A5040125786- Cytokine Signaling Pathways and Interactions
- interferon and immune responses
- Estrogen and related hormone effects
- Cancer Cells and Metastasis
- Lymphoma Diagnosis and Treatment
- Metabolism, Diabetes, and Cancer
- Cancer, Hypoxia, and Metabolism
- Pancreatic and Hepatic Oncology Research
- Histone Deacetylase Inhibitors Research
- Protein Tyrosine Phosphatases
- Telomeres, Telomerase, and Senescence
- CNS Lymphoma Diagnosis and Treatment
- Multiple Sclerosis Research Studies
Université de Montréal
2015-2020
Abstract Most cancers arise in old individuals, which also accumulate senescent cells. Cellular senescence can be experimentally induced by expression of oncogenes or telomere shortening during serial passage culture. In vivo, precursor lesions several cancer types cells, are thought to represent a barrier malignant progression and response the aberrant activation growth signaling pathways (oncogene toxicity). Here, we sought define gene changes associated with cells that bypass oncogenic...
Expression of the suppressor cytokine signaling-1 (SOCS1) is inactivated in hematopoietic and solid cancers by promoter methylation, miRNA-mediated silencing, mutations. Paradoxically, SOCS1 also overexpressed many human cancers. We report here that ability to interact with p53 regulate cellular senescence depends on a structural motif includes tyrosine (Y)80 SH2 domain SOCS1. Mutations this are found at low frequency some cancers, substitution Y80 phosphomimetic residue inhibits p53-SOCS1...
Natalizumab is used as a second-line treatment for multiple sclerosis (MS). Some reports have linked natalizumab to primary central nervous system lymphoma (PCNSL), although few described its management. A 45-year-old woman with Balo’s Concentric Sclerosis presented dizziness, vertigo accompanied by dysarthria, weakness on the left side and blurred vision right eye after fourth dose of natalizumab. Magnetic resonance imaging (MRI) brain biopsy confirmed diagnosis PCNSL. The patient received...
Abstract Reprogrammation of cancer cells into stem-like state is one the most important mechanisms implicated in tumor initiation, metastasis and resistance to chemotherapies. Acquisition cell property directly correlated with level activation ERK/MAPK pathway. Our study focuses on implication downregulation this pathway during transition pancreatic benign neoplasms ductal adenocarcinoma. This transformation acquisition properties. Conversely, hyperactivation ERK using phosphatase inhibitors...
<p>Supplementary data contains additional methods and reagents figures. The figures contain the following information: Supplementary Figure 1 extends figure providing evidence that SOCS1 may interact with hydrophobic motifs present in many transcription factors. 2 supports showing mutations found human cancers affect SOCS1-p53 interacting motif 3 functional characterization of mutants p53 binding. 4 5 SOCS1, p53, YES1 expression levels DLBCL. a description patients' samples using to...
<p>Supplementary data contains additional methods and reagents figures. The figures contain the following information: Supplementary Figure 1 extends figure providing evidence that SOCS1 may interact with hydrophobic motifs present in many transcription factors. 2 supports showing mutations found human cancers affect SOCS1-p53 interacting motif 3 functional characterization of mutants p53 binding. 4 5 SOCS1, p53, YES1 expression levels DLBCL. a description patients' samples using to...
<div>Abstract<p>Expression of the suppressor cytokine signaling-1 (SOCS1) is inactivated in hematopoietic and solid cancers by promoter methylation, miRNA-mediated silencing, mutations. Paradoxically, SOCS1 also overexpressed many human cancers. We report here that ability to interact with p53 regulate cellular senescence depends on a structural motif includes tyrosine (Y)80 SH2 domain SOCS1. Mutations this are found at low frequency some cancers, substitution Y80 phosphomimetic...
<div>Abstract<p>Expression of the suppressor cytokine signaling-1 (SOCS1) is inactivated in hematopoietic and solid cancers by promoter methylation, miRNA-mediated silencing, mutations. Paradoxically, SOCS1 also overexpressed many human cancers. We report here that ability to interact with p53 regulate cellular senescence depends on a structural motif includes tyrosine (Y)80 SH2 domain SOCS1. Mutations this are found at low frequency some cancers, substitution Y80 phosphomimetic...