WorldCat Identities

Dufresne, Marlène (19..-....).

Overview
Works: 5 works in 7 publications in 2 languages and 8 library holdings
Roles: Thesis advisor, Other, Opponent
Publication Timeline
.
Most widely held works by Marlène Dufresne
Rôle du récepteur de la gastrine dans le pancréas endocrine by Stéphane Leung-Theung-Long( Book )

2 editions published in 2005 in French and held by 2 WorldCat member libraries worldwide

Présents dans le pancréas humain fœtal, la gastrine et son récepteur, le récepteur CCK2, pourraient contribuer activement à la différenciation des cellules de l'îlot de Langerhans en induisant l'expression du gène du glucagon dans les cellules alpha. A partir d'un nouveau modèle de cellules alpha pancréatiques exprimant le récepteur CCK2, nous montrons que la gastrine stimule l'expression du gène du glucagon en activant le facteur de transcription Egr-1 via la cascade de signalisation MEK1/ERK1/2. De plus, nous démontrons que Egr-1 est indispensable à l'expression basale du gène du glucagon. Par ailleurs, la capacité de 4 lignées pancréatiques canalaires humaines à exprimer certains gènes du lignage cellulaire endocrine a été étudiée. En réponse à des agents pro-différenciateurs, la lignée BxPC3 semble être un modèle adéquat pour l'étude de la différenciation endocrine dans le pancréas adulte
Régulation et fonctions de l'E3 ubiquitine ligase TRIP12 au cours du cycle cellulaire by Dorian Larrieu( Book )

2 editions published in 2019 in French and held by 2 WorldCat member libraries worldwide

TRIP12 is an E3 ubiquitin ligase that belongs to the HECT (Homologous to the E6-AP Carboxyl Terminus) family. Several proteins are targeted by TRIP12 polyubiquitination which triggers their proteasomal degradation. Among its targets, several proteins are involved in DNA damage responses, chromatin remodelling and p53 pathway activation. Unpublished results of my team showed an increased expression of TRIP12 in pancreatic cancer and pre-neoplastic lesions. My group revealed that TRIP12 polyubiquitinates and provokes the degradation of the transcription factor PTF1a (Pancreas Transcription Factor 1a) stability. Describing for the first time a post-translational regulation of PTF1a. PTF1a is essential in pancreatic development and homeostasis. It inhibits the proliferation of pancreatic cells and is considered as a tumour suppressor gene and. Even if several TRIP12 targets are involved in cellular processes that are tightly cell cycle regulated, the regulation of TRIP12 expression and its functions during the cell cycle was unknown at the beginning of my thesis. I showed that TRIP12 expression and nuclear localization are regulated throughout the cell cycle. I identified an intrinsically disordered domain within the N-terminal region of TRIP12 that permits its interaction to euchromatin. I demonstrated TRIP12 implication in mitosis entry by controlling DNA replication timing Independently of its catalytic activity. TRIP12 is also required for maintaining a correct mitotic progression and chromosomes stability. My results propose TRIP12 as a new chromatin-associated protein that is essential for cell cycle progression and to preserve genome integrity. In the end, my studies will be fundamental to explain the increased expression of TRIP12 protein observed in pancreatic cancer and its impact in carcinogenesis
Exogenous CCK and gastrin stimulate pancreatic exocrine secretion via CCK-A but also via CCK-B/gastrin receptors in the calf by Gwenola Le Dréan( )

1 edition published in 1999 in English and held by 2 WorldCat member libraries worldwide

Chimiosensibilisation de l'adénocarcinome canalaire du pancréas par la perturbation du microenvironnement tumoral et l'augmentation de la biodisponibilité dans la cellule tumorale : effets de la cavitation ultrasonore et de l'inhibition de nrf2 by Marine Camus Duboc( )

1 edition published in 2017 in French and held by 1 WorldCat member library worldwide

Pancreatic ductal adenocarcinoma (PDAC) has increased in incidence over the past decade, leading it to be the fourth lethal cause of cancer in the world with a very poor prognosis, since less than 5% of patients are alive at 5 years. Many advances in the understanding of pancreatic tumorigenesis, notably on the genetic, immune and cellular stroma interactions of the tumor, have led to the development of new treatment strategies in the last decade. However, despite very encouraging pre-clinical results, none of these strategies has yet led to the emergence of a truly effective treatment in comparison with standard chemotherapy. This thesis focused on two innovative therapeutic modalities in the treatment of PDAC at a preclinical stage by studying in vitro (2D and 3D cell cultures) and in vivo (ectopic, orthotopic xenografts) the effects on the tumor growth of an inhibitor of the Nrf2 pathway (involved in oxidative stress), on the first hand, and of a physical element, ultrasound cavitation associated with liposomal chemotherapy, on the second hand. Ultrasound cavitation is a mechanical effect of ultrasound to increase the uptake of molecules or genes in cells. The feasibility and effectiveness of the combination of liposomal chemotherapy targeted by ultrasonic cavitation was evaluated in murin orthotopic models of PDAC. An ultrasound delivery system has been adapted to apply focused inertial cavitation to PDAC xenografts created after the injection of liposomal doxorubicin (L-DOX) according to a preliminary pharmacokinetic study carried out in the murine model. L-DOX, designed on unsaturated phospholipids of dioleoylphosphatidylethanolamine, was known to be stable in the bloodstream and to maximize its accumulation and release of the active drug during ultrasound delivery. This thesis shows that this therapeutic combination (L DOX and inertial cavitation) makes it possible to reduce the tumor volume in vivo in a nude mouse orthotopic model of PDAC. Inertial cavitation may be generated to increase the therapeutic effect of chemotherapybearing liposomes accumulated in the tumor with minimal mechanical effect on the surrounding tissue. Recent studies strongly suggest that Nrf2 is an ideal target against chemoresistance of PDAC. In vitro and in vivo methods were combined to examine the effect of brusatol associated with chemotherapeutic agents on cell death in addition to its impact on oxidative stress (reactive oxygen species and gluthation levels). This thesis demonstrates that the inhibition of the Nrf2 pathway via brusatol, a natural compound derived from Fructus Bruceae, potentiates the effects of chemotherapy and allows the inhibition of tumor growth in vitro on PDAC cell lines. This inhibition is accompanied by a modulation of oxidative stress by brusatol, with increasing ROS and decreasing GSH. In vivo, the combination of brusatol and oxaliplatin reduced tumor volume in two mouse models of PDAC xenograft. These results suggest the efficacy of using brusatol to combat chemoresistance and reinforce the idea that brusatol could be developed as an adjuvant to chemotherapy in PA. Clinical work was also carried out in parallel on an innovative physical treatment modality, endobiliary radiofrequency, in the management of adenoma of the ampoule of Vater, a rare tumor located between the digestive and the bilio-pancreatic systems. The results of this work will also be presented in this thesis
<> by Roxane Pommier( )

1 edition published in 2014 in French and held by 1 WorldCat member library worldwide

 
Audience Level
0
Audience Level
1
  Kids General Special  
Audience level: 0.95 (from 0.93 for Rôle du r ... to 0.97 for Exogenous ...)

Languages