| Literature DB >> 30017245 |
Florian Rambow1, Aljosja Rogiers1, Oskar Marin-Bejar1, Sara Aibar2, Julia Femel3, Michael Dewaele1, Panagiotis Karras1, Daniel Brown4, Young Hwan Chang5, Maria Debiec-Rychter6, Carmen Adriaens1, Enrico Radaelli7, Pascal Wolter8, Oliver Bechter8, Reinhard Dummer9, Mitchell Levesque9, Adriano Piris10, Dennie T Frederick10, Genevieve Boland10, Keith T Flaherty11, Joost van den Oord12, Thierry Voet4, Stein Aerts2, Amanda W Lund3, Jean-Christophe Marine13.
Abstract
Many patients with advanced cancers achieve dramatic responses to a panoply of therapeutics yet retain minimal residual disease (MRD), which ultimately results in relapse. To gain insights into the biology of MRD, we applied single-cell RNA sequencing to malignant cells isolated from BRAF mutant patient-derived xenograft melanoma cohorts exposed to concurrent RAF/MEK-inhibition. We identified distinct drug-tolerant transcriptional states, varying combinations of which co-occurred within MRDs from PDXs and biopsies of patients on treatment. One of these exhibited a neural crest stem cell (NCSC) transcriptional program largely driven by the nuclear receptor RXRG. An RXR antagonist mitigated accumulation of NCSCs in MRD and delayed the development of resistance. These data identify NCSCs as key drivers of resistance and illustrate the therapeutic potential of MRD-directed therapy. They also highlight how gene regulatory network architecture reprogramming may be therapeutically exploited to limit cellular heterogeneity, a key driver of disease progression and therapy resistance.Entities:
Keywords: RXR signaling; cutaneous melanoma; drug tolerance; gene regulatory networks; single cell transcriptomics; targeted therapy
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Year: 2018 PMID: 30017245 DOI: 10.1016/j.cell.2018.06.025
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582