Altering the dosing schedules of cancer treatments might prevent the development of drug resistance, according to a report in Nature this week.

A study in a mouse model of human skin cancer shows that although continuous treatment leads to drug-resistant tumours, intermittent dosing can delay resistance.

Activating mutations in a gene called BRAF are common in melanomas, and BRAF inhibitors such as vemurafenib have shown very promising effects in patients with these tumours, although they generally go on to develop resistance.

To understand the causes and consequences of this resistance, Meghna Das Thakur and colleagues investigate the response of patient-derived melanomas, grafted in mice, to vemurafenib.

They find that in these mouse models, vemurafenib-resistant melanomas become drug-dependent, such that drug discontinuation leads to tumour regression.

Furthermore, they demonstrate that an intermittent dosing schedule can prevent the development of drug resistance. Although the clinical relevance of these findings remains to be shown, the authors suggest that modifying the dosing schedule of vemurafenib may improve its efficacy. 

Source: Nature