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Resistant cancer cells can become dependent on the drug they resisted, as shown for BRAF-inhibitor-resistant melanoma in mice. Stopping the drug for a defined washout and then rechallenging, while tracking the resistance allele in blood tumour DNA, could make the tumour vulnerable to it once more.
Drug addiction has been demonstrated for BRAF-inhibitor-resistant melanoma in mice and reported anecdotally in patients rechallenged after a break. Intermittent dosing prevented resistance in those models. A prospective trial would formalise rechallenge: after progression and a defined washout with an intervening therapy, patients are rechallenged with the original agent and monitored with ctDNA for the resistance allele's decline during the holiday.
Shares Tumour heterogeneity and clonal evolution, Drug resistance (primary and acquired), Osimertinib, Acquired resistance to every therapy.
Shares Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy, Melanoma, Non-small-cell lung cancer.
Shares Tumour heterogeneity and clonal evolution, Osimertinib, Acquired resistance to every therapy, Liquid biopsy (ctDNA).
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy, Liquid biopsy (ctDNA).
Shares Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy, Liquid biopsy (ctDNA), Non-small-cell lung cancer.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy, Melanoma.
Shares Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy, Melanoma, Non-small-cell lung cancer.
Shares Tumour heterogeneity and clonal evolution, Drug resistance (primary and acquired), Acquired resistance to every therapy.