J. Arribas

The efficacy of chemotherapy is limited by intratumoural senescent cells that persist through the upregulation of PD-L2

This study identifies PD-L2 as a marker of therapy-induced senescent cells that suppress chemotherapy efficacy, showing PD-L2 blockade enhances tumour remission in mice.

Gasdermin B over-expression arbitrates HER2-targeted therapy resistance by inducing protective autophagy

This study identifies GSDMB over-expression as a driver of HER2-targeted therapy resistance through autophagy induction and shows that combining lapatinib with chloroquine enhances therapeutic efficacy in GSDMB-positive tumors.

The BRD4S-LOXL2-MED1 interaction at the forefront of cell cycle transcriptional control in triple-negative breast cancer

This study shows that inhibiting LOXL2 and BRD4 together reduces triple-negative breast cancer proliferation by disrupting the BRD4S-LOXL2-MED1 interaction that controls cell cycle gene expression.

Humanized CAR T cells targeting p95HER2

This study develops CAR T cells targeting p95HER2, a tumor-specific antigen, showing efficacy against HER2-amplified tumors and metastases with reduced off-tumor effects.

Personalized Cancer Therapy Prioritization Based on Driver Alteration Co-occurrence Patterns

The paper identifies actionable genomic vulnerabilities in cancer by analyzing driver alteration co-occurrence patterns and validates predictions in mice, improving drug response modeling from patient data.

Maintaining oxidized H3 in heterochromatin is required for the oncogenic capacity of triple-negative breast cancer cells

This study identifies the role of H3K4ox in maintaining heterochromatin structure in TNBC cells and shows its necessity for oncogenic properties.

Reduction of LOXL2-mediated H3K4 oxidation increases chromatin accessibility and promotes chemosensitivity of triple-negative breast cancer cells

This study shows that reducing LOXL2-mediated H3K4 oxidation decreases chromatin compaction and increases chemosensitivity in triple-negative breast cancer cells.