4 h), being its expression in mesenchymal-like GBM also higher than in proneural-like GBM but this latter difference did not reach statistical significance (Fig. 4 h).
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SF3B1 inhibition disrupts malignancy and prolongs survival in glioblastoma patients through BCL2L1 splicing and mTOR/ß-catenin pathways imbalances.
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