Marc Wiesehöfer
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View article: xCT as a potential marker for neuroendocrine cells in high-risk prostate cancer and the relation to AL122023.1-miR-26a/30d/30e axis
xCT as a potential marker for neuroendocrine cells in high-risk prostate cancer and the relation to AL122023.1-miR-26a/30d/30e axis Open
Prostate cancer is the second most common type of cancer in male worldwide. Stromal-epithelial interaction is thought to have a major impact on cancer development and progression. Previous studies have shown that interaction via soluble fa…
View article: Table S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Marker Genes in Clusters from YU-006
View article: Table S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Upregulated pathways in EGFR mutant cell lines transfected with ASCL1
View article: Figure S6 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S6 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
ASCL1 overexpression does not affect PC9 or H1975 cells. Drug response data in two additional lung cancer cell lines overexpressing ASCL1.
View article: Figure S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Drug tolerant residual disease is characterized by profound gene expression, but not mutational, changes compared to untreated tumors. Pyrosequencing results and mapping of bulk RNA-seq reads to mouse and human genome.
View article: Table S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Marker Genes in Clusters from YU-006
View article: Table S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Patient Information
View article: Table S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
WES Summary
View article: Figure S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Drug tolerant residual tumors exhibit variable levels of proliferation and low levels of apoptosis. IHC Quantification and additional IHC results to profile cell proliferation.
View article: Table S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Upregulated pathways in EGFR mutant cell lines transfected with ASCL1
View article: Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Changes in chromatin accessibility in HCC827 and PC9 cells upon ASCL1 expression. Global changes in chromatin accessibility in mutant EGFR lung cancer cell lines following ASCL1 overexpression and osimertinib treatment.
View article: Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
ASCL1 expression activates an EMT transcriptional program in permissive cellular contexts. Expression of individual EMT marker genes in mutant EGFR lung cancer cell lines and PDXs with or without ASCL1 overexpression.
View article: Figure S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Drug tolerant residual tumors exhibit variable levels of proliferation and low levels of apoptosis. IHC Quantification and additional IHC results to profile cell proliferation.
View article: Figure S5 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S5 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Characterization of mutant EGFR lung cancer PDXs at single-cell resolution. Workflow for scRNA-seq on PDXs and single cell data for an additional PDX.
View article: Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
ASCL1 expression activates an EMT transcriptional program in permissive cellular contexts. Expression of individual EMT marker genes in mutant EGFR lung cancer cell lines and PDXs with or without ASCL1 overexpression.
View article: Figure S6 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S6 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
ASCL1 overexpression does not affect PC9 or H1975 cells. Drug response data in two additional lung cancer cell lines overexpressing ASCL1.
View article: Figure S5 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S5 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Characterization of mutant EGFR lung cancer PDXs at single-cell resolution. Workflow for scRNA-seq on PDXs and single cell data for an additional PDX.
View article: Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Expression of signature genes in residual disease in PDXs.
View article: Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Changes in chromatin accessibility in HCC827 and PC9 cells upon ASCL1 expression. Global changes in chromatin accessibility in mutant EGFR lung cancer cell lines following ASCL1 overexpression and osimertinib treatment.
View article: Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Effects of erlotinib and TKI withdrawal on PDX growth.
View article: Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Expression of signature genes in residual disease in PDXs.
View article: Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Effects of erlotinib and TKI withdrawal on PDX growth.
View article: Figure S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S3 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Drug tolerant residual disease is characterized by profound gene expression, but not mutational, changes compared to untreated tumors. Pyrosequencing results and mapping of bulk RNA-seq reads to mouse and human genome.
View article: Table S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S2 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
WES Summary
View article: Table S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Table S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Patient Information
View article: Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S7 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
ASCL1 expression activates an EMT transcriptional program in permissive cellular contexts. Expression of individual EMT marker genes in mutant EGFR lung cancer cell lines and PDXs with or without ASCL1 overexpression.
View article: Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S4 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Expression of signature genes in residual disease in PDXs.
View article: Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Effects of erlotinib and TKI withdrawal on PDX growth.
View article: Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S1 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Effects of erlotinib and TKI withdrawal on PDX growth.
View article: Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts
Figure S8 from ASCL1 Drives Tolerance to Osimertinib in <i>EGFR</i> Mutant Lung Cancer in Permissive Cellular Contexts Open
Changes in chromatin accessibility in HCC827 and PC9 cells upon ASCL1 expression. Global changes in chromatin accessibility in mutant EGFR lung cancer cell lines following ASCL1 overexpression and osimertinib treatment.