Laura M. Millett
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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…
View article: Figure 1 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Figure 1 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 increases PanIN formation in the presence of oncogenic Kras. A, Kaplan–Meier survival curve for human patients with PDAC with KRAS alleles balanced and KRAS alleles imbalanced. KRAS balanced, n = 47; KRAS imbalanced, n = 32…
View article: Supplementary Figure 5 from <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
Supplementary Figure 5 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 sensitizes KPC KrasG12D/fl tumours to MEK1/2 inhibition.
View article: <i>KRAS</i> Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition
<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: The amino acid transporter SLC7A5 drives progression of PI3K-mutant intestinal cancer models and enhances response to MAPK-targeted therapy
The amino acid transporter SLC7A5 drives progression of PI3K-mutant intestinal cancer models and enhances response to MAPK-targeted therapy Open
Colorectal cancer (CRC) is a complex disease with key oncogenic pathways, including Wnt, MAPK, and PI3K, co-operating to drive tumour initiation and progression. Loss-of-function mutations in the Wnt-pathway inhibitor APC are the most prom…
View article: <i>KRAS</i>allelic imbalance drives tumour initiation yet suppresses metastasis in colorectal cancer<i>in vivo</i>
<i>KRAS</i>allelic imbalance drives tumour initiation yet suppresses metastasis in colorectal cancer<i>in vivo</i> Open
Oncogenic KRAS mutations are well-described functionally and are known to drive tumorigenesis. Recent reports describe a significant prevalence of KRAS allelic imbalances or gene dosage changes in human cancers, including loss of the wild-…