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- W4387425965 abstract "Abstract We previously found that T-cell acute lymphoblastic leukemia (T-ALL) requires support from tumor-associated myeloid cells, which activate Insulin Like Growth Factor 1 Receptor (IGF1R) signaling in leukemic blasts. However, IGF1 is not sufficient to sustain T-ALL in vitro, implicating additional myeloid-mediated signals in leukemia progression. Here, we find that T-ALL cells require close contact with myeloid cells to survive. Transcriptional profiling and in vitro assays demonstrate that integrin-mediated cell adhesion activates downstream focal adhesion kinase (FAK)/ proline-rich tyrosine kinase 2 (PYK2), which are required for myeloid-mediated T-ALL support, partly through activation of IGF1R. Blocking integrin ligands or inhibiting FAK/PYK2 signaling diminishes leukemia burden in multiple organs and confers a survival advantage in a mouse model of T-ALL. Inhibiting integrin-mediated adhesion or FAK/PYK2 also reduces survival of primary patient T-ALL cells co-cultured with myeloid cells. Furthermore, elevated integrin pathway gene signatures correlate with higher FAK signaling and myeloid gene signatures and are associated with an inferior prognosis in pediatric T-ALL patients. Together, these findings demonstrate that integrin activation and downstream FAK/PYK2 signaling are important mechanisms underlying myeloid-mediated support of T-ALL progression." @default.
- W4387425965 created "2023-10-08" @default.
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- W4387425965 date "2023-10-07" @default.
- W4387425965 modified "2023-10-11" @default.
- W4387425965 title "Integrin signaling is critical for myeloid-mediated support of T-cell acute lymphoblastic leukemia" @default.
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- W4387425965 doi "https://doi.org/10.1038/s41467-023-41925-z" @default.
- W4387425965 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37805579" @default.
- W4387425965 hasPublicationYear "2023" @default.
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