Cyclin D1 is part of the molecular system regulating the cell cycle G1 to S transition point. Its overexpression, a common finding in carcinomas of the breast, oesophagus, and head and neck, has also been demonstrated in a high percentage of non‐small cell lung carcinomas (NSCLCs). The role of cyclin D1 in NSCLC has been studied by correlating its immunoreactivity with the Ki67 labelling index in paraffin‐embedded, autoclaved surgical samples of 56 NSCLC cases. In addition, flow cytometric determination of ploidy and cell cycle status was carried out on 172 fresh tumour samples from the same cases. Twenty‐four (42·8 per cent) NSCLCs showed positive cyclin D1 immunostaining, a finding which showed no relationship to ploidy pattern, cell cycle phase, histological subtype, or lymph node metastasis, but was significantly associated with the Ki67 labelling index (P=0·03) and with poor cytoplasmic differentiation (P=0·01). Cyclin D1‐positive nuclei were abundant in poorly differentiated zones and absent in the best differentiated areas, particularly in heavily keratinized fields. These data indicate that in NSCLC, cyclin D1 overexpression is not only associated with a high cell proliferation rate, but also seems to play a role in the process of tumour differentiation.

Cluster of differentiation 44 (CD44) encompasses a polymorphic family of cell membrane glycoproteins involved in the mechanism of tumour invasion and metastasis. Since non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) display very different rates of progression, a significant discrepancy in their CD44 expression profiles is to be expected. An immunohistochemical study was undertaken on the expression of standard CD44 (CD44s) and the variant isoforms containing the domains encoded by variant exon 3 (CD44v3) or variant exon 6 (CD44v6) in paraffin-embedded bronchial biopsy specimens from 32 NSCLC cases and 11 SCLC cases. An absolute lack of immunoreactivity for CD44s, CD44v3, and CD44v6 was obtained in every case of SCLC, whereas 28 of the 32 NSCLC cases showed a positive immunoreaction for at least one of the three epitopes investigated. In conclusion, the occurrence of standard and variant CD44 isoforms in NSCLC and their absence in SCLC suggest the possibility that CD44 is in some way instrumental in conditioning the biological behaviour of NSCLC, but not of SCLC, whose metastatic cascade would be set in motion by the activation of hitherto unidentified, CD44-independent pathways.

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