Cutaneous malignant melanoma - immunophenotypic considerations
One of the principal themes of the prolific research on the subject of CMM has been to establish parameters that can predict the clinical outcome. The most useful of these prognostic parameters have been derived from histopathological studies, but none has been consistently reliable. Therefore, other parameters may be presumed to influence the clinical course and a body of evidence acquired from laboratory experimental, pathological and clinical studies suggests that host immune effector mechanisms may be relevant in this regard. Immunohistochemistry provides a means by which histopathologists can attempt to elucidate features of the interaction between tumour cells and host immune effector cells. Such an approach was adopted for the studies presented in this thesis. The T-cell infiltrate associated with CMM, although more intense than that associated with either lentigo maligna or nevocellular nevi, was qualitatively similar with regard to its immunophenotypic characteristics. Natural killer (NK) cells were, however, identified only in association with some cases of CMM. Interleukin-2 (IL-2) was localised principally within melanoma cell nuclei, the uptake of IL-2 by melanoma cells presumably being mediated by the β-chain of the IL-2 receptor which was selectively expressed by tumour cells. Contrary to most previous studies, expression of ICAM-1 and LFA-3 by melanoma and nevus cells was ubiquitous. Expression of these molecules therefore seems unlikely to aid the differential diagnosis of melanocytic lesions and is of doubtful independent prognostic significance. The role that these molecules may have in facilitating host immune responses against tumour cells is unclear; expression of these molecules correlated with neither the intensity of the host inflammatory cell infiltrate nor the presence of regression.