Researchers at Mount Sinai have discovered a previously unknown cause of drug resistance in general subtype of melanoma, one of the most deadly forms of cancer, and, in turn, have discovered a new therapy that could prevent or abolish drug resistance to melanoma patients with a specific gene mutation, according to a study published in Nature Communications in August.
Researchers have identified a novel epigenetic mechanism that causes resistance to standard therapy in melanoma patients with the BRAF mutation in the genes, which are found in about half of all melanomas. The researchers also found a biomarker or biological signature that accompanies this drug resistance: the gene IGFBP2, which is also associated with poor prognosis in patients with melanoma.
Patients with high levels of IGFBP2 could benefit from the combination therapy, which can be created in response to these findings, which inhibit the mutation of BRAF and biological pathways based on IGFBP2, as a multi-purpose approach to the prevention of resistance to drugs or reversing it after its occurrence, research shows. Other studies have shown that it is possible to find IGFBP2 through urine samples, so the impact on the detection and subsequent treatment are great.
"The incidence of cutaneous malignant melanoma is increasing, and its therapeutic management is complex," - said the lead researcher Emily Bernstein, PhD, associate professor of oncological sciences and dermatology at the Icahn School of Medicine at Mount Sinai. "In recent years, there is an extensive therapeutic development for inhibiting key biological targets. Although the majority of patients with advanced metastatic melanoma bearing a BRAF mutation respond to standard therapy, known as MAPK inhibitors, subsequent resistance remains a major clinical problem. "