Shu Xuan Ng
A5080619491- Drug Transport and Resistance Mechanisms
- RNA Interference and Gene Delivery
- Cancer therapeutics and mechanisms
- Ferrocene Chemistry and Applications
- DNA and Nucleic Acid Chemistry
- Protein Degradation and Inhibitors
- Metal complexes synthesis and properties
- Acute Myeloid Leukemia Research
- Retinoids in leukemia and cellular processes
- Antibiotics Pharmacokinetics and Efficacy
- Histone Deacetylase Inhibitors Research
- Click Chemistry and Applications
- Transplantation: Methods and Outcomes
- Organ Transplantation Techniques and Outcomes
- Monoclonal and Polyclonal Antibodies Research
- Liver Disease and Transplantation
National University of Singapore
2023-2024
National University Hospital
2015
Ligand Pharmaceuticals (United States)
2006
Abstract In many cancers, mortality is associated with the emergence of relapse multidrug resistance (MDR). Thus far, investigation cancer mechanisms has largely focused on acquired genetic mutations. Using acute myeloid leukemia (AML) patient-derived xenografts (PDX), we systematically elucidated a basis MDR and identified drug sensitivity in relapsed AML. We derived pharmacologic for 22 AML PDX models using dynamic BH3 profiling (DBP), together genomics transcriptomics. vivo resistant...
<p>Supplemental Table 2 shows sample IDs submitted for RNA-seq.</p>
<p>Supplemental Table 4 shows raw baseline BH3 profiling data on matched pre- and post-resistant AML PDX models.</p>
<p>Supplemental Figure 2 shows RNA-seq signature of drug-resistant AML PDX models.</p>
<p>Supplemental Figure 3 shows MDR mechanisms contribute to drug resistance in AML PDX models.</p>
<p>Supplemental Table 3 shows overlapping gene sets contributing to KEGG pathway enrichment between acquired resistant PDX models and relapsed AML patients.</p>
<p>Supplemental Figure 6 shows drug response data in AML patient samples at diagnosis and relapse.</p>
<p>Supplemental Table 1 shows clinical and genetic characteristics for AML PDXs.</p>
<p>Supplemental Table 1 shows clinical and genetic characteristics for AML PDXs.</p>
<p>Supplemental table legends 1-4.</p>
<p>Supplemental Figure 11 shows comparison of leukemia-related genetic mutations in drug-resistant and parental AML PDX models.</p>
<p>Supplemental Figure 8 shows ex vivo DBP profiling in AML PDX models guides generation of drug-resistant PDXs.</p>
<p>Supplemental Figure 12 shows targeted agents cluster by mechanism of action.</p>
<p>Supplemental Figure 9 shows FLT-3 ITD+ AML cell lines and PDX models are sensitive to inhibitors identified by DBP across compartments.</p>
<p>Supplemental Figure 7 shows relapsed or primary refractory AML patients demonstrate reduced ex vivo drug sensitivity compared to diagnosis patients.</p>
<p>Supplemental Figure 1 shows dynamic BH3 profiling of healthy human CD34+ cells.</p>
<p>Supplemental Figure 11 shows comparison of leukemia-related genetic mutations in drug-resistant and parental AML PDX models.</p>
<p>Supplemental Figure 8 shows ex vivo DBP profiling in AML PDX models guides generation of drug-resistant PDXs.</p>
<p>Supplemental Figure 9 shows FLT-3 ITD+ AML cell lines and PDX models are sensitive to inhibitors identified by DBP across compartments.</p>
<p>Supplemental Figure 12 shows targeted agents cluster by mechanism of action.</p>
<p>Supplemental Figure 5 shows DBP identified drug sensitivities in resistant vs parental AML PDX models.</p>
<p>Supplemental Figure 4 shows differential expression of BCL-2 family related genes and proteins in drug-resistant AML PDX models.</p>
<p>Supplemental Figure 5 shows DBP identified drug sensitivities in resistant vs parental AML PDX models.</p>