Abstract
The value of neuron specific enolase (NSE) immunoreactivity as a marker for small cell lung cancer (SLC) has been assessed using a monoclonal antibody (MCAB) against NSE, MCAB specificity was confirmed using purified enolase isoenzymes, sections of human brain, a panel of lung tumours, neuroendocrine and non-neuroendocrine tumours and normal tissues. Using this MCAB in radioimmunoassay and immunohistochemistry, NSE immunoreactivity was detected in all SCLC material examined. However, considerable reactivity was also observed in a number of non-small cell lung cancer cell lines and tumour biopsy specimens. Furthermore, intratumoral heterogeneity with respect to NSE immunostaining was observed in several cases. Factors which may underlie such intratumoral phenotypic diversity were assessed using flow cytometry together with MCABs directed against both NSE and non-neuronal enolase. Such studies revealed that enolase expression in cells which were no longer actively proliferating differed markedly from that of cells in exponential growth. Furthermore, cells grown under conditions of increasing hypoxia exhibited increased enolase expression relative to those grown under oxygenated conditions. It is concluded from these studies that NSE immunoreactivity per se is an unreliable marker for the SCLC phenotype.
Highlights
All small cell lung cancer (SCLC) cultures designated COR-L were derived from patients clinically diagnosed as having SCLC; non-small cell lung cancer (NSCLC) COR-L23 was derived from a patient having large cell carcinoma of the lung
The finding that SCLC stained positively for neuron specific enolase (NSE), a marker of neuroendocrine cells (Schmechel et al, 1978b; Facer et al, 1980; Gu et al, 1981), has prompted several workers to propose this isoenzyme as a potential marker of the SCLC phenotype (Springall et al, 1984; Sheppard et al, 1984)
N2 exposure (h) observations support the view that SCLC and NSCLC may be related through a differentiation continuum, which probably reflects the differentiation pathway of the bronchial epithelium (Goodwin et al, 1983)
Summary
Purified human NSE and non-neuronal enolase (NNE) was generously donated by Dr R. Lung tumour cultures used in this study include several recently derived in this laboratory from clinical material. The phenotypic characteristics of these cells are fully described elsewhere (BaillieJohnson et al, 1985). All SCLC cultures designated COR-L were derived from patients clinically diagnosed as having SCLC; NSCLC COR-L23 was derived from a patient having large cell carcinoma of the lung. Established SCLC lines FRE, MAR, POC and NSCLC lines MOR and BEN were kindly donated by Dr M. Carney (NCI, Bethesda, USA) and was derived from a SCLC patient
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