Ryan M. Carr
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View article: Spatial Conformation of Pancreatic Cancer Is Associated with Disease Recurrence after Curative-Intent Total Neoadjuvant Therapy
Spatial Conformation of Pancreatic Cancer Is Associated with Disease Recurrence after Curative-Intent Total Neoadjuvant Therapy Open
Pancreatic ductal adenocarcinoma (PDAC) frequently recurs after total neoadjuvant therapy (TNT) and curative-intent resection. Traditional histopathologic response assessments demonstrate that major pathologic response (<5-10% viable resid…
View article: Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer
Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer Open
For over a century, scientists reported the disruption of normal nuclear shape and size in cancer. These changes have long been used as tools for diagnosis and staging of malignancies. However, to date, the mechanisms underlying these aber…
View article: Tumor Landscape Analysis: An Ecologically Informed Framework to Understand Tumor Microenvironments
Tumor Landscape Analysis: An Ecologically Informed Framework to Understand Tumor Microenvironments Open
Tumor microenvironments (TMEs) are spatially complex and dynamic systems shaped by evolutionary pressures, tissue architecture, and cellular interactions. To capture this complexity, we developed the Tumor Landscape Analysis (TLA) pipeline…
View article: Supplementary Figure 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 1 shows correlation of SNP rs1992901 and GLI2 Transcript Expression.
View article: Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 10 shows not differences in H3K4me1 enrichment at Ccnd1 promoter in mutant KRAS cells.
View article: Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 9 shows that Gli2 does not change H3K27Ac enrichment at Ccnd1 promoter downstream of oncogenic KRAS.
View article: Supplementary Table 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 3 includes the sequence of the primers used in our study.
View article: Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 6 describes RNA-seq shows differential gene expression induced by oncogenic KRAS.
View article: Supplementary Figure 5 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 5 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 5 shows the IHC results looking at CD4 and CD8 expression in KC and KCRG mice. The results show no difference in the immune landscape between these mouse models.
View article: Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 8 shows the expression of GLI target genes in all experimental groups.
View article: Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 4 shows the validation of Kras signaling activation and chronic pancreatitis phenotypic examples in KC and KCRG mice.
View article: Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 2 includes the SNP analysis of components of the Hedgehog pathway.
View article: Supplementary Figure 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 2 describes the characterization of the impact Gli2 overexpression in pancreas development. showing that Gli2 loss has no impact on pancreas development or survival in vivo.
View article: Supplementary Figure 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 3 shows Gli2 expression in CRG and KCRG mice and Gli luciferase activity in ΔNGli2-transfected cells.
View article: Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 7 shows how oncogenic KRAS modulates GLI target gene expression.
View article: Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 1 describes the characteristics of the patients used in our study.
View article: Discordant risk factors between pancreatic neuroendocrine neoplasms and pancreatic ductal adenocarcinoma
Discordant risk factors between pancreatic neuroendocrine neoplasms and pancreatic ductal adenocarcinoma Open
Pancreatic neuroendocrine neoplasm (panNEN) is a rare malignancy and the second most common type of pancreatic cancer after pancreatic ductal adenocarcinoma (PDAC), but its etiology is poorly understood. We investigated whether the risk fa…
View article: Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 1 describes the characteristics of the patients used in our study.
View article: Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 1 describes the characteristics of the patients used in our study.
View article: Data from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Data from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Aberrant activation of GLI transcription factors has been implicated in the pathogenesis of different tumor types including pancreatic ductal adenocarcinoma. However, the mechanistic link with established drivers of this disease remains in…
View article: Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 2 includes the SNP analysis of components of the Hedgehog pathway.
View article: Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 8 shows the expression of GLI target genes in all experimental groups.
View article: Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 6 describes RNA-seq shows differential gene expression induced by oncogenic KRAS.
View article: Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 7 shows how oncogenic KRAS modulates GLI target gene expression.
View article: Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 4 shows the validation of Kras signaling activation and chronic pancreatitis phenotypic examples in KC and KCRG mice.
View article: Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 9 shows that Gli2 does not change H3K27Ac enrichment at Ccnd1 promoter downstream of oncogenic KRAS.
View article: Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 6 describes RNA-seq shows differential gene expression induced by oncogenic KRAS.
View article: Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 2 includes the SNP analysis of components of the Hedgehog pathway.