Supplementary Data from INK4 Tumor Suppressor Proteins Mediate Resistance to CDK4/6 Kinase Inhibitors
Supplementary Data from INK4 Tumor Suppressor Proteins Mediate Resistance to CDK4/6 Kinase Inhibitors
Publications
31 shownSupplementary Figure S8 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Cholesterol overload activates AP-1 via ERK signaling to mediate invasion upon GRAMD1B loss in melanoma.</p>
Supplementary Figure S5 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supp. Fig. S5 shows that GRAMD1B is a metastasis suppressor in human melanoma</p>
Supp Table S2 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supplementary Table S2. David GO analysis of AVAST-M signature</p>
Supplementary Figure S7 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Loss of GRAMD1B suppresses de novo cholesterol synthesis in melanoma cells.</p>
Supplementary Figure S2 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>CRISPR Sequencing of MAS2X tumors.</p>
Supp Table S5 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supplementary Table S5. Normalized Counts of transcripts in GRAMD1B KO and NT cells.</p>
Supp Table S4 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supp Table S4 has a list of antibodies and other resources</p>
Supplementary Figure S3 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Validation of gramd1b depletion in zebrafish cells and tumors.</p>
Supplementary Figure S1 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>The AVAST-M trial identifies a signature predictive of metastatic relapse</p>
Supp Table S3 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supp Table S3 has a List of Oligonucleotides Sequences</p>
Supplementary Figure S4 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>An in vivo screen identifies metastasis suppressors in melanoma.</p>
Supp Table S6 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supp Table S6 Differentially Expressed Genes</p>
Supplementary Table 3 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition
<p>ChIP-Seq results</p>
Supplementary Figure 1 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>Characterization of acquired resistance in vitro models</p>
Supplementary Table 2 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>Patients Progression Cell Free DNA data</p>
Supp Table S7 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supp Table S7: GSEA Analysis</p>
Supplementary Figure 3 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>RW7213 cell lines sequencing analysis</p>
Supplementary Figure 5 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>Oncoprint of baseline alterations in CRC patients who developed resistance to KRAS G12C and EGFR inhibitors</p>
Supplementary Figure 2 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>C106 cell lines single cell sequencing analysis</p>
Supplementary Table 1 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition
<p>Sequences of sgRNAs and primers</p>
Supplementary Figures from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition
<p>Supplementary Figures S1-S25</p>
Supplementary Figure 6 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>C106 resistant cells drug withdrawal and Patient #12 MSK-Impact data</p>
Supplementary Table 3 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>Patients Longitudinal Cell Free DNA data</p>
Supplementary Table 2 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition
<p>CRISPR screen results</p>
Supplementary Figure from INK4 Tumor Suppressor Proteins Mediate Resistance to CDK4/6 Kinase Inhibitors
Supplementary Figure from INK4 Tumor Suppressor Proteins Mediate Resistance to CDK4/6 Kinase Inhibitors
Supplementary Table 1 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>Patients Characteristics</p>
Supplementary Figure 4 from Molecular Characterization of Acquired Resistance to KRAS<sup>G12C</sup>–EGFR Inhibition in Colorectal Cancer
<p>Generation of acquired resistance PDX model</p>
Supplementary Figure S6 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Loss of GRAMD1B promotes tumor cell invasion in human melanoma cells</p>
Supplementary Table 4 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition
<p>RNA-Seq results</p>
Supp Table S1 from Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma
<p>Supplementary Table S1. List of genes predictive of metastasis from AVAST-M trial. </p>
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- Publications
- 31
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- 0000-0002-3873-315X
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