Temozolomide demonstrates efficacy equal to that of DTIC and is an oral alternative for patients with advanced metastatic melanoma.

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Our data suggest that the angiogenic serum factors VEGF, bFGF, and IL-8 are useful predictive markers for overall and progression-free survival in melanoma patients.

Clusterin (CLU) has been implicated in various cell functions involved in carcinogenesis and tumour progression. There are two known CLU protein isoforms generated in human cells. A nuclear form of CLU protein (nCLU) is proapoptotic, and a secretory form (sCLU) is prosurvival. CLU expression has been associated with tumorigenesis of various malignancies, including tumours of prostate, colon, and breast. Furthermore, CLU expression is modulated by many factors that are believed to regulate tumour growth and/or apoptosis, including 1,25-dihydroxyvitamin D 3 , transforming growth factor beta-1, ultraviolet radiation, and IR. sCLU upregulation appears to be a general molecular stress response. Presently, preliminary results indicate that therapeutic modalities targeting CLU may be effective in cancer treatment. However, such strategies should make sure that nCLU is not eliminated or reduced. This review summarizes our present understanding of the importance of CLU in various physiological functions including tumour growth, and discusses its relevance to future cancer therapy.

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BACKGROUND The nonclassic human major histocompatibility complex class I antigens human leukocyte antigen (HLA)–G are proposed to protect tumor cells from natural killer cell lysis. In the current study, the authors measured soluble HLA‐G molecules (sHLA‐G) in serum from patients with malignant melanoma. METHODS Soluble HLA‐G was determined in serum samples of 190 melanoma patients with various stages of disease, with or without current therapy including interferon (IFN)–α and different cytostatics in comparison to 126 healthy controls by using a two‐step enzyme‐linked immunoadsorbent assay. RESULTS Serum sHLA‐G was significantly (P < 0.0005) elevated in melanoma patients (mean ± standard error of the mean [SEM] = 41.95 ± 2.15 ng/mL) compared with healthy controls (mean ± SEM = 22.92 ± 1.51 ng/mL). Univariate analysis revealed a correlation of sHLA‐G serum level with advanced stages of disease (P < 0.001) and tumor load (P < 0.05). Patients undergoing immunotherapy with IFN‐α (n = 31) showed an increased serum sHLA‐G (mean ± SEM = 62.05 ± 7.58 ng/mL; P < 0.0005), whereas other treatment regimens (n = 24) did not influence sHLA‐G serum concentrations. Multivariate analysis revealed treatment with IFN‐α as the only impact factor for elevated serum sHLA‐G, lacking any correlation with stage of disease or tumor burden. Furthermore, IFN‐α was found to upregulate HLA‐G cell surface expression on circulating monocytes. sHLA‐G serum level was not associated with recurrence free or overall survival. CONCLUSIONS This study shows increased sHLA‐G serum concentrations in melanoma patients and additional enhancement upon treatment with IFN‐α. The level of serum sHLA‐G, however, had no negative impact on patients' prognosis. Cancer 2001;92:369–76. © 2001 American Cancer Society.

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