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( A ) Heatmap showing copy number variations (CNV) of premalignant (n=1), early stage (n=11), and end stage (n=34) NCpE tumors in chromosomes 1-19. There is variability in copy number profiles across all tumors, with an enrichment in the end-stage tumors. ( B ) Gene ontology Biological Process (GO BP) enrichment analysis comparing representative enriched terms of highly expressed genes between BRAF-wildtype (WT) and BRAF-mutant NCpE tumors. The dot size represents the number of genes, and the color scale reflects the significance level. ( C ) Heatmap depicting the expression patterns of stemness, proliferation, developmental, HGG-associated, and Ras-Mapk-associated genes across early stage BRAF-WT (n=7), early stage BRAF-mutant (n=5), end stage BRAF-WT (n=7) and end stage BRAF-mutant (n=4) NCpE tumors. ( D–F ) Normalized expression levels of Braf across early and end-stage samples; **** p <0.0001. ( D ), between Braf -WT and Braf mutant samples in early stage samples ( E ), and between Braf -WT and Braf mutant samples in end stage samples ( F ). ( G ) Relative cell viability of NCpE-derived tumor cells and to BRAF <t>inhibitors:</t> Naporafenib, Exarafenib, Belverafenib, and Dabrafenib; and <t>MEK</t> inhibitors: Cobimetinib and Trametinib (all used at 5 mM). NCpE-derived cells were of early-stage BRAF-mutant (N=2), end-stage BRAF-mutant (N=2), and end-stage BRAF-WT (N=4) status. Data shown represent mean ± [SEM] normalized to the DMSO-treated control. ( H ) Normalized expression levels of Braf , Map2k1 , and Map2k2 across the end stage NCpE-tumor derived cell lines.
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( A ) Heatmap showing copy number variations (CNV) of premalignant (n=1), early stage (n=11), and end stage (n=34) NCpE tumors in chromosomes 1-19. There is variability in copy number profiles across all tumors, with an enrichment in the end-stage tumors. ( B ) Gene ontology Biological Process (GO BP) enrichment analysis comparing representative enriched terms of highly expressed genes between BRAF-wildtype (WT) and BRAF-mutant NCpE tumors. The dot size represents the number of genes, and the color scale reflects the significance level. ( C ) Heatmap depicting the expression patterns of stemness, proliferation, developmental, HGG-associated, and Ras-Mapk-associated genes across early stage BRAF-WT (n=7), early stage BRAF-mutant (n=5), end stage BRAF-WT (n=7) and end stage BRAF-mutant (n=4) NCpE tumors. ( D–F ) Normalized expression levels of Braf across early and end-stage samples; **** p <0.0001. ( D ), between Braf -WT and Braf mutant samples in early stage samples ( E ), and between Braf -WT and Braf mutant samples in end stage samples ( F ). ( G ) Relative cell viability of NCpE-derived tumor cells and to BRAF <t>inhibitors:</t> Naporafenib, Exarafenib, Belverafenib, and Dabrafenib; and <t>MEK</t> inhibitors: Cobimetinib and Trametinib (all used at 5 mM). NCpE-derived cells were of early-stage BRAF-mutant (N=2), end-stage BRAF-mutant (N=2), and end-stage BRAF-WT (N=4) status. Data shown represent mean ± [SEM] normalized to the DMSO-treated control. ( H ) Normalized expression levels of Braf , Map2k1 , and Map2k2 across the end stage NCpE-tumor derived cell lines.
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( A ) Heatmap showing copy number variations (CNV) of premalignant (n=1), early stage (n=11), and end stage (n=34) NCpE tumors in chromosomes 1-19. There is variability in copy number profiles across all tumors, with an enrichment in the end-stage tumors. ( B ) Gene ontology Biological Process (GO BP) enrichment analysis comparing representative enriched terms of highly expressed genes between BRAF-wildtype (WT) and BRAF-mutant NCpE tumors. The dot size represents the number of genes, and the color scale reflects the significance level. ( C ) Heatmap depicting the expression patterns of stemness, proliferation, developmental, HGG-associated, and Ras-Mapk-associated genes across early stage BRAF-WT (n=7), early stage BRAF-mutant (n=5), end stage BRAF-WT (n=7) and end stage BRAF-mutant (n=4) NCpE tumors. ( D–F ) Normalized expression levels of Braf across early and end-stage samples; **** p <0.0001. ( D ), between Braf -WT and Braf mutant samples in early stage samples ( E ), and between Braf -WT and Braf mutant samples in end stage samples ( F ). ( G ) Relative cell viability of NCpE-derived tumor cells and to BRAF <t>inhibitors:</t> Naporafenib, Exarafenib, Belverafenib, and Dabrafenib; and <t>MEK</t> inhibitors: Cobimetinib and Trametinib (all used at 5 mM). NCpE-derived cells were of early-stage BRAF-mutant (N=2), end-stage BRAF-mutant (N=2), and end-stage BRAF-WT (N=4) status. Data shown represent mean ± [SEM] normalized to the DMSO-treated control. ( H ) Normalized expression levels of Braf , Map2k1 , and Map2k2 across the end stage NCpE-tumor derived cell lines.
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( A ) Heatmap showing copy number variations (CNV) of premalignant (n=1), early stage (n=11), and end stage (n=34) NCpE tumors in chromosomes 1-19. There is variability in copy number profiles across all tumors, with an enrichment in the end-stage tumors. ( B ) Gene ontology Biological Process (GO BP) enrichment analysis comparing representative enriched terms of highly expressed genes between BRAF-wildtype (WT) and BRAF-mutant NCpE tumors. The dot size represents the number of genes, and the color scale reflects the significance level. ( C ) Heatmap depicting the expression patterns of stemness, proliferation, developmental, HGG-associated, and Ras-Mapk-associated genes across early stage BRAF-WT (n=7), early stage BRAF-mutant (n=5), end stage BRAF-WT (n=7) and end stage BRAF-mutant (n=4) NCpE tumors. ( D–F ) Normalized expression levels of Braf across early and end-stage samples; **** p <0.0001. ( D ), between Braf -WT and Braf mutant samples in early stage samples ( E ), and between Braf -WT and Braf mutant samples in end stage samples ( F ). ( G ) Relative cell viability of NCpE-derived tumor cells and to BRAF inhibitors: Naporafenib, Exarafenib, Belverafenib, and Dabrafenib; and MEK inhibitors: Cobimetinib and Trametinib (all used at 5 mM). NCpE-derived cells were of early-stage BRAF-mutant (N=2), end-stage BRAF-mutant (N=2), and end-stage BRAF-WT (N=4) status. Data shown represent mean ± [SEM] normalized to the DMSO-treated control. ( H ) Normalized expression levels of Braf , Map2k1 , and Map2k2 across the end stage NCpE-tumor derived cell lines.

Journal: bioRxiv

Article Title: Convergence on BRAF and MAPK Signaling in Glioma Development in a P53-ENU model

doi: 10.64898/2026.02.23.707201

Figure Lengend Snippet: ( A ) Heatmap showing copy number variations (CNV) of premalignant (n=1), early stage (n=11), and end stage (n=34) NCpE tumors in chromosomes 1-19. There is variability in copy number profiles across all tumors, with an enrichment in the end-stage tumors. ( B ) Gene ontology Biological Process (GO BP) enrichment analysis comparing representative enriched terms of highly expressed genes between BRAF-wildtype (WT) and BRAF-mutant NCpE tumors. The dot size represents the number of genes, and the color scale reflects the significance level. ( C ) Heatmap depicting the expression patterns of stemness, proliferation, developmental, HGG-associated, and Ras-Mapk-associated genes across early stage BRAF-WT (n=7), early stage BRAF-mutant (n=5), end stage BRAF-WT (n=7) and end stage BRAF-mutant (n=4) NCpE tumors. ( D–F ) Normalized expression levels of Braf across early and end-stage samples; **** p <0.0001. ( D ), between Braf -WT and Braf mutant samples in early stage samples ( E ), and between Braf -WT and Braf mutant samples in end stage samples ( F ). ( G ) Relative cell viability of NCpE-derived tumor cells and to BRAF inhibitors: Naporafenib, Exarafenib, Belverafenib, and Dabrafenib; and MEK inhibitors: Cobimetinib and Trametinib (all used at 5 mM). NCpE-derived cells were of early-stage BRAF-mutant (N=2), end-stage BRAF-mutant (N=2), and end-stage BRAF-WT (N=4) status. Data shown represent mean ± [SEM] normalized to the DMSO-treated control. ( H ) Normalized expression levels of Braf , Map2k1 , and Map2k2 across the end stage NCpE-tumor derived cell lines.

Article Snippet: The MEK inhibitors were obtained from Cedarlane/MedChemExpress (Cobimetinib, HY-13064; Tremetinib, HY-10999).

Techniques: Mutagenesis, Expressing, Derivative Assay, Control