Ontology highlight
ABSTRACT:
PROVIDER: PRJNA611679 | ENA |
REPOSITORIES: ENA
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Project description:In this study, we show that in a spider mite species, Tetranychus urticae, genetic changes do not drive experimental range expansions. We performed two experiments, each with two treatments, wherein mite populations were allowed to expand their habitat range. In a first experiment, we either replaced migrating females with females from the parental stock populations (Replacement From Stock) or left the migrants unmanipulated (Control). In a second experiment, we compared the range expansions of non-evolving, genetically inbred, populations (Iso) with those of evolving, genetically diverse, populations (Mix). Transcriptomic analysis supported other lines of evidence showing that experimental range expansion was driven by kin competition and not by genetic changes (see also Van Petegem et al, 2017). Only 21 differentially expressed genes were found.
2018-12-05 | GSE105408 | GEO
Project description:Barrett’s esophagus is a condition in which the squamous epithelium of the esophagus is replaced with a metaplastic crypt-structured epithelium and progresses to esophageal adenocarcinoma in a minority of cases. It is an ideal human system in which to study the evolutionary dynamics of progression. Previous results suggested that there is a low mutation rate in Barrett’s, based on measures of whole biopsies. However, it was unclear if this was due to a low mutation rate in crypts or a high mutation rate in crypts with a low clonal expansion rate. We used phylogenetic analyses to study copy-number alterations in the epithelium of 67 whole biopsies and 291 single crypts from those biopsies in 8 individuals with Barrett’s esophagus, including 4 cancer progressors. While crypts contained some private mutations, the mutation load and inferred mutation rate in crypts were similar to those in whole biopsies; the latter thus being a reasonable substrate for studies of the mutational process. Diversity between biopsies and within biopsies were strongly correlated. Mutations were more frequent near the gastro-esophageal junction and genomic instability appeared to precede genome doubling, leading to clonal expansions in two cases. This suggests that progression is driven by rare, carcinogenic alterations of large effect, rather than the gradual accumulation of many alterations of small effect, and explains why most patients with Barrett’s esophagus do not progress to esophageal adenocarcinoma. These results shed light on the evolutionary dynamics underlying neoplastic progression in Barrett’s esophagus. Batch 7 of 7
2018-01-30 | GSE99429 | GEO
Project description:Barrett’s esophagus is a condition in which the squamous epithelium of the esophagus is replaced with a metaplastic crypt-structured epithelium and progresses to esophageal adenocarcinoma in a minority of cases. It is an ideal human system in which to study the evolutionary dynamics of progression. Previous results suggested that there is a low mutation rate in Barrett’s, based on measures of whole biopsies. However, it was unclear if this was due to a low mutation rate in crypts or a high mutation rate in crypts with a low clonal expansion rate. We used phylogenetic analyses to study copy-number alterations in the epithelium of 67 whole biopsies and 291 single crypts from those biopsies in 8 individuals with Barrett’s esophagus, including 4 cancer progressors. While crypts contained some private mutations, the mutation load and inferred mutation rate in crypts were similar to those in whole biopsies; the latter thus being a reasonable substrate for studies of the mutational process. Diversity between biopsies and within biopsies were strongly correlated. Mutations were more frequent near the gastro-esophageal junction and genomic instability appeared to precede genome doubling, leading to clonal expansions in two cases. This suggests that progression is driven by rare, carcinogenic alterations of large effect, rather than the gradual accumulation of many alterations of small effect, and explains why most patients with Barrett’s esophagus do not progress to esophageal adenocarcinoma. These results shed light on the evolutionary dynamics underlying neoplastic progression in Barrett’s esophagus. Batch 3 of 7
2018-01-30 | GSE99268 | GEO
Project description:Barrett’s esophagus is a condition in which the squamous epithelium of the esophagus is replaced with a metaplastic crypt-structured epithelium and progresses to esophageal adenocarcinoma in a minority of cases. It is an ideal human system in which to study the evolutionary dynamics of progression. Previous results suggested that there is a low mutation rate in Barrett’s, based on measures of whole biopsies. However, it was unclear if this was due to a low mutation rate in crypts or a high mutation rate in crypts with a low clonal expansion rate. We used phylogenetic analyses to study copy-number alterations in the epithelium of 67 whole biopsies and 291 single crypts from those biopsies in 8 individuals with Barrett’s esophagus, including 4 cancer progressors. While crypts contained some private mutations, the mutation load and inferred mutation rate in crypts were similar to those in whole biopsies; the latter thus being a reasonable substrate for studies of the mutational process. Diversity between biopsies and within biopsies were strongly correlated. Mutations were more frequent near the gastro-esophageal junction and genomic instability appeared to precede genome doubling, leading to clonal expansions in two cases. This suggests that progression is driven by rare, carcinogenic alterations of large effect, rather than the gradual accumulation of many alterations of small effect, and explains why most patients with Barrett’s esophagus do not progress to esophageal adenocarcinoma. These results shed light on the evolutionary dynamics underlying neoplastic progression in Barrett’s esophagus. Batch 4 of 7
2018-01-30 | GSE99269 | GEO