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University of Otago research provides insights into an underlying mechanism that could explain why new cancer therapies to treat metastatic melanoma do not always work on patients, paving the way for predicting which patients will benefit from certain drugs.
Their findings shed much needed light on why new immune checkpoint inhibitor therapies such as nivolumab and pembrolizumab- approved by the New Zealand Government for the first time in 2016 to treat metastatic melanoma do not work on many patients. The new immunotherapeutic drugs herald a significant advancement in a cure for cancer.
But while they can be effective for some melanoma patients, for others the therapies do not work at all, and most eventually become resistant to immunotherapy treatments. One of the key components of the immune checkpoint mechanism is a protein on the surface of cancer cells called PD-L1 which can potentially be receptive to or block immunotherapy.
The researchers showed that an epigenetic modification-DNA modifications that do not directly alter the DNA sequence, but instead change the frequency by which a cell uses specific genes – specifically DNA methylation, influences whether PD-L1 is expressed on the cancer cell surface. Melanoma is a global problem, “biomarkers” are tools to select which patients benefit from which cancer therapies. Presently, there are no reliable biomarkers for predicting benefit from immune therapy in melanoma.
Epigenetic therapies could be used in clinical trials in combination with immunotherapy in melanoma to treat patients. DNA methylation is an epigenetic mechanism that plays a key role in switching genes “on” or “off” and helps to determine cellular function. Generally, DNA methylation silences gene expression and has been implicated in cancer.
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