These are often central, in main or segmental bronchi, or peripheral. They may show an endobronchial growth pattern or infiltrate between the cartilaginous rings initially, in time destroying them to invade surrounding tissue. The tumour is solid, grey/white but may show cavitation (Figure 19; see colour plate section). Such cavity formation may cause clinical misdiagnosis as apical cavitating tuberculosis. Very rarely both diseases may co-exist. There is often related bronchiectasis and obstructive pneumonitis, due to bronchial obstruction. The pneumonitis causes both radiological and macroscopic problems in definition of the true extent of the tumour. This problem may be accentuated if there is a prominent inflammatory component to the tumour.
Adjacent to the tumour there may be carcinoma in situ as well as chronic bronchitic changes. In addition, there is squamous metaplasia and reserve cell hyperplasia. The tumour shows varying degrees of squamous differentiation, lying in a fibrous stroma with a varying amount of acute and chronic inflammation. Foci of recent and old haemorrhage are seen. Well-differentiated tumours show keratin pearls and keratinization (Figure 20; see colour plate section). Intercellular bridges should be sought and paradoxically can be best identified with a mucin stain. Rarely mucin can be seen in the malignant cells but more than 10% of the tumour should show a distinctive glandular component before an adenosquamous carcinoma is diagnosed. Tumour giant cells imply a poor prognosis. Clear cell change, due to glycogen accumulation, is also a feature of some tumours but has no prognostic connotation. The nuclei are hyperchromatic and may show prominent nucleoli. The tumour may encircle the bronchus and a fibre-optic biopsy may only reveal fibrosis.
Squamous cell carcinomas manifest earlier than other types of pulmonary malignancy because of obstructive symptoms. They may involve lymph nodes by direct spread. There may be lymphatic and vascular invasion, but the prognostic significance of vascular invasion in non-small-cell carcinoma is uncertain. Some studies suggest that vascular invasion indicates a poor prognosis, others show it has no effect on survival, since the tumour-associated desmoplasia causes occlusive intimal fibrosis in thin walled pulmonary arteries and veins.
A small subgroup of squamous carcinomas is termed basaloid carcinoma. This tumour grows exophytically in proximal bronchi. Mediastinal pleura or adipose tissue are often invaded. There is a solid lobular or anastamotic trabecular pattern with small, moderately pleomorphic, cuboidal or fusiform cells. There is peripheral pallisading and a high mitotic rate. Other subtypes of squamous carcinomas are clear cell, not to be confused with adeno-carcinoma, papillary, pleomorphic and spindle cell and small cell variant of squamous.
Conditions to be considered in the differential diagnosis are florid squamous metaplasia in the bronchus or states associated with an inflammatory process, dysplasia, which if high grade can be very difficult to distinguish on a small biopsy, any benign lung tumour with squamous metaplasia on the surface, especially granular cell myoblastoma, benign squamous cell papilloma, tumours with a squamous component, such as carcinosarcoma, spindle cell sarcomas, metastatic tumours with a squamous appearance, including sarcomas, which can be primary or secondary, and meso-thelioma. Special stains, including mucins and cyto-keratins, are often helpful in determining the cell of origin and in some cases the site.
It may be difficult with poorly differentiated tumours to differentiate squamous from adenocarcinoma. In such cases if mucin stains are diffusely negative the term 'non-small cell carcinoma' is used. This enables medical oncologists to give appropriate treatment, as they need to distinguish this tumour from small-cell lung carcinoma.
Treatment depends on the stage of the disease. Cases with stage IIIA disease or less are treated by surgery though the role of surgery has yet to be established in N2 and N3 disease. Other options for more advanced disease are radiotherapy, either direct beam or intraluminal, brachytherapy and chemotherapy.
Prognosis depends on the stage. Five-year survival rates are stage I, 50%, stage II, 30% and stage IIIA, approximately 10% (Mountain, 1988).
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