Tirso Pons

Diacylglycerol kinase zeta dictates CD40-mediated immune synapse formation, mTORC1 signaling and plasma cell fate in B lymphocytes

This study shows DGKζ is essential for CD40-mediated immune synapse formation, mTORC1 signaling, and plasma cell differentiation in B cells.

A genome-wide analysis identifies DIDO3 binding at active chromatin and topological boundaries in mouse stem cells

This study identifies DIDO3 binding at active chromatin and topological boundaries in mouse stem cells, linking it to chromatin organization and transcriptional regulation.

A computational and structural analysis of germline and somatic variants affecting the DDR mechanism, and their impact on human diseases and prostate cancer progression

The paper analyzes germline and somatic variants in DDR genes, showing somatic variants cluster in functional regions and differ from germline variants in prostate cancer patients.

The chromatin reader Dido3 is a regulator of the gene network that controls B cell differentiation

This study shows that DIDO3 deficiency disrupts B cell differentiation by altering transcription factor expression and somatic recombination.

Unique genomic features and deeply-conserved functions of long non-coding RNAs in the Cancer LncRNA Census (CLC)

The paper introduces the Cancer LncRNA Census (CLC), a curated resource of lncRNAs with causative roles in cancer, and shows their genomic and evolutionary features.

Integrative pathway enrichment analysis of multivariate omics data

ActivePathways integrates multivariate omics data to identify enriched pathways, revealing cancer driver genes and prognostic pathways in breast cancer.

Whole-exome sequencing of plasma cell-free DNA portrays the somatic mutation landscape of refractory metastatic colorectal cancer and enables the discovery of mutated KDR/VEGFR2 receptors as modulators of anti-angiogenic therapies.

This study uses whole-exome sequencing of plasma cell-free DNA to analyze somatic mutations in metastatic colorectal cancer and identifies KDR/VEGFR2 mutations affecting anti-angiogenic therapy response.