James C. Cusack
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The Impact of the Gut Microbiome, Environment, and Diet in Early-Onset Colorectal Cancer Development Open
Traditionally considered a disease common in the older population, colorectal cancer is increasing in incidence among younger demographics. Evidence suggests that populational- and generational-level shifts in the composition of the human …
View article: Weakly supervised segmentation models as explainable radiological classifiers for lung tumour detection on CT images
Weakly supervised segmentation models as explainable radiological classifiers for lung tumour detection on CT images Open
Purpose Interpretability is essential for reliable convolutional neural network (CNN) image classifiers in radiological applications. We describe a weakly supervised segmentation model that learns to delineate the target object, trained wi…
Ultrasound Guided Cryoablation of Morton’s Neuroma: Case Series Including Post-Ablation MRI Appearances Open
Category: Midfoot/Forefoot; Other Introduction/Purpose: Morton’s neuroma (MN) is a very common compressive neuropathy of the interdigital nerve. Non- operative management is recommended initially and many therapies have been described. Cry…
Supplementary Figure 4 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 4 - PDF file 44K, CRM1 inhibition induces a statistically significant increase in caspase-3/7 activity as single therapy or in combination with BRAF inhibition
Supplementary Figure 1 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 1 - PDF file 29K, CRM1 and BRAF inhibition decrease melanoma cell proliferation and are synergistic in vitro
Supplementary Methods and Figure Legends from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Methods and Figure Legends - PDF 133K, Supplementary methods and figure legends
Supplementary Figure 1 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 1 - PDF file 29K, CRM1 and BRAF inhibition decrease melanoma cell proliferation and are synergistic in vitro
Supplementary Figure 6 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 6 - PDF file 57K, CRM1/BRAF inhibition in PTEN null/BRAF mutant melanoma Xenograft model
Data from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Resistance to BRAF inhibitor therapy places priority on developing BRAF inhibitor-based combinations that will overcome de novo resistance and prevent the emergence of acquired mechanisms of resistance. The CRM1 receptor mediates the nucle…
Supplementary Figure 7 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 7 - PDF file, TP53 knockdown in A375 reduces the effect of CRM1 inhibition on A375 proliferation but not on caspase-3/7 activity
Supplementary Figure 3 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 3 - PDF 313K, CRM1 inhibition induces cell cycle arrest and increases cell death when combined with BRAF inhibition
Data from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Resistance to BRAF inhibitor therapy places priority on developing BRAF inhibitor-based combinations that will overcome de novo resistance and prevent the emergence of acquired mechanisms of resistance. The CRM1 receptor mediates the nucle…
Supplementary Figure 7 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 7 - PDF file, TP53 knockdown in A375 reduces the effect of CRM1 inhibition on A375 proliferation but not on caspase-3/7 activity
Supplementary Figure 2 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 2 - PDF 191K, CRM1 inhibition induces cell cycle arrest and increases cell death when combined with BRAF inhibition
Supplementary Figure 3 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 3 - PDF 313K, CRM1 inhibition induces cell cycle arrest and increases cell death when combined with BRAF inhibition
Supplementary Figure 4 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 4 - PDF file 44K, CRM1 inhibition induces a statistically significant increase in caspase-3/7 activity as single therapy or in combination with BRAF inhibition
Supplementary Figure 5 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 5 - PDF file 894K, CRM1 inhibition leads to delayed tumor growth independent of BRAF or NRAS status in melanoma xenograft models
Supplementary Figure 6 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 6 - PDF file 57K, CRM1/BRAF inhibition in PTEN null/BRAF mutant melanoma Xenograft model
Supplementary Methods and Figure Legends from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Methods and Figure Legends - PDF 133K, Supplementary methods and figure legends
Supplementary Figure 2 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 2 - PDF 191K, CRM1 inhibition induces cell cycle arrest and increases cell death when combined with BRAF inhibition
Supplementary Figure 5 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 5 - PDF file 894K, CRM1 inhibition leads to delayed tumor growth independent of BRAF or NRAS status in melanoma xenograft models
Data from Activation of PI3K Signaling in Merkel Cell Carcinoma Open
Purpose: Merkel cell carcinoma (MCC) is an aggressive cutaneous neuroendocrine tumor, often metastatic at presentation, for which current chemotherapeutic regimens are largely ineffective. As its pathogenesis is still unknown, we hypothesi…
Supplementary Table 2 from Activation of PI3K Signaling in Merkel Cell Carcinoma Open
PDF file - 62K
View article: Data from Minimal Residual Disease Detection using a Plasma-only Circulating Tumor DNA Assay in Patients with Colorectal Cancer
Data from Minimal Residual Disease Detection using a Plasma-only Circulating Tumor DNA Assay in Patients with Colorectal Cancer Open
Purpose:Detection of persistent circulating tumor DNA (ctDNA) after curative-intent surgery can identify patients with minimal residual disease (MRD) who will ultimately recur. Most ctDNA MRD assays require tumor sequencing to identify tum…
Data from XPO1 Inhibition Enhances Radiation Response in Preclinical Models of Rectal Cancer Open
Purpose: Combination of radiation with radiosensitizing chemotherapeutic agents improves outcomes for locally advanced rectal cancer. Current treatment includes 5-fluorouracil–based chemoradiation prior to surgical resection; however patho…
Supplementary Table 1 from Activation of PI3K Signaling in Merkel Cell Carcinoma Open
PDF file - 25K
Supplementary Table 1 from Activation of PI3K Signaling in Merkel Cell Carcinoma Open
PDF file - 25K
Supplementary Figures 1-4 from XPO1 Inhibition Enhances Radiation Response in Preclinical Models of Rectal Cancer Open
Supplementary Figure 1. Selinexor induces HT29 and LoVo cell apoptosis; Supplementary Figure 2. Combination of radiation and Selinexor reduces tumor cell radiation survival; Supplementary Figure 3. Body weight of female nude mice; Suppleme…
Supplementary Table 4 from Activation of PI3K Signaling in Merkel Cell Carcinoma Open
PDF file - 52K