Thomas G. Paulson
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View article: 3D pathology-guided microdissection
3D pathology-guided microdissection Open
Traditional micro- and macro-dissection techniques enable the extraction of localized regions in thin tissue sections for molecular analysis. Despite the growing use of 3D microscopy, analogous methods for volumetric microdissection are la…
View article: Histopathology-based Spatial Profiling of Immune and Molecular Features Predicts Cancer risk in Barrett’s Esophagus
Histopathology-based Spatial Profiling of Immune and Molecular Features Predicts Cancer risk in Barrett’s Esophagus Open
Background Improved cancer risk stratification is needed to differentiate high-risk individuals with Barrett’s esophagus (BE) from low-risk populations to reduce overtreatment and improve outcome. The evolution of BE towards adenocarcinoma…
View article: Breakage fusion bridge cycles drive high oncogene number with moderate intratumoural heterogeneity
Breakage fusion bridge cycles drive high oncogene number with moderate intratumoural heterogeneity Open
Oncogene amplification is a key driver of cancer pathogenesis. Both breakage fusion bridge (BFB) cycles and extrachromosomal DNA (ecDNA) can lead to high oncogene copy numbers, but the impact of BFB amplifications on intratumoral heterogen…
View article: Community assembly modeling of microbial evolution within Barrett’s esophagus and esophageal adenocarcinoma
Community assembly modeling of microbial evolution within Barrett’s esophagus and esophageal adenocarcinoma Open
Mathematical modeling of somatic evolution, a process impacting both host cells and microbial communities in the human body, can capture important dynamics driving carcinogenesis. Here we considered models for esophageal adenocarcinoma (EA…
View article: Breakage fusion bridge cycles drive high oncogene copy number, but not intratumoral genetic heterogeneity or rapid cancer genome change
Breakage fusion bridge cycles drive high oncogene copy number, but not intratumoral genetic heterogeneity or rapid cancer genome change Open
SUMMARY Oncogene amplification is a major driver of cancer pathogenesis. Breakage fusion bridge (BFB) cycles, like extrachromosomal DNA (ecDNA), can lead to high copy numbers of oncogenes, but their impact on intratumoral heterogeneity, tr…
View article: Extrachromosomal DNA in the cancerous transformation of Barrett’s oesophagus
Extrachromosomal DNA in the cancerous transformation of Barrett’s oesophagus Open
View article: Supplementary Table S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Table S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Population characteristics of study subjects.
View article: Supplementary Figure S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Processes applied for SCA feature selection, prediction model development and cross-validation in the study.
View article: Supplementary Methods from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Methods from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Supplementary Methods from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
View article: Supplementary Methods from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Methods from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Supplementary Methods from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
View article: Supplementary Figure S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Schematic describing SCA datasets and statistical methods used in model training, comparisons, cross-validations, and figures.
View article: Supplementary Figure S4 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S4 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
ROC for combined T1+T2 data. The model was trained by repeatedly using a randomly drawn 2/3 of the combined T1+T2 data for training, and testing on the reserved 1/3 of the data. The average AUC of 10,000 ROC from the reserved test data is …
View article: Data from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Data from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Cancers detected at a late stage are often refractory to treatments and ultimately lethal. Early detection can significantly increase survival probability, but attempts to reduce mortality by early detection have frequently increased overd…
View article: Supplementary Figure S3 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S3 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
ROC for T1 using Jackknife method. The model was trained on T1 data with one sample left out and tested on the left out T1 sample (AUC=0.86). The ROC curve is established based on the testing results of the 248 left-out samples.
View article: Supplementary Figure S4 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S4 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
ROC for combined T1+T2 data. The model was trained by repeatedly using a randomly drawn 2/3 of the combined T1+T2 data for training, and testing on the reserved 1/3 of the data. The average AUC of 10,000 ROC from the reserved test data is …
View article: Supplementary Table S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Table S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
List of 86 regions selected as a panel of predictors for EA risk prediction and frequency of SCA in these regions in nonprogressors, progressors and in an independent set of six EA samples.
View article: Supplementary Figure S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Processes applied for SCA feature selection, prediction model development and cross-validation in the study.
View article: Supplementary Table S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Table S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
List of 86 regions selected as a panel of predictors for EA risk prediction and frequency of SCA in these regions in nonprogressors, progressors and in an independent set of six EA samples.
View article: Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus
Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus Open
All cancers are believed to arise by dynamic, stochastic somatic genomic evolution with genome instability, generation of diversity, and selection of genomic alterations that underlie multistage progression to cancer. Advanced esophageal a…
View article: Supplementary Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus
Supplementary Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus Open
PDF file 2119K, Supplementary Table S1, Cohort characteristics. Supplementary Table S2, Mean SCA and mean percent of probes with SCA per biopsy in time windows. Supplementary Table S3, SCA with similar frequency in progressors and nonprogr…
View article: Supplementary Table S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Table S1 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Population characteristics of study subjects.
View article: Data from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Data from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Cancers detected at a late stage are often refractory to treatments and ultimately lethal. Early detection can significantly increase survival probability, but attempts to reduce mortality by early detection have frequently increased overd…
View article: Supplementary Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus
Supplementary Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus Open
PDF file 2119K, Supplementary Table S1, Cohort characteristics. Supplementary Table S2, Mean SCA and mean percent of probes with SCA per biopsy in time windows. Supplementary Table S3, SCA with similar frequency in progressors and nonprogr…
View article: Supplementary Figure S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S2 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
Schematic describing SCA datasets and statistical methods used in model training, comparisons, cross-validations, and figures.
View article: Supplementary Figure S3 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus
Supplementary Figure S3 from Assessment of Esophageal Adenocarcinoma Risk Using Somatic Chromosome Alterations in Longitudinal Samples in Barrett's Esophagus Open
ROC for T1 using Jackknife method. The model was trained on T1 data with one sample left out and tested on the left out T1 sample (AUC=0.86). The ROC curve is established based on the testing results of the 248 left-out samples.
View article: Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus
Data from Temporal and Spatial Evolution of Somatic Chromosomal Alterations: A Case-Cohort Study of Barrett's Esophagus Open
All cancers are believed to arise by dynamic, stochastic somatic genomic evolution with genome instability, generation of diversity, and selection of genomic alterations that underlie multistage progression to cancer. Advanced esophageal a…
View article: Supplementary Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma
Supplementary Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma Open
Supplementary Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma
View article: Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma
Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma Open
Purpose: Chromosomal instability, as assessed by many techniques, including DNA content aneuploidy, loss of heterozygosity, and comparative genomic hybridization, has consistently been reported to be common in cancer and rare in nor…
View article: Supplementary Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma
Supplementary Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma Open
Supplementary Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma
View article: Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma
Data from Chromosomal Instability and Copy Number Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma Open
Purpose: Chromosomal instability, as assessed by many techniques, including DNA content aneuploidy, loss of heterozygosity, and comparative genomic hybridization, has consistently been reported to be common in cancer and rare in nor…