a) E0771 Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed by SHG, To-pro-3 staining for all nuclei, and collagen fibre individualization. Scale bar: 50 µm. ( b, c) M-Wnt (WT n = 8 tumours, KO n = 4 tumours) and AT-3 (n = 5 tumours/group) Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed for infiltrating CD3 + T cells normalized by total cells via IHC. ( d–g) M-Wnt and AT-3 Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed for collagen fibre alignment (d, e) and fibre length (f, g), n = 4 tumours/group. ( h–j) E0771, n = 5 tumours/group (h), M-Wnt, n = 4 tumours/group (i) and AT-3, n = 4/group (j) Ddr1-WT/KO tumours transplanted from Rag1 −/− to C57BL/6 hosts were analysed for fibre numbers by the CT-Fire software. ( k–m) E0771 Ddr1-WT/KO tumours (WT n = 10 tumours, KO n = 8 tumours) from immunodeficient Rag1 −/− hosts were analysed for collagen fibre alignment (k), fibre length (l) and fibre numbers (m) by the CT-Fire software. ( n) Growth curves of E0771 Ddr1-KO tumours in immunocompetent hosts that were intratumorally injected with recombinant WT and mutant Fc-ECD (WT: n = 10 tumours, W54A: n = 9 tumours). ( o) Representative images of E0771 Ddr1-KO tumours treated with recombinant WT or mutant Fc-ECD in C57BL/6 hosts as analysed by SHG, To-pro-3 staining, and collagen fibre individualization. Scale bar: 50 µm. ( p) Quantification of collagen fibre alignment in WT and mutant Fc-ECD treated tumours (n = 5 tumours/group). ( q) Enumeration of infiltrating CD3 + T cells normalized by total cells via IHC (WT: n = 4 tumours, KO: n = 3 tumours). Values represent mean ± SEM. p value as indicated, two-tailed Student’s t-test for all tests except for tumour volumes, which were done by two-way ANOVA. Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, DC, USA

Masana M, Su YA, Liebl C, Wang XD, Jansen L, Westerholz S et al. The stress-inducible actin-interacting protein DRR1 shapes social behavior. Psychoneuroendocrinology 2014; 48: 98–110.Department of Anatomy and Cell Biology, School of Medicine and Health Sciences, The George Washington University, Washington, DC, USA

Department of Pathology, School of Medicine and Health Sciences, The George Washington University, Washington, DC, USAKishida S, Mu P, Miyakawa S, Fujiwara M, Abe T, Sakamoto K et al. Midkine promotes neuroblastoma through Notch2 signaling. Cancer Res 2013; 73: 1318–1327.

Meng, W. et al. Efficient generation of monoclonal antibodies from single rhesus macaque antibody secreting cells. MAbs 7, 707–718 (2015). Deng ZH, Gomez TS, Osborne DG, Phillips-Krawczak CA, Zhang JS, Billadeau DD . Nuclear FAM21 participates in NF-kappa B-dependent gene regulation in pancreatic cancer cells. J Cell Sci 2015; 128: 373–384.Takai, K. et al. Discoidin domain receptor 1 (DDR1) ablation promotes tissue fibrosis and hypoxia to induce aggressive basal-like breast cancers. Genes Dev. 32, 244–257 (2018). For Scotland, 2011 data is shown (update coming soon, the Scottish census was delayed by a year unlike the rest of the UK).

Le PU, Angers-Loustau A, de Oliveira RM, Ajlan A, Brassard CL, Dudley A et al. DRR drives brain cancer invasion by regulating cytoskeletal-focal adhesion dynamics. Oncogene 2010; 29: 4636–4647. Mertins, P. et al. Proteogenomics connects somatic mutations to signalling in breast cancer. Nature 534, 55–62 (2016). Baarlink C, Wang H, Grosse R . Nuclear actin network assembly by formins regulates the SRF coactivator MAL. Science 2013; 340: 864–867.

Careers

Kaur, A. et al. Remodeling of the collagen matrix in aging skin promotes melanoma metastasis and affects immune cell motility. Cancer Discov. 9, 64–81 (2019). Leitinger, B. Discoidin domain receptor functions in physiological and pathological conditions. Int. Rev. Cell Mol. Biol. 310, 39–87 (2014). Takahashi Y, Sipp D, Enomoto H . Tissue interactions in neural crest cell development and disease. Science 2013; 341: 860–863.