Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Newsletter IMODI #4 - October 2017

128 views

Published on

ZOOM ON: Acute myeloid leukemia: what’s new?
• NEWS: Publication by JE Sarry
• IMODI around the world: Meet the experts!
• FOCUS on: INSERM U1037 Research lab
• FOLLOW US: Be the first to get our new models

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

Newsletter IMODI #4 - October 2017

  1. 1. NEWSLETTER n°4 - October 2017 www.imodi-cancer.org ZOOM ON:Acute myeloid leukemia • NEWS: Publication by JE Sarry • IMODI around the world: Meet the experts! • FOCUS on: INSERM U1037 Research lab • FOLLOW US: Be the first to get our new models Acute myeloid leukemia (AML) is an aggressive hematological malignancy characterized by the accumulation of immature myeloid precursors with resultant peripheral blood cytopenias. The median age at diagnosis of AML is 67 years and outcomes vary according to clinical and laboratory parameters. However, for most patients, outcomes remain poor with high rates of relapse. According to data from the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute, the median overall survival of patients over 66 years withAMLislessthan19monthsdespiteintensivetherapy.Thus,overallsurvivalisapproximately 35% at two years and some subgroups have a less than 5% two-year survival. For the last 43 years, the standard of care has been 3+7 combination chemotherapy, with three days of an anthracycline and seven days of cytarabine. Recently, there have been dramatic advances in our understanding of AML biology and genetics. This new knowledge is now being translated into better predictive markers and novel therapies in this disease. The new therapies being developed for AML include drugs targeting specific mutated proteins (FLT3-ITD, IDH1/2 mutant) and dysregulated pathways such as signaling, apoptosis and mitochondrial metabolism. Epigenetic dysregulation is a key driver of AML biology and new epigenetic therapies (rearranged MLL, DOT1L, EZH 1/2 and LSD1 inhibitors) are one of many exciting developments for this disease. Novel immune- (anti-CD33, CD123, CD47 or BiTE) and cell-based therapies are also under development. Hypermetabolic cancer cells resist to chemotherapy in acute myeloid leukemia A study led by Dr. JE. Sarry and his Team RESISTAML of the Cancer Research Centre of Toulouse (Inserm, France) and involving Toulouse University Hospital (Prof. C. Récher, IUCT-O, France), Metabolomic and Fluxomic Core Unit (Prof. JC. Portais, METATOUL INSA, France) and Toulouse Animal Unit (Dr. Y. Barreira, UMS006, ANEXPLO, France), revealed new findings about the in vivo mechanisms of drug resistance in human acute myeloid leukemia. Oncodesign will be present at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics: October 26-30, Philadelphia, USA, Hall E JoinModul-BioattheLeadersinBiobankingCongress-October25-27,Nashville,USA Join CTI-Biotech to the Bulgarian Association for Personalized Medicine – BAPEMED conference - November 3-4, Plovdiv University, Bulgaria Biofortis will make a bioinformatic presentation at the PRI Pharmabiotics event - March 14-15, 2018, Paris, FRANCE Acute myeloid leukemia (AML) : what’s new? DrJ.ESarry’steamhasdiscoverednewresistancemechanismsofAML Meet OUR experts Read the article Read the article Where to meet our experts ZOOMNEWSIMODI AROUNDTHEWORLD © IMODI Cancer - October 2017 - All right reserved - www.imodi-cancer.org - news@imodi-cancer.frPage 1 on 2 Next > Dr Jean-Emmanuel SARRY - INSERM U1037 MEETING    
  2. 2. NEWSLETTER n°4 - October 2017 www.imodi-cancer.org The french IMODI (Innovative MODels Initiative) consortium is dedicated to the development, the characterization and the commercialization of new preclinical models in oncology. IMODI is a public-private consortium of 18 partners pooling their ressources for the development of more valuable models of cancer in order to decrease the attrition rate of clinical development of novel anti-cancer agents. Science and technology developments: Despite a high rate of complete remission after treatment with genotoxic agents, the prognosis is very poor in human acute myeloid leukemia (AML). Indeed, 5-year overall survival is about 30 to 40% in patients younger than 60 years old and less than 20% in patients over 60 years. Front-line chemotherapy based on a combination of an anthracycline (eg. daunorubicin, DNR, or idarubicin, IDA) and a nucleoside analogue (eg. cytarabine, AraC) is highly effective in ablating leukemic cells, but distant relapses are observed in the majority of patients, characterized by a refractory phase during which no other treatment has shown any efficacy thus far (Tallman et al. 2005; Burnett et al. 2011). Relapses are caused by tumor regrowth initiated by resistant leukemic clones (RLCs). The biology of therapeutic resistance currently represents an active area of research. However, the molecular mechanisms underlying AML chemoresistance are still poorly understood, especially in the in vivo context. The goal of our Team is to understand the causes of drug resistance for the development of new treatments eradicating RLCs and overcoming patient relapses. Our hypothesis is that RLCs have specific mitochondrial energetic and metabolic features mediated by metabolic interactions with stromal cells, which modulates their therapeutic resistance in the tumoral niche. For that, using diverse metabolomic, transcriptomic, pharmacological and functional approaches as well as patient samplesandanewlydevelopedAML-engraftedimmunodeficient models (Sarry et al. 2011, Farge et al. 2017), we propose to 1/ elucidate the stemness and functional heterogeneity of RLCs in response to genotoxics in vivo, and to 2/ determine how reprogrammed mitochondrial energy and metabolic signaling networks drive the drug resistance of RLCs in vivo. Jean-Emmanuel Sarry’s team is part of Oncodevice, IMODI, Labex TOUCAN & PHUC CAPTOR. IMODI at a glance Model and treat the diversity of cancers INSERM U1037 Research lab: to understand the drug resistance in acute myeloid leukemia Read detailled article 2013/01/01: Creation of the consortium 2013/09/01:Signature of the consortium agreement 2015/10/01:Signature of the 1st licence agreement 7 years: duration of the 1rst R&D phase 150 Researchers 6 SMEs 4 pharmaceutical industries 8 Academic institutions FOCUS © IMODI Cancer - October 2017 - All rights reserved - www.imodi-cancer.org - news@imodi-cancer.fr Developing PDX models and cellular assays Modelling the human tumour microenvironment in mice Studying the relationship between microbiota and cancer Designedby:EssentielMARKETING IMODI’s partners 122 PDX models are now available through our web-catalogue. You can quickly search the models that fits your needs. The next version of the IMODI web-catalogue will offer you a wide range of models with the new products like PDX-derived cell lines, ex-vivo assays and bio-collection of tumor, plasma and stools. Follow us and be the first to know about the latest product developments. Follow-us : Be the first to get our new models Discover WEB-CATALOGUE

×