Brain Pathology

Cover image for Vol. 27 Issue 3

Edited By: Seth Love

Impact Factor: 5.256

ISI Journal Citation Reports © Ranking: 2015: 6/79 (Pathology); 18/193 (Clinical Neurology); 33/256 (Neurosciences)

Online ISSN: 1750-3639

Mini-Symposium: Adamantinomatous Craniopharyngioma and Xanthomatous Lesions of the Sella

  • Models of human adamantinomatous craniopharyngioma tissue: Steps toward an effective adjuvant treatment

    Models of human adamantinomatous craniopharyngioma tissue: Steps toward an effective adjuvant treatment

    Subcellular characterization of ACP based on immunohistochemistry. Double immunohistochemistry (A) showing budding ACP tumor (line) into adjacent brain tissue (asterisk) with beta-catenin accumulating cell clusters (red) at the tip of the finger-shaped tumor protrusion. Detection of activated EGFR (EGFR-P, green) reveals co-localization within the beta- catenin accumulating cells (yellow) in the merged view, demonstrating co-activation of Wnt signaling and EGFR signaling pathway within the same cells at the invasion front. Solid ACP areas reveal a different marker expression (B). The beta-catenin accumulating cells are marked in red with the corresponding marker profile summarized in the red box. Cells surrounding the mostly whirl-shaped beta-catenin enriched cells (light blue) express enhanced levels of claudin-1, involved in tight junction formation and the epithelial cell adhesion molecule EpCAM.

  • Genetically engineered mouse models of craniopharyngioma: an opportunity for therapy development and understanding of tumor biology

    Genetically engineered mouse models of craniopharyngioma: an opportunity for therapy development and understanding of tumor biology

    Genetically engineered mouse models of ACP. A) Embryonic model. Over-activation of the WNT pathway in the developing pituitary results in large cystic/solid tumors. Clusters of cells accumulating nucleo-cytoplasmic beta-catenin (arrows) are present in both human ACP and murine (E18.5) pretumoral pituitaries. B) Inducible model. Tamoxifen-induced activation of the WNT pathway at 6 weeks of age results in the formation of beta-catenin accumulating clusters followed by tumor formation. However, lineage tracing with yellow fluorescent protein (YFP) shows that tumors are not derived from clusters and do not contain activated beta-catenin suggesting a non-cell autonomous mechanism of tumorigenesis. Clusters secrete numerous factors, e.g. SHH, BMPs, FGFs and inflammatory modulators potentially inducing tumorigenesis in a paracrine manner (Reprinted from Cell Stem Cell, 13, Andoniadou CL, Matsushima D, Mousavy Gharavy SN, Signore M, Mackintosh AI, Schaeffer M, Gaston-Massuet C, Mollard P, Jacques TS, Le Tissier P, et al., Sox2(C) stem/progenitor cells in the adult mouse pituitary support organ homeostasis and have tumor-inducing potential, pp 433–445, Copyright 2013, with permission from Elsevier).

  • Proteomics in pediatric cystic craniopharyngioma

    Proteomics in pediatric cystic craniopharyngioma

    Proteomic integrated platform.

  • Review of xanthomatous lesions of the sella

    Review of xanthomatous lesions of the sella

    Coronal magnetic resonance images (MRI), with gadolinium. a, b. This patient (#2) required two neurosurgical resections to control the growth of her sellar region mass; the appearance prior to each resection is shown. c. Patient #9 was one of two that was monitored over time with serial MRIs, which clearly show the growth of the lesion over time.

  • Models of human adamantinomatous craniopharyngioma tissue: Steps toward an effective adjuvant treatment
  • Genetically engineered mouse models of craniopharyngioma: an opportunity for therapy development and understanding of tumor biology
  • Proteomics in pediatric cystic craniopharyngioma
  • Review of xanthomatous lesions of the sella

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