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  • Characterization of the spectrum of trivalent VAV1-mutation-driven tumours using a gene-edited mouse model.

Characterization of the spectrum of trivalent VAV1-mutation-driven tumours using a gene-edited mouse model.

Molecular oncology (2022-07-28)
Javier Robles-Valero, Lucía Fernández-Nevado, Myriam Cuadrado, Luis Francisco Lorenzo-Martín, Isabel Fernández-Pisonero, Antonio Abad, Esther Redín, Luis Montuenga, Dionisio Martín-Zanca, Anna Bigas, Moisés Mallo, Mercedes Dosil, Xosé R Bustelo
ABSTRACT

Mutations in the VAV1 guanine nucleotide exchange factor 1 have been recently found in peripheral T cell lymphoma and nonsmall-cell lung cancer (NSCLC). To understand their pathogenic potential, we generated a gene-edited mouse model that expresses a VAV1 mutant protein that recapitulates the signalling alterations present in the VAV1 mutant subclass most frequently found in tumours. We could not detect any overt tumourigenic process in those mice. However, the concurrent elimination of the Trp53 tumour suppressor gene in them drives T cell lymphomagenesis. This process represents an exacerbation of the normal functions that wild-type VAV1 plays in follicular helper T cells. We also found that, in combination with the Kras oncogene, the VAV1 mutant version favours progression of NSCLC. These data indicate that VAV1 mutations play critical, although highly cell-type-specific, roles in tumourigenesis. They also indicate that such functions are contingent on the mutational landscape of the tumours involved.

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Bovine Serum Albumin, cold ethanol fraction, pH 5.2, ≥96%
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Anti-phospho-Histone H3 (Ser10) Antibody, Mitosis Marker, Upstate®, from rabbit
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Anti-Clara Cell Secretory Protein Antibody, serum, Upstate®
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