferentiated
lesions containing little keratin.
Pathophysiology 2 Small cell/oat cell/anaplastic lung cancer is a highly
Lung cancer is characterised by multiple genetic alter- malignant tumour arising from bronchial epithelium,
ations: but with properties of neuroendocrine cells contain-
1 In >90% of small cell lung cancers the p53 and rb tu- ing secretory granules. Tumours are centrally located
mour suppressor genes are both mutated, and >50% and are associated with a rapid growth rate with
and 20% respectively in non-small cell lung cancer. metastases almost invariable at presentation. Often
2 Activation of dominant oncogenes – for example, mu- associated with ectopic ADH and ACTH secretion
tations in ras genes are associated with 20% of non- (water/sodium retention and Cushing’s syndrome).
small cell lung cancer and confer a poor prognosis, 3 Adenocarcinoma characteristically develops as a pe-
while tumour amplification of c-myc is associated ripheral tumour, but may arise from the main
with a poor prognosis in small cell lung cancer. bronchus. A proportion are thought to arise from pre-
3 Some of these genetic alterations are seen in pre- existing lung scars. It is the most common bronchial
neoplastic lesions such as hyperplasia, dysplasia and carcinoma associated with asbestos and is propor-
carcinoma-in-situ of the bronchial epithelium, but it tionallymorecommoninnon-smokers.Histologically
appears that as many as 10 of these mutations are four patterns are seen:
needed for the development of lung cancer. Acinar – prominent gland-like spaces.
Papillary – fronds of tumour on thin septa.

Clinical features Solid carcinoma – poorly differentiated with mucin
Cough or worsening of a pre-existing cough is the most production.
common early symptom, but may be ignored. Haemop- Alveolar cell carcinoma derived from alveolar or
tysis due to ulceration of a tumour is the next most com- bronchial epithelial cells (Clara cells and type II
mon. Dyspnoea, a dull central chest ache or pleuritic pneumocytes). These may exist as isolated pe-
pain, or slowly resolving chest infection are all common. ripheral nodules, but they characteristically spread
Clubbing and systemic features (weight loss, anorexia through the lung along alveolar septa (seen on chest
and malaise) or complications from metastatic deposits X-ray as areas of alveolar shadowing). Half are mul-
may also be presenting features. tifocal infiltrative tumours, which replace areas of
lunginamannerresemblingpneumonicconsolida-
Macroscopy/microscopy tion.Cellsaretall,columnarandrelativelyuniform,
Because of their pathological behaviour malignancies have few mitoses and secrete mucin (sometimes co-
of the lung are divided into ‘small cell’ and ‘non-small pious). The remaining half are single grey masses
cell’. This is useful clinically on deciding treatment. But up to 10 cm in diameter made up of cuboidal cells
histologically, lung carcinoma is divided into four cell with hyperchromatic nuclei.