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PH-RS09

Benign bronchial tumours and pre-invasive lesions

How the bronchial and alveolar linings pass through recognisable pre-invasive stages on the way to lung cancer, and how benign tumours such as hamartomas and papillomas grow, block airways or turn up as a nodule on a scan.

By the end, you can

  • Relate the cells of the bronchial and alveolar lining to the squamous, glandular and neuroendocrine lesions they give rise to.
  • Describe the sequence from squamous metaplasia through dysplasia to carcinoma in situ in the central bronchi.
  • Distinguish atypical adenomatous hyperplasia, adenocarcinoma in situ and minimally invasive adenocarcinoma.
  • Describe the structure of a pulmonary hamartoma and of bronchial papillomas.
  • Explain why a central lesion causes obstruction and bleeding while a peripheral one is usually found by chance.
  • Recognise the classic microscopic features, nodule imaging and tests of precursor lesions, hamartomas and carcinoid tumours, and explain how stopping smoking, resection, bronchoscopic treatment and somatostatin analogues act on them.

What it is

Pre-invasive (precursor) lesions of the lung are proliferations of atypical epithelial cells that have not yet invaded the underlying tissue: squamous dysplasia and carcinoma in situ in the central bronchi, atypical adenomatous hyperplasia and adenocarcinoma in situ in the periphery, and diffuse neuroendocrine cell hyperplasia. Benign tumours of the lung, such as the pulmonary hamartoma and bronchial papillomas, grow by expansion and do not invade or metastasise. Both are far less common than lung cancer.

4 types to tell apart
Squamous precursor lesions
Squamous dysplasia (mild, moderate, severe) and carcinoma in situ, arising in metaplastic squamous epithelium of the larger bronchi; precursors of squamous cell carcinoma.
Glandular precursor lesions
Atypical adenomatous hyperplasia and adenocarcinoma in situ, growing along alveolar walls in the periphery; precursors of adenocarcinoma.
Neuroendocrine precursor lesion
Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH), from which tumourlets and carcinoid tumours can arise.
Benign tumours
Pulmonary hamartoma (the commonest), bronchial papillomas, adenomas such as sclerosing pneumocytoma, and benign salivary-gland-type tumours.

US spelling: tumours → tumors.

Normal function

The cells that line the airways

The bronchi are lined by . sweep a layer of mucus, made by , up towards the larynx, and small on the are the stem cells that replace them. Scattered among them are neuroendocrine cells, single or in small clusters, which sense oxygen and release peptides and amines such as serotonin.

Further out the lining thins. Bronchioles are lined by ciliated cells and dome-shaped club cells, and the alveoli by flat type I and cuboidal type II pneumocytes; type II cells make surfactant and replace the alveolar lining after injury. Submucosal glands, cartilage and smooth muscle support the larger airways.

In the usual explanation, each cell type gives rise to its own group of lesions: basal cells to squamous lesions in the central bronchi, club cells and type II pneumocytes to glandular lesions in the periphery, neuroendocrine cells to neuroendocrine lesions, and the supporting mesenchyme to tumours such as the hamartoma.

Point to it on the model