TY  - JOUR
AU  - Romero, Octavio A
AU  - Vilarrubi, Andrea
AU  - Alburquerque-Bejar, Juan J
AU  - Gomez, Antonio
AU  - Andrades, Alvaro
AU  - Trastulli, Deborah
AU  - Pros, Eva
AU  - Setien, Fernando
AU  - Verdura, Sara
AU  - Farré, Lourdes
AU  - Martín-Tejera, Juan F
AU  - Llabata, Paula
AU  - Oaknin, Ana
AU  - Saigi, Maria
AU  - Piulats, Josep M
AU  - Matias-Guiu, Xavier
AU  - Medina, Pedro P
AU  - Vidal, August
AU  - Villanueva, Alberto
AU  - Sanchez-Cespedes, Montse
PY  - 2021
DO  - 10.1038/s41467-021-24618-3
UR  - http://hdl.handle.net/10668/18200
T2  - Nature communications
AB  - Despite the genetic inactivation of SMARCA4, a core component of the SWI/SNF-complex commonly found in cancer, there are no therapies that effectively target SMARCA4-deficient tumours. Here, we show that, unlike the cells with activated MYC oncogene,...
LA  - en
KW  - Animals
KW  - Antineoplastic Agents
KW  - Benzazepines
KW  - Cell Line, Tumor
KW  - Cell Survival
KW  - DNA Helicases
KW  - Drug Resistance, Neoplasm
KW  - Gene Expression
KW  - Histone Deacetylase Inhibitors
KW  - Histone Demethylases
KW  - Histones
KW  - Humans
KW  - Jumonji Domain-Containing Histone Demethylases
KW  - Mice
KW  - Neoplasms
KW  - Nuclear Proteins
KW  - Pyrimidines
KW  - Transcription Factors
KW  - Transcriptional Activation
TI  - SMARCA4 deficient tumours are vulnerable to KDM6A/UTX and KDM6B/JMJD3 blockade.
TY  - research article
VL  - 12
ER  -