Insulinomas are rare neuroendocrine tumors arising from pancreatic β cells, characterized by aberrant proliferation and altered insulin secretion, leading to glucose homeostasis failure. With the aim of uncovering the role of noncoding regulatory regions and their aberrations in the development of these tumors, we coupled epigenetic and transcriptome profiling with whole-genome sequencing. As a result, we unraveled somatic mutations associated with changes in regulatory functions.
View Article and Find Full Text PDFWe explore the physics of topological lattice models immersed in c-QED architectures for arbitrary coupling strength with the photon field. We propose the use of the cavity transmission as a topological marker and study its behaviour. For this, we develop an approach combining the input-output formalism with a Mean-Field plus fluctuations description of the setup.
View Article and Find Full Text PDFMacroH2A histone variants have a function in gene regulation that is poorly understood at the molecular level. We report that macroH2A1.2 and macroH2A2 modulate the transcriptional ground state of cancer cells and how they respond to inflammatory cytokines.
View Article and Find Full Text PDFPurpose Of Review: Type 1 diabetes (T1D) develops as a consequence of a combination of genetic predisposition and environmental factors. Combined, these events trigger an autoimmune disease that results in progressive loss of pancreatic β cells, leading to insulin deficiency. This article reviews the current knowledge on the genetics of T1D with a specific focus on genetic variation in pancreatic islet regulatory networks and its implication to T1D risk and disease development.
View Article and Find Full Text PDFWe propose a driving protocol which allows us to use quantum dot arrays as quantum simulators for 1D topological phases. We show that by driving the system out of equilibrium, one can imprint bond order in the lattice (producing structures such as dimers, trimers, etc.) and selectively modify the hopping amplitudes at will.
View Article and Find Full Text PDFIn recent years, cancer genomics has provided new insights into genetic alterations and signaling pathways involved in thyroid cancer. However, the picture of the molecular landscape is not yet complete. DNA methylation, the most widely studied epigenetic mechanism, is altered in thyroid cancer.
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