Simon T. Barry
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View article: A New Approach to Large Multiomics Data Integration
A New Approach to Large Multiomics Data Integration Open
Data reduction and data mining are common practices for handling large-scale data from wide-ranging sources, but high-dimensional omics and imaging data sets present difficult challenges for feature extraction and data mining due to the la…
View article: Tumor-associated neutrophil precursors impair homologous DNA repair and promote sensitivity to PARP inhibition
Tumor-associated neutrophil precursors impair homologous DNA repair and promote sensitivity to PARP inhibition Open
Tumor evolution is one of the major mechanisms responsible for acquiring therapy-resistant and more aggressive cancer clones. Whether the tumor microenvironment through immune-mediated mechanisms might promote the development of more aggre…
View article: Virtual Histological Staining as a Tool for Extending Renal Segmentation Across Stains
Virtual Histological Staining as a Tool for Extending Renal Segmentation Across Stains Open
In renal histopathology, the routine clinical use of several histological stains presents challenges for the direct application of stain-specific deep learning-based analysis tools to whole-slide images. We present an approach to the in si…
View article: KEAP1 and STK11/LKB1 alterations enhance vulnerability to ATR inhibition in KRAS mutant non-small cell lung cancer
KEAP1 and STK11/LKB1 alterations enhance vulnerability to ATR inhibition in KRAS mutant non-small cell lung cancer Open
KRAS mutations frequently co-occur with alterations in STK11/LKB1 and/or KEAP1, defining an aggressive subset of lung cancers resistant to immuno- and chemotherapy. While LKB1 loss is associated with vulnerability to DNA damage response-ba…
View article: Spatial metabolomics informs the use of clinical imaging for improved detection of cribriform prostate cancer
Spatial metabolomics informs the use of clinical imaging for improved detection of cribriform prostate cancer Open
Cribriform prostate cancer (crPCa) is associated with poor clinical outcomes, yet its accurate detection remains challenging due to the poor sensitivity of standard-of-care diagnostic tools. Here, we use untargeted spatial metabolomics to …
View article: Multimodal profiling unveils a reversible breast basal-like cell state in AKT-inhibitor resistant tumours
Multimodal profiling unveils a reversible breast basal-like cell state in AKT-inhibitor resistant tumours Open
The PI3K/AKT/mTOR pathway is central to cell metabolism and growth. However, pharmacological inhibition of the pathway is not uniformly effective across cancer types, or even within a single cancer model. In this study, we leverage oblique…
View article: Figure 4 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Figure 4 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Genetic targeting of p110β and its interaction with RAC1 sensitizes to MEK1/2 inhibition in vitro and in vivo.A, Left, flow cytometry–based cell-cycle profiling of WM266.4 cells following indicated 24-hour treatment. Right, proportion of W…
View article: Figure 2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Figure 2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Functional loss of PREX2 function sensitizes to MAPK inhibition in vitro and in vivo. A, Left, Kaplan–Meier overall survival of mice with the indicated genotypes and treatments. BRAF PTEN + vehicle (n = 8; median survival, 12.5 days) vs. B…
View article: Data from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Data from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Metastatic melanoma remains a major clinical challenge. Large-scale genomic sequencing of melanoma has identified bona fide activating mutations in RAC1, which are associated with resistance to BRAF-targeting therapies. Targeting the RAC1-…
View article: Supplementary Figures S1-S10 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Supplementary Figures S1-S10 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Supplementary Figures S1-S10 with associated figure legends.
View article: Supplementary Table S1 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Supplementary Table S1 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Reverse Phase Protein Array antibodies
View article: Supplementary Figures S1-S10 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Supplementary Figures S1-S10 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Supplementary Figures S1-S10 with associated figure legends.
View article: Supplementary Table S2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Supplementary Table S2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Cancer subtypes abbreviations
View article: Supplementary Table S1 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Supplementary Table S1 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Reverse Phase Protein Array antibodies
View article: Figure 5 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Figure 5 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Therapeutic targeting of MEK1/2 and the RAC1 effector p110β has marked therapeutic efficacy in melanoma in vivo. A, Left, Kaplan–Meier overall survival of mice harboring WM266.4 subcutaneous xenografts treated with vehicle (n = 5; median s…
View article: Supplementary Table S2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Supplementary Table S2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Cancer subtypes abbreviations
View article: Figure 3 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma
Figure 3 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma Open
Cotargeting of MEK1/2 and the RAC1 effector p110β suppresses growth of melanoma lines in vitro. A, Left, relative confluence of WM266.4 cells treated with indicated treatments over time. Representative of a minimum of five independent expe…
View article: Use of metabolic imaging to monitor heterogeneity of tumour response following therapeutic mTORC1/2 pathway inhibition
Use of metabolic imaging to monitor heterogeneity of tumour response following therapeutic mTORC1/2 pathway inhibition Open
The PI3K–mTOR–AKT pathway regulates tumour proliferation, gene expression and metabolism, but pathway inhibition induces heterogeneous feedback reactivation, limiting anti-tumour responses. Measuring heterogeneity of pathway inhibition in …
View article: List of Consortium Members from Visualizing Cancer Heterogeneity at the Molecular and Cellular Levels: Lessons from Rosetta
List of Consortium Members from Visualizing Cancer Heterogeneity at the Molecular and Cellular Levels: Lessons from Rosetta Open
Cancer Research UK Rosetta Grand Challenge consortium list of members
View article: Supplementary Figure 1 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Supplementary Figure 1 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Increased fibrosis in wild-type Kras deficient PanINs.
View article: Supplementary Figure 2 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Supplementary Figure 2 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Release from AZD6244 treatment results in rapid acinar to ductal metaplasia in KC KrasG12D/fl.
View article: Data from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Data from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Pancreatic cancer is characterized by the prevalence of oncogenic mutations in KRAS. Previous studies have reported that altered KRAS gene dosage drives progression and metastasis in pancreatic cancer. Whereas the role of oncogenic KRAS mu…
View article: Figure 3 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Figure 3 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Loss of WT KRAS induces increased MAPK signaling in KPC KrasG12D/fl. A, Experimental schematic representing mice imaged once weekly by ultrasound from 6 weeks of age to clinical endpoint to follow tumor growth over time. B, Tumor volume re…
View article: Supplementary Figure 6 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Supplementary Figure 6 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
MEK1/2 inhibition in KPC KrasG12D/fl mice with established tumours reverses enrichment of immune response related gene programmes.
View article: Supplementary Figure 4 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Supplementary Figure 4 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Loss of wild-type KRAS does not alter PI3K-AKT signalling.
View article: Supplementary Figure 3 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Supplementary Figure 3 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Acceleration of pancreatic tumour initiation after loss of wild-type Kras in KPC KrasG12D/fl mice.
View article: Figure 4 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Figure 4 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Late-stage intervention with MEK1/2 inhibition improves survival of KPC KrasG12D/fl mice. A, Experimental schematic. KPC KrasG12D/+ and KPC KrasG12D/fl mice were palpated for tumor burden, with palpable tumor burden confirmed by ultrasound…
View article: Figure 2 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Figure 2 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition Open
Early intervention with AZD6244 reduces PanIN burden in KrasG12D/fl mice. A, Experimental schematic. KC KrasG12D/fl were treated from day 42 for 28 days with vehicle or AZD6244 and sampled at day 70. B, Representative hematoxylin and eosin…