Calming Down Immune Cells Could Hold Key to Melanoma Treatment

The gist: New research has shed light on why some patients’ melanoma tumors resist standard treatment. The scientists found that certain immune system cells produce chemical signals that may protect melanoma cells, and keep them from being destroyed. To get around this, the researchers say, drugs that affect the immune system (immunotherapy) could be combined with standard melanoma treatment. Indeed, such a combination is already being tested in a clinical trial—a research study with volunteer patients.

“Immune cells may be responsible for drug resistance in melanoma patients, according to research published in Cancer Discovery.”Cancer Research UK scientists at The University of Manchester found that chemical signals produced by a type of immune cell, called macrophages, also act as a survival signal for .

“When the researchers blocked the macrophages’ ability to make this signal – called TNF alpha – melanoma tumours were much smaller and easier to treat.

“When melanoma patients are given chemotherapy or radiotherapy it causes inflammation, increasing the number of macrophages in the body – and raising the levels of TNF alpha. This research suggests that targeting this chemical ‘survival signal’ could lead to new ways to treat the disease.”


Evidence of Epidermal Growth Factor Receptor Expression in Uveal Melanoma: Inhibition of Epidermal Growth Factor-Mediated Signalling by Gefitinib and Cetuximab Triggered Antibody-Dependent Cellular…

“Despite advances in surgery and radiotherapy of uveal melanoma (UM), many patients develop distant metastases that poorly respond to therapy. Improved therapies for the metastatic disease are therefore urgently needed. Expression of the epidermal growth factor receptor (EGFR), a target of kinase inhibitors and humanised antibodies in use for several cancers, had been reported. Forty-eight human UMs were analysed by expression profiling. Signalling was tested in three EGFR expressing UM cell lines by Western blotting using phosphorylation specific antibodies for EGFR and the downstream mediators AKT (v-akt murine thymoma viral oncogene homolog) and extracellular signal-regulated kinase (ERK). Evidence for signalling in tumours was obtained through the application of a UM-specific EGF-signature. The EGFR specific kinase inhibitor, Gefitinib and the humanised monoclonal antibody, Cetuximab, were tested for their effect on EGFR signalling. Natural killer cell mediated antibody-dependent cellular cytotoxicity (ADCC) and tumour necrosis factor α (TNF-α) release was analysed for Cetuximab.”