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Articles by Andre Levchenko
SPINK1-COL18A1 crosstalk shapes epigenome and drives cancer stemness in pancreatic ductal adenocarcinoma
STS-LTS microarray result analysis Differential expression analysis was done by limma 3.58.185 by including both batch and STS/LTS group as variables in the design formula.
Disruption of WNT/Notch signaling in pancreatic cancer reveals tumors depend on the intricate equilibrium of malignant cell states
Keywords intratumoral heterogeneity pancreas cancer tissue organization lineage tracing lineage ablation WNT Notch gene perturbation Get full text access Log in, subscribe or purchase for full access. References 1. Barker, N. ∙ Clevers, H. Leucine-rich repeat-containing G-protein-coupled receptors as markers of adult stem cells Gastroenterology. 2010; 138:1681-1696 2. Murtaugh, L.C. ∙ Keefe, M.D. Regeneration and repair of the exocrine pancreas Annu. Rev. Physiol. 2015; 77:229-249 3. Ge, Y. ∙ Fuchs, E.
Cas12a-knock-in mice for multiplexed genome editing, disease modelling and immune-cell engineering - Nature Biomedical Engineering
Abstract The pleiotropic effects of human disease and the complex nature of gene-interaction networks require knock-in mice allowing for multiplexed gene perturbations. Here we describe a series of knock-in mice with a C57BL/6 background and with the conditional or constitutive expression of LbCas12a or of high-fidelity enhanced AsCas12a, which were inserted at the Rosa26 locus.
Tunability of calcium dynamics by signaling inputs and cell-cell communication in pancreatic beta cells
Abstract In addition to frequently occurring stable all-or-none responses, live cells can display more complex response dynamics, e.g., oscillations in the activity/concentration of biomolecules.
Single-Cell Measurements and Modeling and Computation of Decision-Making Errors in a Molecular Signaling System with Two Output Molecules
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Dynamic decoding of VEGF signaling and coordinated control of multiple phenotypes by the Src-TEM4-YAP pathway
Abstract Responses of endothelial cells to elevated levels of Vascular Endothelial Growth Factor (VEGF), frequently accompanying local decrease in oxygen supply, include loosening of cell contacts, rearrangement of cells in the process of vessel remodeling and ultimately, angiogenic growth. How these complex processes, occurring on diverse time scales, are coordinated and how they are guided by a single key signaling input, is still incompletely understood.
Single Cell Measurements and Modeling and Computation of Decision Making Errors in a Molecular Signaling System with Two Output Molecules
Abstract A cell constantly receives signals and takes different fates accordingly. Given the uncertainty rendered by signal transduction noise, the cell may incorrectly perceive the signals. It may mistakenly behave as if there is a signal - although there is none, or may miss the presence of a signal that actually exists.
Experimental and Phylogenetic Evidence for Correlated Gene Expression Evolution between Dermal and Endometrial Fibroblasts: implications for the evolution of cancer malignancy
New Results doi: https://doi.org/10.1101/2023.07.08.548194 Abstract Changes in transcriptional gene expression is a dominant mode of evolution, mostly driven by mutations at cis-regulatory regions. Mutations can affect gene expression in multiple cell types if the same cis-regulatory elements are used by different cell types. As a consequence, changes in gene expression in one cell type may be associated with similar gene expression changes in another cell type.
Epigenetics as a mediator of plasticity in cancer
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Epigenetics as a mediator of plasticity in cancer
LATEST NEWS Plasticity of cancer cell phenotypes During differentiation, cells adopt phenotypic states of progressive specificity. Cancer cells violate this property, instead adopting increased plasticity of structure and function. Epigenetic change has been considered a developmental landscape that can channel specific differentiation events and define and constrain distinct phenotypic and gene expression states.
Evolution of placental invasion and cancer metastasis are causally linked
Abstract Among mammals, placental invasion is correlated with vulnerability to malignancy. Animals with more invasive placentation (for example, humans) are more vulnerable to malignancy. To explain this correlation, we propose the hypothesis of ‘Evolved Levels of Invasibility’ proposing that the evolution of invasibility of stromal tissue affects both placental and cancer invasion. We provide evidence for this using an in vitro model.
A Loss of Epigenetic Control Can Promote Cell Death through Reversing the Balance of Pathways in a Signaling Network
Epigenetic control of regulatory networks is only partially understood. Expression of Insulin-like growth factor-II (IGF2) is controlled by genomic imprinting, mediated by silencing of the maternal allele. Loss of imprinting of IGF2 (LOI) is linked to intestinal and colorectal cancers, causally in murine models and epidemiologically in humans. However, the molecular underpinnings of the LOI phenotype are not clear.
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