What is it about?
We integrated hundreds of exomes and whole-genomes from B-cell lymphoma and Chronic Lymphocitic Leukemia (CLL) patients into a single analysis. Using new bioinformatic tools, we were able to construct the landscape of mutational drivers in B-cell tumors, pointing towards dozens of recurrently mutated genes and derregulated pathways. This information provides a better understanding of lymphoma biology, and can be used to develop new targeted therapies aiming to disrupt the aberrant activation of some pathways in lymphomagenesis.
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Why is it important?
I believe this is an important analysis because it is the first of its class exclusively dedicated to B-cell tumors. These tumors are very heterogeneous in their clinical presentation, but all arise from B-cells in different stages of maturation. The results translated into the discovery of new potential drug targets (e.g., DTX-1), aberrantions involving immune check-point regulators (CD83), and the skewed distribution of muations in tyrosine kinase genes (e.g., SGK-1) in aggresive lymphomas compared with low-grade tumors. Finally, we could also detect recurrent mutations in interleukin genes and their receptors, which probably indicate a functional role in autocrine singalling during lymphoma development and progression.
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This page is a summary of: Detection of new drivers of frequent B-cell lymphoid neoplasms using an integrated analysis of whole genomes, PLoS ONE, May 2021, PLOS, DOI: 10.1371/journal.pone.0248886.
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