Translational projects

The “Sheinth” laboratory aims at developing a dynamic translational research on cancers through an interactive group of scientists and clinicians affiliated to INSERM, Paul Strauss Cancer Center, and Strasbourg University Hospitals.
Our goal is to propose innovative and more efficient treatments by deciphering the causes behind the variability in therapeutic responses. Our strategy is to characterise the impact of chemo/chemo-radiation therapies on the interactions between the cancer cells and the specific metabolic and cellular microenvironment with the object at discovering key effectors that might represent prognostic markers and/or drugable targets. More precisely, we are focusing on the contribution of epigenetic processes in the interplay between metabolic stress response pathway activated by the microenvironment and gene regulations driven by the complex family of the p53 tumor suppressor gene (p53,p 63, p73). We are mostly focusing on cancers of the aero-digestive system (i.e. gastric, oesophagus, colon, head & neck, lung) as well as healthy tissues affected by the therapies (muscle, nervous system)

To address these question, we propose a translational research that indudes fundamental molecular studies extending them into the pathophysiological context using animal models (i.e. transgenics gastric cancer mouse model) and dinical investigations (i.e. biobanks for gastric and head/neck cancer). Our results are also the bases for the development of innovative mono or combined therapies targeting the cellular metabolism, which already led to several patents. We believe that our projects will uncover innovative tolls for treatment decision malin and therapeutic protocols that will be translated from bench to bed in the frame of clinical trials. The rapid transfert for our findings will be facilitated in the future by the proximity of the ICANS.

The ongoing complementary projects are:

  • Investigate the impact of organometallic-based chemotherapies (i.Ie oxaliplatin) in the metabolit stress signalling pathways (UPR, Hif1/2, mTor,…) that respond to the tumor-specific metabolic (i.e. hypoxia, pH, redox stress) and cellular (i.e. immune & neuronal cells) microenvironment.

  • Identify the contribution of the p53 family in the metabolic stress response and the impact of HPV infection in this process – Etablish the consequences on cancer cell immunogenicity, tumor response and prognosis.

  • Characterise the epigenetic processes (i.e., miRNA, acetylation/HDAC, methylation/DM) that participate in metabolic stress response and their interaction with the p53 family (p53, p63, p73).

  • Combined RNA/DNA deep sequencing, previously generated omic data (methylome, miRome, transcriptome, genetic anomalies) and bioinformatics to identity prognostic and drugable targets in biopsies (tumor/circulating cells) specimen of gastric and head/neck cancers related to metabolic and epigenetic stress response.

  • Develop innovative mono or combined chemotherapies that target the cellular response by using for example the unique redox property of organometallic compounds and inhibitors for selected HDAC and DM evaluate their impact on the immunogenic reaction.

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