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Brady, Samuel W; McQuerry, Jasmine A; Qiao, Yi; Piccolo, Stephen R; Shrestha, Gajendra; Jenkins, David F; Layer, Ryan M; Pedersen, Brent S; Miller, Ryan H; Esch, Amanda; Selitsky, Sara R; Parker, Joel S; Anderson, Layla A; Dalley, Brian K; Factor, Rachel E; Reddy, Chakravarthy B; Boltax, Jonathan P; Li, Dean Y; Moos, Philip J; Gray, Joe W; Heiser, Laura M; Buys, Saundra S; Cohen, Adam L; Johnson, W Evan; Quinlan, Aaron R; Marth, Gabor; Werner, Theresa L; Bild, Andrea H
Nature communications, 11/2017, Letnik: 8, Številka: 1Journal Article
Metastatic breast cancer remains challenging to treat, and most patients ultimately progress on therapy. This acquired drug resistance is largely due to drug-refractory sub-populations (subclones) within heterogeneous tumors. Here, we track the genetic and phenotypic subclonal evolution of four breast cancers through years of treatment to better understand how breast cancers become drug-resistant. Recurrently appearing post-chemotherapy mutations are rare. However, bulk and single-cell RNA sequencing reveal acquisition of malignant phenotypes after treatment, including enhanced mesenchymal and growth factor signaling, which may promote drug resistance, and decreased antigen presentation and TNF-α signaling, which may enable immune system avoidance. Some of these phenotypes pre-exist in pre-treatment subclones that become dominant after chemotherapy, indicating selection for resistance phenotypes. Post-chemotherapy cancer cells are effectively treated with drugs targeting acquired phenotypes. These findings highlight cancer's ability to evolve phenotypically and suggest a phenotype-targeted treatment strategy that adapts to cancer as it evolves.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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