Purpose: Fibrosis is a common late complication of radiation therapy. Molecular dysregulations leading to fibrosis have been characterized for the coding part of the genome, notably those involving the TGFB1 gene network. However, because a large part of the human genome encodes RNA transcripts that are not translated into proteins, exploring the involvement of the noncoding part of the genome in fibrosis susceptibility and development was the aim of this work.
View Article and Find Full Text PDFMetabarcoding DNA sequencing has revolutionized the study of microbial communities. Third-generation sequencing producing long reads had opened up new perspectives. Obtaining the full-length ribosomal RNA gene would permit one to reach a better taxonomic resolution at the species or the strain level.
View Article and Find Full Text PDFAlthough it is well established that 5 to 15% of radiotherapy patients exhibit severe side-effects in non-cancerous tissues, the molecular mechanisms involved are still poorly known, and the links between cellular and tissue radiosensitivity are still debated. We here studied fibroblasts from non-irradiated skin of patients with severe sequelae of radiotherapy, to determine whether specific basal cell activities might be involved in susceptibility to side-effects in normal tissues. Compared to control cells, patient fibroblasts exhibited higher radiosensitivity together with defects in DNA repair.
View Article and Find Full Text PDF