Nora Bayani

UCSF Helen Diller Family Comprehensive Cancer Center — United States

Medicine · Health Sciences

13h-index4.6kcitations53works0.42yr avg
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Research Topics

Cancer Cells and Metastasis(14), Bioinformatics and Genomic Networks(11), Melanoma and MAPK Pathways(11), HER2/EGFR in Cancer Research(8), Gene expression and cancer classification(7)

Publications53 total

Data from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 6 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Table 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 5 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 7 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 3 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 1 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Dataset from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 4 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 8 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Table 1 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Supplementary Figure 9 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025Open Access
Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Cancer Discovery·2025· 6 citedOpen Access
Data from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
2023Open Access
Supplementary Figure 1 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
2023Open Access
Supplementary Figure 2 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
2023Open Access
Supplementary Figure Legends 1-2 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
2023Open Access
Supplementary Tables 1-6 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
2023Open Access
Data from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
2023Open Access
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Frequent Co-authors

Joe W. Gray(32), Olga K. Mirzoeva(27), Paul T. Spellman(25), Laura M. Heiser(25), Heidi S. Feiler(24), Richard M. Neve(17), Nicholas J. Wang(17), Reyno Delrosario(16), Quân Tran(16), Allan Balmain(16), James E. Korkola(15), Gordon B. Mills(15), Leslie A. Lange(14), Eve Kandyba(14), Kyle Halliwill(14), Laura Riva(14), John DiGiovanni(14), Ludmil B. Alexandrov(14), Frank McCormick(13), Debopriya Das(13)