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Tissue architecture delineates field cancerization in BRAFV600E-induced tumor development

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F22%3A00082396" target="_blank" >RIV/00023001:_____/22:00082396 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11150/22:10442769

  • Result on the web

    <a href="https://journals.biologists.com/dmm/article/15/2/dmm048887/271800/Tissue-architecture-delineates-field-cancerization" target="_blank" >https://journals.biologists.com/dmm/article/15/2/dmm048887/271800/Tissue-architecture-delineates-field-cancerization</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1242/dmm.048887" target="_blank" >10.1242/dmm.048887</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Tissue architecture delineates field cancerization in BRAFV600E-induced tumor development

  • Original language description

    Cancer cells hijack developmental growth mechanisms but whether tissue morphogenesis and architecture modify tumorigenesis is unknown. Here, we characterized a new mouse model of sporadic thyroid carcinogenesis based on inducible expression of BRAF carrying a Val600 Glu (V600E) point mutation (BRAFV600E) from the thyroglobulin promoter (TgCreERT2). Spontaneous activation of this Braf-mutant allele due to leaky activity of the Cre recombinase revealed that intrinsic properties of thyroid follicles determined BRAF-mutant cell fate. Papillary thyroid carcinomas developed multicentrically within a normal microenvironment. Each tumor originated from a single follicle that provided a confined space for growth of a distinct tumor phenotype. Lineage tracing revealed oligoclonal tumor development in infancy and early selection of BRAFV600E kinase inhibitor-resistant clones. Somatic mutations were few, non-recurrent and limited to advanced tumors. Female mice developed larger tumors than males, reproducing the gender difference of human thyroid cancer. These data indicate that BRAFV600E-induced tumorigenesis is spatiotemporally regulated depending on the maturity and heterogeneity of follicles. Moreover, thyroid tissue organization seems to determine whether a BRAF- mutant lineage becomes a cancerized lineage. The TgCreERT2; BrafCA/+ sporadic thyroid cancer mouse model provides a new tool to evaluate drug therapy at different stages of tumor evolution.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30109 - Pathology

Result continuities

  • Project

  • Continuities

    N - Vyzkumna aktivita podporovana z neverejnych zdroju

Others

  • Publication year

    2022

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Disease Models and Mechanisms

  • ISSN

    1754-8403

  • e-ISSN

    1754-8411

  • Volume of the periodical

    15

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    16

  • Pages from-to

    "Art. no. dmm048887"

  • UT code for WoS article

    000767197800001

  • EID of the result in the Scopus database

    2-s2.0-85113846120