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. 2019 Oct 28;217(1):e20181184. doi: 10.1084/jem.20181184

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© 2019 Haeger et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 1. — Collective invasion as primary invasion pattern in sarcoma and melanoma xenografts. (A) Schematic view defining tumor core and collective invasion zone (CI) of tumors growing in the deep dermis of the mouse monitored intravitally through an imaging window. (B) Collective invasion strands of human HT-1080 sarcoma (left; day 7; see also Video 1) and MV3 melanoma xenografts (right; day 8; see also Video 2). Tumor cells stably express nuclear H2B-EGFP and cytoplasmic DsRed2. Alexa Fluor 660–conjugated dextran contrastsperfused blood vessels. Second harmonic generation (SHG) visualizes muscle and collagen fibers. Arrowheads, alignment of invasion strands with perfused blood vessels. Scale bar, 100 µm. (C) Prevalence of invasion types, including individual cells, detached clusters, or collective strands connected to the core (day 5–7). Data represent the means and SD from five (HT-1080) and three (MV3) tumors. Per tumor, on average 150 (HT-1080) and 300 (MV3) cells were analyzed. (D) Distribution of ALCAM along cell–cell junctions (arrowheads) in invading tumor strands. Maximum-intensity projections (overview) and individual sections (insets) from confocal 3D stacks. Diffuse background fluorescence originates from fat (F) and myofibers (M). Scale bars, 100 µm (overview); 10 µm (insets).