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. Author manuscript; available in PMC: 2018 Jun 5.
Published in final edited form as: Nature. 2016 Oct 31;539(7629):390–395. doi: 10.1038/nature20132

Figure 1. LKB1 inactivation synergizes with KRASG12D to potentiate glycolysis, serine metabolism, and tumourigenesis.

Figure 1

a. Representative pancreas histology of the indicated genotypes of mice at 20–25-weeks (n=4/genotype). b, Subcutaneous tumour growth of KL cells expressing empty vector (KL) or LKB1 (rescue) (n=8/group). c, d, Ductal cells tested for glucose uptake (c) (n=6, independent replicates), and (d) lactate secretion (n=3). e, Oxygen consumption rates in K and KL cells under nutrient replete conditions (n=21). f, Fates of glycolytic intermediates. g, GSEA showing enrichment of serine/glycine/one-carbon network18 (K cells, n=3; KL cells, n=4). NES=Normalized Enrichment Score. h, i, Isotopomer abundance of U13C-glucose-derived M+3 pyruvate (h) or serine (i) (n=3, biological replicates). Data pooled from three (e) or representative of two (d) experiments. Error bars: s.e.m. (b), s.d. (c,d,g,h). *P<0.05, **P<0.01, ***P<0.001.