AI Article Synopsis
- * Researchers found that knocking out BTG1 increases the severity of the disease, especially when paired with Bcl2 overexpression.
- * Additionally, they identified a partnership between BTG1 and the protein BCAR1, leading to enhanced cell migration when BTG1 is mutated or deleted, which can potentially be treated with SRC inhibitors like dasatinib.
Article Abstract
Understanding the functional role of mutated genes in cancer is required to translate the findings of cancer genomics into therapeutic improvement. BTG1 is recurrently mutated in the MCD/C5 subtype of diffuse large B-cell lymphoma (DLBCL), which is associated with extranodal dissemination. Here, we provide evidence that Btg1 knock out accelerates the development of a lethal lymphoproliferative disease driven by Bcl2 overexpression. Furthermore, we show that the scaffolding protein BCAR1 is a BTG1 partner. Moreover, after BTG1 deletion or expression of BTG1 mutations observed in patients with DLBCL, the overactivation of the BCAR1-RAC1 pathway confers increased migration ability in vitro and in vivo. These modifications are targetable with the SRC inhibitor dasatinib, which opens novel therapeutic opportunities in BTG1 mutated DLBCL.
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| http://dx.doi.org/10.1182/blood.2022016943 | DOI Listing |
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