Melanoma is often infiltrated by inflammatory and immune cells that might either maintain chronic inflammation therefore promoting tumor growth or mount an anti-tumor response to control tumor outcome. In this setting, Th1-orientated lymphocyte infiltration is associated with a better outcome in melanoma. Although the IFN-Induced Protein CXCL10 is expressed by Th-1 immune cells, its receptor was also shown to be involved in melanoma progression and metastasis.

To investigate the CXCL10 mediated anti-tumoral response in vivo, and its clinical relevance.

C57BL/6 mice bearing B16F1 melanoma were treated intraperitoneally with an adenovirus vector expressing CXCL10. Besides, PBMC from twenty patients, ten with melanoma in remission and ten with melanoma in progression, were assessed for their content in cytokine/chemokine using a 30-plex assay, and for their ability to modulate melanoma invasion in vitro in Transwell^® chambers coated with matrigel^®

Treatment with CXCL10 reduced melanoma tumor growth in C57BL/6 mice compared to control in vivo, and melanoma invasion in vitro. Screening of 30 cytokines/chemokines proteins expression showed that only CXCL10 was significantly increased in patients in remission compared to patients in progression. Only PBMC from patients in remission significantly reduced melanoma cell invasiveness in an ex vivo Transwell^® assay. Accordingly, this inhibitory effect was also observed with PBMC culture media from patients with melanoma in remission.

The quantitative increase in CXCL10 production, together with its ability to limit melanoma progression, shows the potential benefit of this chemokine to control melanoma progression or metastasis.

Copyright © 2010 British Association of Dermatologists.

PMID: 21155750 [PubMed - as supplied by publisher] Source: National Library of Medicine.