Dean C. Singleton
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View article: Whole‐genome CRISPR‐Cas9 knockout screens identify <i>SHOC2</i> as a genetic dependency in <i>NRAS</i>‐mutant melanoma
Whole‐genome CRISPR‐Cas9 knockout screens identify <i>SHOC2</i> as a genetic dependency in <i>NRAS</i>‐mutant melanoma Open
View article: Megakaryocyte maturation involves activation of the adaptive unfolded protein response
Megakaryocyte maturation involves activation of the adaptive unfolded protein response Open
Endoplasmic reticulum stress triggers the unfolded protein response (UPR) to promote cell survival or apoptosis. Transient endoplasmic reticulum stress activation has been reported to trigger megakaryocyte production, and UPR activation ha…
View article: Clinical relevance and therapeutic predictive ability of hypoxia biomarkers in head and neck cancer tumour models
Clinical relevance and therapeutic predictive ability of hypoxia biomarkers in head and neck cancer tumour models Open
Tumour hypoxia promotes poor patient outcomes, with particularly strong evidence for head and neck squamous cell carcinoma (HNSCC). To effectively target hypoxia, therapies require selection biomarkers and preclinical models that can accur…
View article: Megakaryocyte maturation involves activation of the adaptive unfolded protein response
Megakaryocyte maturation involves activation of the adaptive unfolded protein response Open
Endoplasmic reticulum stress triggers the unfolded protein response (UPR) to promote cell survival or apoptosis. Transient endoplasmic reticulum stress activation has been reported to trigger megakaryocyte production, and UPR activation ha…
View article: Supplementary Figure 1 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 1 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
The expression of bicarbonate transporters in a panel of cell lines relative to the expression of β actin.
View article: Supplementary Figure 3 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 3 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Hypoxic induction of bicarbonate transporters in U87 between 24 and 96 hours and in DLD-1 at 72 hours.
View article: Supplementary Figure 4 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 4 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Hypoxic induction of SLC4A4, SLC4A5 and SLC4A9 at 1% oxygen in Ls174T, U87 and MDA-MB-231 between 24 and 72 hours.
View article: Supplementary Figure Legends from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure Legends from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Detailed Supplementary Figure Legends
View article: Supplementary Figure 7 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 7 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
S0859 treatment does not reduce DLD-1 spheroid growth rate but does reduce the number of Ki67 positive U87 cells in spheroids.
View article: Supplementary Figure 6 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 6 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Acidic pH does not reduce 2D cell survival in combination with SLC4A4 or SLC4A9 knockdown in U87, MDA-MB-231 and LS174T.
View article: Supplementary Figure 4 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 4 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Hypoxic induction of SLC4A4, SLC4A5 and SLC4A9 at 1% oxygen in Ls174T, U87 and MDA-MB-231 between 24 and 72 hours.
View article: Supplementary Figure 8 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 8 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
NDBT inhibition or knockdown increases the intracellular pH gradients, and doxycycline does not reduce the growth of U87 shCTL xenografts.
View article: Supplementary Figure 2 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 2 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Hypoxic induction of bicarbonate transporters in Ls174T between 24 and 96 hours.
View article: Supplementary Figure 6 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 6 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Acidic pH does not reduce 2D cell survival in combination with SLC4A4 or SLC4A9 knockdown in U87, MDA-MB-231 and LS174T.
View article: Data from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Data from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Tumor hypoxia is associated clinically with therapeutic resistance and poor patient outcomes. One feature of tumor hypoxia is activated expression of carbonic anhydrase IX (CA9), a regulator of pH and tumor growth. In this study, we invest…
View article: Supplementary Figure Legends from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure Legends from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Detailed Supplementary Figure Legends
View article: Supplementary Figure 2 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 2 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Hypoxic induction of bicarbonate transporters in Ls174T between 24 and 96 hours.
View article: Supplementary Figure 5 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 5 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Validation of HIF1α and HIF2α knockdown by quantitative-PCR in Ls174T.
View article: Supplementary Figure 5 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 5 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Validation of HIF1α and HIF2α knockdown by quantitative-PCR in Ls174T.
View article: Supplementary Figure 8 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 8 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
NDBT inhibition or knockdown increases the intracellular pH gradients, and doxycycline does not reduce the growth of U87 shCTL xenografts.
View article: Supplementary Figure 7 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 7 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
S0859 treatment does not reduce DLD-1 spheroid growth rate but does reduce the number of Ki67 positive U87 cells in spheroids.
View article: Supplementary Figure 1 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 1 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
The expression of bicarbonate transporters in a panel of cell lines relative to the expression of β actin.
View article: Supplementary Figure 3 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Supplementary Figure 3 from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Hypoxic induction of bicarbonate transporters in U87 between 24 and 96 hours and in DLD-1 at 72 hours.
View article: Data from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth
Data from Disrupting Hypoxia-Induced Bicarbonate Transport Acidifies Tumor Cells and Suppresses Tumor Growth Open
Tumor hypoxia is associated clinically with therapeutic resistance and poor patient outcomes. One feature of tumor hypoxia is activated expression of carbonic anhydrase IX (CA9), a regulator of pH and tumor growth. In this study, we invest…
View article: In vitro breast cancer models for studying mechanisms of resistance to endocrine therapy
In vitro breast cancer models for studying mechanisms of resistance to endocrine therapy Open
The development of endocrine resistance is a common reason for the failure of endocrine therapies in hormone receptor-positive breast cancer. This review provides an overview of the different types of in vitro models that have been develop…
View article: Patient-Derived Xenograft and Organoid Models for Precision Medicine Targeting of the Tumour Microenvironment in Head and Neck Cancer
Patient-Derived Xenograft and Organoid Models for Precision Medicine Targeting of the Tumour Microenvironment in Head and Neck Cancer Open
Patient survival from head and neck squamous cell carcinoma (HNSCC), the seventh most common cause of cancer, has not markedly improved in recent years despite the approval of targeted therapies and immunotherapy agents. Precision medicine…
View article: Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in triple-receptor negative breast cancer
Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in triple-receptor negative breast cancer Open
Background Glutamine serves as an important nutrient with many cancer types displaying glutamine dependence. Following cellular uptake glutamine is converted to glutamate in a reaction catalysed by mitochondrial glutaminase. This glutamate…
View article: Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in Triple-receptor Negative Breast Cancer
Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in Triple-receptor Negative Breast Cancer Open
Background Glutamine serves as an important nutrient with many cancer types displaying glutamine dependence. Following cellular uptake glutamine is converted to glutamate in a reaction catalysed by mitochondrial glutaminase. This glutamate…
View article: Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in Triple-receptor Negative Breast Cancer
Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in Triple-receptor Negative Breast Cancer Open
Background Glutamine serves as an important nutrient with many cancer types displaying glutamine dependence. Following cellular uptake glutamine is converted to glutamate in a reaction catalysed by mitochondrial glutaminase. This glutamate…
View article: N-Methyl-D-Aspartate Receptor Hypofunction in Meg-01 Cells Reveals a Role for Intracellular Calcium Homeostasis in Balancing Megakaryocytic-Erythroid Differentiation
N-Methyl-D-Aspartate Receptor Hypofunction in Meg-01 Cells Reveals a Role for Intracellular Calcium Homeostasis in Balancing Megakaryocytic-Erythroid Differentiation Open
The release of calcium ions (Ca2+) from the endoplasmic reticulum (ER) and related store-operated calcium entry (SOCE) regulate maturation of normal megakaryocytes. The N-methyl-D-aspartate (NMDA) receptor (NMDAR) provides an additional me…