Non-mammalian models of multiple endocrine neoplasia type 2

  1. Ross L Cagan
  1. Department of Cell, Developmental and Regenerative Biology, School of Biomedical Sciences, Icahn School of Medicine, New York, New York, USA
  1. Correspondence should be addressed to R L Cagan: ross.cagan{at}
  1. Figure 1

    (A, C and D) Targeting a fluorescent probe specifically to the thyroid (thyroglobulin-TdTomato) highlighted the zebrafish follicular cells. Thyroid structure was disrupted by co-targeting human BRAF(V600E). Reproduced, under the terms of the original CC BY licence, from Anelli et al. (2017). Panel B shows a sagittal section of adult thyroid follicles, which are associated with the ventral aorta and gills. Reproduced, with permission, from Bourque & Houvras (2011).

  2. Figure 2

    In contrast to control larval wing epithelia (panels A, C), activating SRC activity via CSK knockdown (B, D) led loss of apical junctions (P120-catenin, green), EMT and basal migration of transformed cells. Red: nuclear-localized RFP. E: schematic of panel D. Panel E reprinted from Developmental Cell, volume 10, Vidal M, Larson DE & Cagan RL, Csk-deficient boundary cells are eliminated from normal Drosophila epithelia by exclusion, migration, and apoptosis, pages 33–44, Copyright (2006), with permission from Elsevier.

  3. Figure 3

    (A) Oncogenic RET isoforms. ICD, intracellular domain. (B) In contrast to controls, cells expressing KIF5B-RET (green) expressed phosphorylated EGFR as they underwent EMT and migrated basally. Bottom panel shows a closeup of invadopodia-like processes expressing phosphorylated EGFR (red) and phosphorylated SRC (not shown). Panel B reproduced, under the terms of the original CC BYNCND licence, from Das & Cagan (2017).

  4. Figure 4

    (A) Vandetanib suppressed RET-mediated transformation of eye epithelia. Reproduced, with permission from the Genetics Society of America, from Read et al. (2005). (B) AD80 acts through altered networks. Reproduced, with permission, from Dar et al. (2012).

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