Matthew C. Stubbs
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View article: Assessment of CD73 activity in breast cancer-derived small extracellular vesicles: application to monitoring of patients’ responses to immunotherapy
Assessment of CD73 activity in breast cancer-derived small extracellular vesicles: application to monitoring of patients’ responses to immunotherapy Open
View article: BIRC5 upregulation enhances DNMT3A-mutant T-ALL cell survival and pathogenesis
BIRC5 upregulation enhances DNMT3A-mutant T-ALL cell survival and pathogenesis Open
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematopoietic neoplasm. Although the prognosis of pediatric T-ALL has improved with intensified chemotherapy regimens, this benefit has largely not translated to the adult T-ALL …
View article: A randomised controlled trial of plasma exchange compared to standard of care in the treatment of severe COVID-19 infection (COVIPLEX)
A randomised controlled trial of plasma exchange compared to standard of care in the treatment of severe COVID-19 infection (COVIPLEX) Open
COVID-19 disease is associated with a hyperinflammatory, pro-thrombotic state and a high mortality. Our primary objective was to assess the change in inflammatory and thrombotic markers associated with PEX, and secondary objectives were to…
View article: Data from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Data from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Impairing the BET family coactivator BRD4 with small-molecule inhibitors (BETi) showed encouraging preclinical activity in treating acute myeloid leukemia (AML). However, dose-limiting toxicities and limited clinical activity dampened the …
View article: Table S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Table S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Table S1: Metabolomics Raw Data
View article: Figure S4 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S4 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S4: UK5099 does not enhance the efficacy of BETi in preventing MOLM-13 chimerism. NSGS mice were engrafted with MOLM-13 cells and treated with vehicle control, BETi (50 mg/kg) 5 times a week, twice daily and/or UK5099 (40 mg/kg) thr…
View article: Figure S3 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S3 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S3: CRISPR technology disrupts target genes. Expressions of (A) BRD4, (B, C) LDHB, and (C) MCT1 were disrupted in the indicated cell lines by CRISPR. The percent indel efficiency of the genetic disruption was quantified by TIDE anal…
View article: Data from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Data from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Impairing the BET family coactivator BRD4 with small-molecule inhibitors (BETi) showed encouraging preclinical activity in treating acute myeloid leukemia (AML). However, dose-limiting toxicities and limited clinical activity dampened the …
View article: Figure S4 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S4 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S4: UK5099 does not enhance the efficacy of BETi in preventing MOLM-13 chimerism. NSGS mice were engrafted with MOLM-13 cells and treated with vehicle control, BETi (50 mg/kg) 5 times a week, twice daily and/or UK5099 (40 mg/kg) thr…
View article: Figure S3 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S3 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S3: CRISPR technology disrupts target genes. Expressions of (A) BRD4, (B, C) LDHB, and (C) MCT1 were disrupted in the indicated cell lines by CRISPR. The percent indel efficiency of the genetic disruption was quantified by TIDE anal…
View article: Table S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Table S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Table S2: Characteristics of AML patient samples tested with BETi.
View article: Figure S5 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S5 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S5: Oxamate displays minimal toxicity to AML myeloblasts alone. AML myeloblasts were cultured for 72 hr with BETi (0.15 µM) and indicated lactate utilization inhibitors (AZD3965, UK5099, oxamate = 0.1 µM) and viability quantified us…
View article: Figure S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S1: Glutaminolysis and fatty acid oxidation does not allow MOLM-13 to metabolically bypass BET inhibition. (A) MV-4-11 and MOLM-13 cells were cultured for 72 hr with BETi (0.15 µM) and viability quantified using a fluorescent plate …
View article: Table S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Table S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Table S2: Characteristics of AML patient samples tested with BETi.
View article: Figure S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S2: Maximal respiration in MOLM-13 cells is unaffected by the addition of BETi and/or lactate utilization inhibitors. MV-4-11 and MOLM-13 cells were cultured for 72 hr with indicated treatments (BETi = 0.15 µM; AZD3965, UK5099, oxam…
View article: Figure S5 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S5 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S5: Oxamate displays minimal toxicity to AML myeloblasts alone. AML myeloblasts were cultured for 72 hr with BETi (0.15 µM) and indicated lactate utilization inhibitors (AZD3965, UK5099, oxamate = 0.1 µM) and viability quantified us…
View article: Figure S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S2 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S2: Maximal respiration in MOLM-13 cells is unaffected by the addition of BETi and/or lactate utilization inhibitors. MV-4-11 and MOLM-13 cells were cultured for 72 hr with indicated treatments (BETi = 0.15 µM; AZD3965, UK5099, oxam…
View article: Figure S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Figure S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Figure S1: Glutaminolysis and fatty acid oxidation does not allow MOLM-13 to metabolically bypass BET inhibition. (A) MV-4-11 and MOLM-13 cells were cultured for 72 hr with BETi (0.15 µM) and viability quantified using a fluorescent plate …
View article: Table S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Table S1 from Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Table S1: Metabolomics Raw Data
View article: Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia
Lactate Utilization Enables Metabolic Escape to Confer Resistance to BET Inhibition in Acute Myeloid Leukemia Open
Impairing the BET family coactivator BRD4 with small-molecule inhibitors (BETi) showed encouraging preclinical activity in treating acute myeloid leukemia (AML). However, dose-limiting toxicities and limited clinical activity dampened the …
View article: Caplacizumab Added to Plasma Exchange and Immunosuppression Accelerates Recovery and Improves Survival in Immune-Mediated TTP: An International Real-World Study of the IWG-TTP (The Capla 1000 Project)
Caplacizumab Added to Plasma Exchange and Immunosuppression Accelerates Recovery and Improves Survival in Immune-Mediated TTP: An International Real-World Study of the IWG-TTP (The Capla 1000 Project) Open
View article: Supplementary Table 2 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Supplementary Table 2 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Exome sequencing results.
View article: Supplementary Figures from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Supplementary Figures from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Supplementary Figures 1-7
View article: Supplementary Table 2 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Supplementary Table 2 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Exome sequencing results.
View article: Supplementary Figures from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Supplementary Figures from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Supplementary Figures 1-7
View article: Data from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Data from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Myeloproliferative neoplasms (MPN) are chronic blood diseases with significant morbidity and mortality. Although sequencing studies have elucidated the genetic mutations that drive these diseases, MPNs remain largely incurable with a signi…
View article: Supplementary Table 1 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Supplementary Table 1 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Hematological comparison of MF patients versus PDXs
View article: Supplementary Table 1 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Supplementary Table 1 from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Hematological comparison of MF patients versus PDXs
View article: Data from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms
Data from A Humanized Animal Model Predicts Clonal Evolution and Therapeutic Vulnerabilities in Myeloproliferative Neoplasms Open
Myeloproliferative neoplasms (MPN) are chronic blood diseases with significant morbidity and mortality. Although sequencing studies have elucidated the genetic mutations that drive these diseases, MPNs remain largely incurable with a signi…
View article: Data from Selective Inhibition of HDAC1 and HDAC2 as a Potential Therapeutic Option for B-ALL
Data from Selective Inhibition of HDAC1 and HDAC2 as a Potential Therapeutic Option for B-ALL Open
Purpose: Histone deacetylase inhibitors (HDACi) have recently emerged as efficacious therapies that target epigenetic mechanisms in hematologic malignancies. One such hematologic malignancy, B-cell acute lymphoblastic leukemia (B-AL…