A5041372659- Chromatin Remodeling and Cancer
- Immune cells in cancer
- interferon and immune responses
- Protein Degradation and Inhibitors
- Histone Deacetylase Inhibitors Research
- Immune Cell Function and Interaction
- CRISPR and Genetic Engineering
- Epigenetics and DNA Methylation
- Cancer, Hypoxia, and Metabolism
- RNA regulation and disease
- RNA modifications and cancer
- Genomics and Chromatin Dynamics
European Institute of Oncology
2021-2024
Istituti di Ricovero e Cura a Carattere Scientifico
2024
Institut d'Investigació Biomédica de Bellvitge
2020-2021
Institut Català d'Oncologia
2019
Abstract Despite the genetic inactivation of SMARCA4 , a core component SWI/SNF-complex commonly found in cancer, there are no therapies that effectively target SMARCA4-deficient tumours. Here, we show that, unlike cells with activated MYC oncogene, refractory to histone deacetylase inhibitor, SAHA, leading aberrant accumulation H3K27me3. -mutant also an impaired transactivation and significantly reduced levels demethylases KDM6A/UTX KDM6B/JMJD3, strong dependency on these demethylases, so...
Abstract Caloric Restriction (CR) has established anti-cancer effects, but its clinical relevance and molecular mechanism remain largely undefined. Here, we investigate CR’s impact on several mouse models of Acute Myeloid Leukemias, including Promyelocytic Leukemia, a subtype strongly affected by obesity. After an initial marked anti-tumor effect, lethal disease invariably re-emerges. Initially, CR leads to cell-cycle restriction, apoptosis, inhibition TOR insulin/IGF1 signaling. The...
Innate immune responses to coronavirus infections are highly cell specific. Tissue-resident macrophages, which infected by severe acute respiratory syndrome 2 (SARS-CoV-2) in patients but inconsistently vitro, exert critical conflicting effects secreting both antiviral type I interferons (IFNs) and tissue-damaging inflammatory cytokines. Steroids, the only class of host-targeting drugs approved for treatment disease 2019 (COVID-19), indiscriminately suppress responses, possibly impairing...
Abstract Double-stranded RNAs (dsRNAs) are potent immunostimulatory nucleic acids of viral origin but also physiologically produced by mammalian cells. Recent studies demonstrated that elevating dsRNA levels, either exogenously through mimetics like Polyinosinic-polycytidylic acid (pI:C) or endogenously epigenetic modulation retroviral elements, can elicit anticancer effects. In response to dsRNA, cells a dual consisting in Interferon (IFN) production and translational shutdown associated,...
Abstract Double-stranded RNAs (dsRNAs) are potent immunostimulatory nucleic acids of viral origin but also physiologically produced by mammalian cells. Recent studies demonstrated that elevating dsRNA levels, either exogenously through mimetics like Polyinosinic-polycytidylic acid (pI:C) or endogenously epigenetic modulation retroviral elements, can elicit anticancer effects. In response to dsRNA, cells a dual consisting in Interferon (IFN) production and translational shutdown associated,...
Summary Despite the genetic inactivation of SMARCA4 , a core component SWI/SNF-complex commonly found in cancer, there are no therapies that effectively target SMARCA4-deficient tumours. Here, we show that, unlike cells with activated MYC oncogene, refractory to histone deacetylase inhibitor, SAHA, leading aberrant accumulation H3K27me3. This is associated impaired transactivation and significantly reduced levels demethylases KDM6A/UTX KDM6B/JMJD3, which confer strong dependency on KDM6s...
Abstract Tissue-resident macrophages exert critical but conflicting effects on the progression of coronavirus infections by secreting both anti-viral type I Interferons and tissue-damaging inflammatory cytokines. Steroids, only class host-targeting drugs approved for Covid19, indiscriminately suppress responses, possibly impairing viral clearance, provide limited clinical benefit. Here we set up a mouse in vitro co-culture system that reproduces macrophage response to SARS-CoV2 seen patients...
Abstract Despite the genetic inactivation of SMARCA4, a core component SWI/SNF-complex commonly found in cancer, there are no therapies that effectively target SMARCA4-deficient tumours. Here, we show that, unlike cells with activated MYC oncogene, SMARCA4 refractory to histone deacetylase inhibitor, SAHA, leading aberrant accumulation H3K27me3. This is associated impaired transactivation and significantly reduced levels demethylases KDM6A/UTX KDM6B/JMJD3, strong dependency on these...