Arquiv0s N@ao Definid0s par@ us0 pess0@l
Ontology highlight
ABSTRACT:
INSTRUMENT(S): UPLC HRMS
ORGANISM(S): Op
SUBMITTER: 
Yasmin Bento Campani
PROVIDER: MSV000095649 | MassIVE | Mon Aug 19 16:42:00 BST 2024
REPOSITORIES: MassIVE
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Primary endpoints: Le critère de jugement principal est la survie sans progression à 3 ans. La survie sans progression est définie par le délai entre la date d’inclusion du patient et la date de la progression ou du décès, quelle qu’en soit la cause. Seuls les patients entièrement réséqués suite à la chirurgie maximale et aptes à recevoir la chimiothérapie seront pris en compte.
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Project description:In mammals, homologous chromosomes rarely pair outside meiosis. One exception is the X chromosome, which transiently pairs during X-chromosome inactivation (XCI). How two chromosomes find each other in 3D space is not known. Here, we reveal a required interaction between the X-inactivation center (Xic) and the telomere in mouse embryonic stem (ES) cells. The subtelomeric, pseudoautosomal regions (PARs) of the two sex chromosomes (X and Y) also undergo pairing in both female and male cells. PARs transcribe a class of telomeric RNA, dubbed PAR-TERRA, which accounts for a vast majority of all TERRA transcripts. PAR-TERRA binds throughout the genome, including to the PAR and Xic. During X-chromosome pairing, PAR-TERRA anchors the Xic to the PAR, creating a ‘tetrad’ of pairwise homologous interactions (Xic–Xic, PAR–PAR, and Xic–PAR). Xic pairing occurs within the tetrad. Depleting PAR-TERRA abrogates pairing and blocks initiation of XCI, whereas autosomal PAR-TERRA induces ectopic pairing. We propose a ‘constrained diffusion model’ in which PAR-TERRA creates an interaction hub to guide Xic homology searching during XCI.
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Project description:Primary objectives: Evaluer l’efficacité du traitement sur le taux de réponse objective (RECIST)
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Project description:Ferroptosis is a unique iron-dependent form of non-apoptotic cell death characterized by devastating lipid peroxidation. Whilst growing evidence suggests that ferroptosis is a type of autophagy-dependent cell death, the underlying molecular mechanisms regulating ferroptosis are largely unknown. In this study, through an unbiased RNA-sequencing screening, we demonstrate the activation of a multi-faceted tumor-suppressor protein Par-4/PAWR during ferroptosis. Functional studies reveal that genetic depletion of Par-4 effectively blocks ferroptosis, whereas Par-4 overexpression sensitizes cells to undergo ferroptosis. More importantly, we have determined that Par-4-triggered ferroptosis is mechanistically driven by the autophagic machinery. Upregulation of Par-4 promotes activation of ferritinophagy (autophagic degradation of ferritin) via the nuclear receptor co-activator 4 (NCOA4), resulting in excessive release of free labile iron and, hence, enhanced lipid peroxidation and ferroptosis. Inhibition of Par-4 dramatically suppresses the NCOA4-mediated ferritinophagy signaling axis. Our results also establish that Par-4 activation positively correlates with reactive oxygen species (ROS) production, which is critical for ferritinophagy-mediated ferroptosis. Furthermore, Par-4 knockdown effectively blocked ferroptosis-mediated tumor suppression in the mouse xenograft models. Collectively, these findings reveal that Par-4 has a crucial role in ferroptosis, which could be further exploited for cancer therapy.
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Project description:Primary objectives: o Estimer l’observance chez des patients traités par capecitabine (Xeloda), une chimiothérapie orale, pour un cancer colorectal ou mammaire suivant deux techniques complémentaires :• par système électronique individuel enregistrant l’heure et la date à laquelle le patient prélève ses pilules avant leur ingestion supposée• des prélèvements pharmacocinétiques couplés à une modélisation pharmacocinétique de population du Xeloda et des métabolites afin d’imputer l’observance sur les dernières prises précédant le prélèvement.
Primary endpoints: a) MESURE DE L’OBSERVANCE ET EVALUATION DU PROFIL TYPE DU PATIENT :
Etape Io Comptage des pilules restantes dans les blisterso Modélisation PK pour estimer l’observance des dernières priseso Auto-questionnaire à l’inclusion et entretien semi-directif dans les 2 mois suivant la fin du cycle 6 de traitement.Etape IIo Comptage des pilules restantes dans les piluliers à bouchon électroniqueo Analyse des temps d’ouverture des piluliers à bouchon électronique pour estimer l’observance sur la totalité du cycle.o Modélisation PK pour estimer l’observance sur les dernières prisesAuto-questionnaire à l’inclusion et entretien semi-directif dans les 2 mois suivant la fin du cycle 6 de traitement.
b) CRITÈRES D’ÉVALUATION clinique :
Lors de chaque visite du patient correspondant à la fin d’un cycle de traitement, soit toutes les 3 semaineso Un personnel de l’équipe clinique vérifiera avec le patient que les effets secondaires ont bien été notés dans son Carnet de Liaison, ce pour chaque semaine du cycle de traitement. Il (ou elle) complètera éventuellement le Carnet de Liaison sur les indications du patiento Le Carnet de Liaison sera photocopiéo Les toxicités notées dans le Carnet de Liaison seront quottées suivant le système de classification du National Cancer Institute of Canada Common Toxicity Criteria (NCIC CTC) pour chaque semaine du cycle.o Evaluation tumorale
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Project description:Prostate apoptosis response-4 (Par-4) is a tumor suppressor protein that is extensively investigated in cancer. The objective of this study is to determine the physiological function of Par-4 in normal cells. Our findings indicated that genetic loss of Par-4 in mice primarily results in adipocyte hypertrophy and obesity, and secondary leads to hepatic steatosis and insulin resistance. Moreover, we noted that Par-4 is downregulated in human subjects who are likely to become obese in the future, thereby serving as a predictor of obesity. Importantly, ChIP-Seq indicated that MDM2 is a target of Par-4 protein, which is known to function as a transcriptional coregulator. We show that Par-4 loss upregulates MDM2 target protein p53, and that p53 further induces complement factor C3 and its proteolytic fragment acylation stimulating protein (ASP), an adipokine that is known to be causally associated with obesity. These studies led to the identification of the Par-4-MDM2-p53-C3/ASP axis in regulation of obesity by Par-4.
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Project description:PAR-1 is known to be involved in the transition from non-metastatic to metastatic melanoma. We sought to determine the downstream target genes regulated by PAR-1 to determine how PAR-1 is contributing to the metastatic melanoma phenotype.
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Project description:Protease-activated receptor-2 (PAR-2), a G protein-coupled receptor activated by trypsin and coagulant factors, plays broad spectrum of physiological and pathological roles especially in cancer development. In this study, we used PAR-2 activating peptide to mimic the action of trypsin to trigger PAR-2 signaling pathway and effects of PAR-2 activation on gene expression in human pancreatic cancer cell line BxPC-3 investigated by microarray analysis. Through DAVID bioinformatic resources, we observed that activated PAR-2-mediated genes are summarized to two different pathways, renal cell carcinoma and NFkB pathway. In renal cell carcinoma pathway, activated PAR-2 dysregulated hypoxia-inducible factors and its target genes, including glucose transporter 1 (GLUT1), transforming growth factor-b (TGF-b) and vascular endothelial growth factor-A (VEGF-A). In addition, activated PAR-2 induced MAPK signaling and transcriptional factors, such as JUN, MAP2K1 and ETS1. The regulation of these genes by PAR-2 assumed that PAR-2 signaling was associated with cancer progression. On the other hand, activated PAR-2 upregulated interleukin-1b (IL-1b) and toll-like receptor 4 (TLR4) related with NFkB activation, which indicated that PAR-2 signaling may cause cancer-related inflammation. In conclusion, PAR-2 may be a factor to regulate cancer progression and inflammation.
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