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Patients with advanced (defined as unresectable or metastatic) v-Raf mouse sarcoma virus oncogene homolog B V600 (BRAFV600) mutated melanoma patients who were previously treated with v-Raf mouse sarcoma virus oncogene homolog B (BRAFV600) )/mitogen-activated protein kinase (MEK) inhibitors and programmed cell death 1 (PD-1) and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) immunotherapy have progressed after immunothera.
In a prospective phase 2 clinical trial of 25 patients who discontinued BRAF-/MEK inhibitor therapy at least 12 weeks prior to enrollment, the objective response rate (ORR) was 32% and the disease control rate (DCR) was 7
Hydroxychloroquine prevents autophagy-driven resistance and improves the efficacy of BRAF-/MEK-inhibitors in preclinical melanoma mode.
Following the safety run-in phase, in the Phase 2 portion of the trial, patients were randomly assigned between prior treatment with dabrafenib, trametinib, and hydroxychloroquine (experimental arm) or dabrafenib and trametinib, with the potential to add hydroxychloroquine upon documented tumor progression Chloroquine (concurrent control grou.
CONSORT plot (AE, adverse event; DAB, dabrafenib; HCQ, hydroxychloroquine; pt(s), patient; PD, progressive disease; TRA, trametinib):
Best objective response in the intent-to-treat population:
Best objective response in the intent-to-treat population:In conclusion, ongoing studies are investigating this drug combination in less pretreated populatio.
Selection of patients to receive hydroxychloroquine can be based on the expression of autophagy markers (eg, microtubule-associated protein 1 light chain 3β) on tumor samples at baseline or on treatment, while patients without this signature can receive other treatments
References: Awada G, Schwarze JK, Tijtgat J, Fasolino G, Kruse V, Neyns.
References: Awada G, Schwarze JK, Tijtgat J, Fasolino G, Kruse V, Neyns.
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