about
Mito-priming as a method to engineer Bcl-2 addiction.Limited mitochondrial permeabilization causes DNA damage and genomic instability in the absence of cell death.TIF1γ interferes with TGFβ1/SMAD4 signaling to promote poor outcome in operable breast cancer patients.Mitochondrial apoptosis: killing cancer using the enemy within.Mitochondrial permeabilization engages NF-κB-dependent anti-tumour activity under caspase deficiency.Src tyrosine kinase inhibits apoptosis through the Erk1/2- dependent degradation of the death accelerator Bik.Does Molecular Genotype Provide Useful Information in the Management of Radioiodine Refractory Thyroid Cancers? Results of a Retrospective Study.BCL-XL directly modulates RAS signalling to favour cancer cell stemness.Amniotic fluid glial fibrillary acidic protein (AF-GFAP), a biomarker of open neural tube defects.Molecular testing of BRAF, RAS and TERT on thyroid FNAs with indeterminate cytology improves diagnostic accuracy.Breast cancer targeting through inhibition of the endoplasmic reticulum-based apoptosis regulator Nrh/BCL2L10.Predictive factors of outcome in poorly differentiated thyroid carcinomas.What Does This Mutation Mean? The Tools and Pitfalls of Variant Interpretation in Lymphoid Malignancies.Comparison of RT-qPCR and Nanostring in the measurement of blood interferon response for the diagnosis of type I interferonopathiesTif1γ is essential for the terminal differentiation of mammary alveolar epithelial cells and for lactation through SMAD4 inhibitionKilling the Killer: PARC/CUL9 promotes cell survival by destroying cytochrome CThe apoptosis inhibitor Bcl-xL controls breast cancer cell migration through mitochondria-dependent reactive oxygen species productionApplication of Mito-Priming to Generate BCL-2 Addicted CellsMitochondrial inner membrane permeabilisation enables mtDNA release during apoptosisReply to Dr Ozden et alEffect of Buparlisib, a Pan-Class I PI3K Inhibitor, in Refractory Follicular and Poorly Differentiated Thyroid CancerTERT promoter mutations identify a high-risk group in metastasis-free advanced thyroid carcinomaConcomitant GNA11 and SF3B1 mutations in two cases of melanoma associated with blue naevusCOPA Syndrome as a Cause of Lupus NephritisDermoscopic features in BRAF and NRAS primary cutaneous melanoma: association with peppering and blue-white veilClinical efficacy of the optimal biological dose in early-phase trials of anti-cancer targeted therapiesmTORC1 Activation Requires DRAM-1 by Facilitating Lysosomal Amino Acid Efflux
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description
researcher ORCID ID = 0000-0003-3768-2378
@en
wetenschapper
@nl
name
Jonathan Lopez
@ast
Jonathan Lopez
@en
Jonathan Lopez
@es
Jonathan Lopez
@nl
type
label
Jonathan Lopez
@ast
Jonathan Lopez
@en
Jonathan Lopez
@es
Jonathan Lopez
@nl
prefLabel
Jonathan Lopez
@ast
Jonathan Lopez
@en
Jonathan Lopez
@es
Jonathan Lopez
@nl
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0000-0003-3768-2378