Shawn C. Chafe
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View article: 29 SNAT2 AS A NOVEL TARGETABLE VULNERABILITY IN RECURRENT GLIOBLASTOMA
29 SNAT2 AS A NOVEL TARGETABLE VULNERABILITY IN RECURRENT GLIOBLASTOMA Open
Glioblastoma (GBM) is the most fatal primary brain tumour. Standard-of-care consists of surgical resection followed by chemo-radiotherapy, but the tumour almost always recurs. There are currently no effective treatments at recurrence, and …
View article: PRCA-06 GENOME-WIDE IN VIVO CRISPR ACTIVATION SCREEN IDENTIFIES BACE1 AS A THERAPEUTIC VULNERABILITY OF LUNG CANCER BRAIN METASTASIS
PRCA-06 GENOME-WIDE IN VIVO CRISPR ACTIVATION SCREEN IDENTIFIES BACE1 AS A THERAPEUTIC VULNERABILITY OF LUNG CANCER BRAIN METASTASIS Open
Brain metastasis occurs in up to 40% of patients with non-small cell lung cancer (NSCLC). Considerable genomic heterogeneity exists between the primary lung tumor and respective brain metastasis; however, the identity of the genes capable …
View article: A genome-wide in vivo CRISPR activation screen identifies BACE1 as a therapeutic vulnerability of lung cancer brain metastasis
A genome-wide in vivo CRISPR activation screen identifies BACE1 as a therapeutic vulnerability of lung cancer brain metastasis Open
Brain metastasis occurs in up to 40% of patients with non–small cell lung cancer (NSCLC). Considerable genomic heterogeneity exists between the primary lung tumor and respective brain metastasis; however, the identity of the genes capable …
View article: Identification of intratumoral bacteria that enhance breast tumor metastasis
Identification of intratumoral bacteria that enhance breast tumor metastasis Open
The central, mortality-associated hallmark of cancer is the process of metastasis. It is increasingly recognized that bacteria influence multiple facets of cancer progression, but the extent to which tumor microenvironment-associated bacte…
View article: Pan-cancer<i>N</i>-glycoproteomic atlas of patient-derived xenografts uncovers FAT2 as a therapeutic target for head and neck cancers
Pan-cancer<i>N</i>-glycoproteomic atlas of patient-derived xenografts uncovers FAT2 as a therapeutic target for head and neck cancers Open
SUMMARY Cell surface proteins offer significant cancer therapeutic potential attributable to their accessible membrane localization and central role in cellular signaling. Despite this, their promise remains largely untapped due to the tec…
View article: TMET-34. PYROPTOSIS IS AN ACQUIRED VULNERABILITY OF BRAIN METASTASES
TMET-34. PYROPTOSIS IS AN ACQUIRED VULNERABILITY OF BRAIN METASTASES Open
Metastasis, the spread of cancer cells from one part of the body to another, is a leading cause of death among cancer patients. Three particularly dangerous forms of metastases are the spread of lung, skin, and breast cancers to the brain.…
View article: De novo GTP synthesis is a metabolic vulnerability for the interception of brain metastases
De novo GTP synthesis is a metabolic vulnerability for the interception of brain metastases Open
Patients with brain metastases (BM) face a 90% mortality rate within one year of diagnosis and the current standard of care is palliative. Targeting BM-initiating cells (BMICs) is a feasible strategy to treat BM, but druggable targets are …
View article: Supplementary Figure S4 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S4 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S4 shows that the combined loss of CAIX activity and the GSH synthesis axis of Gln metabolism increases cytotoxicity of hypoxic cancer cells.
View article: Supplementary Figure S6 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S6 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S6 shows IHC staining for 4-HNE in SUM159PT tumors, demonstrating that co-targeting CAIX/XII activity and GSH synthesis increases lipid peroxidation in vivo.
View article: Supplementary Figure S3 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S3 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S3 shows heatmaps showing the drug combination responses for cytotoxicity of cancer cells in hypoxia induced by SLC-0111 in combination with inhibition of Gln metabolism.
View article: Supplementary Figure S2 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S2 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S2 shows that CAIX catalytic activity and the CAIX intracellular domain regulate Gln uptake by hypoxic cancer cells.
View article: Supplementary Figure S4 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S4 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S4 shows that the combined loss of CAIX activity and the GSH synthesis axis of Gln metabolism increases cytotoxicity of hypoxic cancer cells.
View article: Data from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Data from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
The ability of tumor cells to alter their metabolism to support survival and growth presents a challenge to effectively treat cancers. Carbonic anhydrase IX (CAIX) is a hypoxia-induced, metabolic enzyme that plays a crucial role in pH regu…
View article: Supplementary Table S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Table S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Table S1 lists the shRNA sequences used to knock down gene expression of SLC1A5, GLS1 and GCLC in cancer cells.
View article: Supplementary Figure S5 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S5 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S5 shows heatmaps demonstrating that combined inhibition of CAIX activity and GCLC or RSL3 synergize to increase cytotoxicity of hypoxic cancer cells.
View article: Supplementary Figure S6 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S6 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S6 shows IHC staining for 4-HNE in SUM159PT tumors, demonstrating that co-targeting CAIX/XII activity and GSH synthesis increases lipid peroxidation in vivo.
View article: Supplementary Figure S3 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S3 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S3 shows heatmaps showing the drug combination responses for cytotoxicity of cancer cells in hypoxia induced by SLC-0111 in combination with inhibition of Gln metabolism.
View article: Supplementary Figure S2 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S2 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S2 shows that CAIX catalytic activity and the CAIX intracellular domain regulate Gln uptake by hypoxic cancer cells.
View article: Supplementary Table S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Table S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Table S1 lists the shRNA sequences used to knock down gene expression of SLC1A5, GLS1 and GCLC in cancer cells.
View article: Supplementary Figure S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S1 shows data describing the characterization of the interaction between SLC1A5 and CAIX in cancer cells.
View article: Supplementary Figure S5 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S5 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S5 shows heatmaps demonstrating that combined inhibition of CAIX activity and GCLC or RSL3 synergize to increase cytotoxicity of hypoxic cancer cells.
View article: Supplementary Figure S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells
Supplementary Figure S1 from A Carbonic Anhydrase IX/SLC1A5 axis regulates glutamine metabolism dependent ferroptosis in hypoxic tumor cells Open
Supplementary Figure S1 shows data describing the characterization of the interaction between SLC1A5 and CAIX in cancer cells.
View article: TRSC-04 DE NOVO GTP SYNTHESIS IS A METABOLIC VULNERABILITY FOR THE INTERCEPTION OF BRAIN METASTASES
TRSC-04 DE NOVO GTP SYNTHESIS IS A METABOLIC VULNERABILITY FOR THE INTERCEPTION OF BRAIN METASTASES Open
Patients with brain metastases (BM) face a 90% mortality rate within one year of diagnosis and the current standard of care is mainly palliative. Targeting BM-initiating cells (BMIC) is a feasible strategy to treat BM, but druggable target…
View article: Supplementary Data 1 from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases
Supplementary Data 1 from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases Open
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View article: Supplementary Data 1 from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases
Supplementary Data 1 from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases Open
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View article: Data from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases
Data from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases Open
Purpose:Brain metastases (BM) are mainly treated palliatively with an expected survival of less than 12 months after diagnosis. In many solid tumors, the human neural stem cell marker glycoprotein CD133 is a marker of a tumor-initiating ce…
View article: Data from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases
Data from Intratumoral Delivery of Chimeric Antigen Receptor T Cells Targeting CD133 Effectively Treats Brain Metastases Open
Purpose:Brain metastases (BM) are mainly treated palliatively with an expected survival of less than 12 months after diagnosis. In many solid tumors, the human neural stem cell marker glycoprotein CD133 is a marker of a tumor-initiating ce…
View article: Data from A Carbonic Anhydrase IX/SLC1A5 Axis Regulates Glutamine Metabolism Dependent Ferroptosis in Hypoxic Tumor Cells
Data from A Carbonic Anhydrase IX/SLC1A5 Axis Regulates Glutamine Metabolism Dependent Ferroptosis in Hypoxic Tumor Cells Open
The ability of tumor cells to alter their metabolism to support survival and growth presents a challenge to effectively treat cancers. Carbonic anhydrase IX (CAIX) is a hypoxia-induced, metabolic enzyme that plays a crucial role in pH regu…
View article: Supplementary Figure S5 from A Carbonic Anhydrase IX/SLC1A5 Axis Regulates Glutamine Metabolism Dependent Ferroptosis in Hypoxic Tumor Cells
Supplementary Figure S5 from A Carbonic Anhydrase IX/SLC1A5 Axis Regulates Glutamine Metabolism Dependent Ferroptosis in Hypoxic Tumor Cells Open
Supplementary Figure S5 shows heatmaps demonstrating that combined inhibition of CAIX activity and GCLC or RSL3 synergize to increase cytotoxicity of hypoxic cancer cells.