New avenues to suppress adaptation of cancer cells to efficacy of drugs in standard and prospective therapies are critically needed to improve treatment outcomes. While many current anti-cancer drugs are initially efficacious, most eventually lead to resistance and patient relapse. Drug treatment induces cell stress response, which may allow some of the tumour cells to survive. These may adapt into drug-resistant malignancy during chemotherapy by rounds of clonal selection of existing or acquired transcriptional, epigenetic and genetic alterations. We wish to identify malignant-specific rapid responses to drug stress and find new compounds that would block such responses and reduce the adaptation rate.