R
J
Last name: ROUX
First name: Jérémie
International audience
International audience
Cell response heterogeneity upon treatment is the main obstacle in developing efficacious cancer drugs in preclinical research. Although single-cell tudies have revealed the depth of cellular heterogeneity observed between in tumor cells, the regulatory impact of cell variability on therapeutic esponse remains unclear.To gain a deeper...
Isogenic cells can respond differently to cytotoxic drugs, such as the tumor necrosis factor-related apoptosis inducing ligand (TRAIL), with only a fraction committing to apoptosis. Since non-genetic transient resistance to TRAIL has been shown to dependent on caspase-8 dynamics at the receptor level in vitro, here we investigate the core...
International audience
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Abstract Single-cell multimodal technologies reveal the scales of cellular heterogeneity impairing cancer treatment, yet cell response dynamics remain largely underused to decipher the mechanisms of drug resistance they take part in. As the phenotypic heterogeneity of a clonal cell population informs on the capacity of each single-cell to...
The apoptotic signaling pathway designates a set of biochemical reactions involved in programmed cell death. One of the triggering mechanisms of apoptosis is the binding of death ligands to death receptors on the cell membrane, a known stimulus for the activation of the so-called extrinsic apoptosis signaling pathway. Stimulation by death...
Cell response heterogeneity upon treatment is a main obstacle in preclinical development of efficacious cancer drugs, due to the emergence of drug-tolerant cells. We have previously developed a single-cell pipeline called Fate-seq to profile drug-tolerant persisters, based on predictions oftheir drug response. To automatize and increase the...
Cell response heterogeneity upon drug treatment is a leading cause of reduced drug efficacy in preclinical cancer research. Although single-cell studies have revealed the depth of cellular heterogeneity observed between in tumor cells, the regulatory impact of cell variability on therapeutic response remains unclear. Here, we present a new ODE...
International audience
International audience
Cell response heterogeneity upon treatment is a main obstacle in preclinical development of efficacious cancer drugs, due to the emergence of drug-tolerant cells. We have previously developed a single-cell workflow, Fate-Seq (1,2), to profile drug-tolerant persisters. Fate-Seq is based on the prediction of the drug response of each cells that...
International audience
International audience
Initiating cell death in malignant cells through the activation of death receptors 4 and 5 (DR4/5) is a cancer therapeutic strategy re-entering a phase of intensive investigation due to recent advances that improved ligand activity, pharmacokinectics and lowered side effects (Wajant et al. Cancer Lett 2013). However, most drugs induce...
A central problem in the multi-omics era is to bridge the gap between genes/proteins of heterogeneous expression (call them sources) and proteins already known to be involved in a specific cell response signalling pathway (call them targets). Insights on this problem are of special interest to unveil the molecular basis of individual cell...
Prioritizing genes for their role in drug sensitivity, is an important step in understanding drugs mechanisms of action and discovering new molecular targets for co-treatment. To formalize this problem, we consider two sets of genes X and P respectively composing the gene signature of cell sensitivity at the drug IC 50 and the genes involved in...
Prioritizing genes for their role in drug sensitivity, is an important step in understanding drugs mechanisms of action and discovering new molecular targets for co-treatment. To formalize this problem, we consider two sets of genes X and P respectively composing the gene signature of cell sensitivity at the drug IC 50 and the genes involved in...
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Prioritizing genes for their role in drug sensitivity, is an important step in understanding drugs mechanisms of action and discovering new molecular targets for co-treatment. To formalize this problem, we consider two sets of genes X and P respectively composing the gene signature of cell sensitivity at the drug IC 50 and the genes involved in...