Mitchell Flagg
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Transcriptional subtypes of glottic cancer characterized by differential activation of canonical oncogenic programming Open
Background There is a paucity of data concerning molecular heterogeneity among glottic squamous cell carcinoma, and the clinical implications thereof. Methods Data corresponding to glottic squamous cell carcinoma were derived from The Canc…
View article: Supplementary Figure 2 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients
Supplementary Figure 2 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients Open
PDF file - 212K, Fig. S2. Ligand-dependent PDGFRβ stimulation promotes the proliferation of erlotinib-treated glioblastoma cells.
View article: Data from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients
Data from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients Open
Acquired resistance to tyrosine kinase inhibitors (TKI) represents a major challenge for personalized cancer therapy. Multiple genetic mechanisms of acquired TKI resistance have been identified in several types of human cancer. However, th…
View article: Data from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients
Data from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients Open
Acquired resistance to tyrosine kinase inhibitors (TKI) represents a major challenge for personalized cancer therapy. Multiple genetic mechanisms of acquired TKI resistance have been identified in several types of human cancer. However, th…
View article: Supplementary Figure 2 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients
Supplementary Figure 2 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients Open
PDF file - 212K, Fig. S2. Ligand-dependent PDGFRβ stimulation promotes the proliferation of erlotinib-treated glioblastoma cells.
View article: Supplementary Figure 1 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients
Supplementary Figure 1 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients Open
PDF file - 199K, Fig. S1. EGFRvIII and wild type EGFR signaling regulate PDGFRβ in vitro.
View article: Supplementary Figure 1 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients
Supplementary Figure 1 from De-Repression of <i>PDGFRβ</i> Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients Open
PDF file - 199K, Fig. S1. EGFRvIII and wild type EGFR signaling regulate PDGFRβ in vitro.
View article: Table S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription
Table S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Survival analysis of Institutional HPV positive tumors by ecDNA and hybrid classification.
View article: Figure S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription
Figure S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Principal component analyses of utilization of canonical HPV splice sites in institutional and TCGA cohorts.
View article: Figure S3 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription
Figure S3 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Downstream expression at site of integration of human/viral hybrid RNA sequence.
View article: Supplementary Legend from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription
Supplementary Legend from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Supplementary Legend
Supplementary Legend from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Supplementary Legend
View article: Table S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription
Table S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Survival analysis of Institutional HPV positive tumors by ecDNA and hybrid classification.
Table S1 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Clinical Data of Institutional Cohort.
Figure S1 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Output from Amplicon Architect of the institutional and TCGA cohorts. URL: dx.doi.org/10.6084/m9.figshare.13520087
Data from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Purpose:Human papillomavirus (HPV) plays a major role in oncogenesis and circular extrachromosomal DNA (ecDNA) is found in many cancers. However, the relationship between HPV and circular ecDNA in human cancer is not understood.Experimenta…
Table S2 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
List of Genes Upregulated With ecDNA.
Figure S2 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Non-canonical virus structures.
Figure S4 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Principal component analyses of utilization of canonical HPV splice sites in institutional and TCGA cohorts.
Figure S3 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Downstream expression at site of integration of human/viral hybrid RNA sequence.
Figure S1 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Output from Amplicon Architect of the institutional and TCGA cohorts. URL: dx.doi.org/10.6084/m9.figshare.13520087
Figure S5 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Verification of full-length transcript identified by Amplicon Architect.
Table S1 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Clinical Data of Institutional Cohort.
Table S3 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Survival analysis of TCGA HPV positive tumors by ecDNA and hybrid classification.
Table S2 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
List of Genes Upregulated With ecDNA.
Figure S2 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Non-canonical virus structures.
Figure S5 from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Verification of full-length transcript identified by Amplicon Architect.
Data from Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription Open
Purpose:Human papillomavirus (HPV) plays a major role in oncogenesis and circular extrachromosomal DNA (ecDNA) is found in many cancers. However, the relationship between HPV and circular ecDNA in human cancer is not understood.Experimenta…