Olga K. Mirzoeva

University of California, San Francisco — United States

Medicine · Health Sciences

21h-index4.0kcitations91works1.72yr avg
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Research Topics

Pancreatic and Hepatic Oncology Research(31), Cancer Cells and Metastasis(18), Melanoma and MAPK Pathways(12), Cancer Genomics and Diagnostics(11), Cancer Mechanisms and Therapy(9)

Publications91 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
Stem-cell states converge in multistage cutaneous squamous cell carcinoma development
Science·2024· 21 cited
The interplay between dormant mutated cells and tumor promotion by chronic tissue damage in determining cancer risk
bioRxiv (Cold Spring Harbor Laboratory)·2024Open Access
Gene networks reveal stem-cell state convergence during preneoplasia and progression to malignancy in multistage skin carcinogenesis
2023· 2 citedOpen Access
Supplementary Figure Legends from Subtype-Specific MEK-PI3 Kinase Feedback as a Therapeutic Target in Pancreatic Adenocarcinoma
2023Open Access
Supplementary Table 1 from Subtype-Specific MEK-PI3 Kinase Feedback as a Therapeutic Target in Pancreatic Adenocarcinoma
2023Open Access
Supplementary Figure 1 from Subtype-Specific MEK-PI3 Kinase Feedback as a Therapeutic Target in Pancreatic Adenocarcinoma
2023Open Access
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Frequent Co-authors

W. Michael Korn(23), Nora Bayani(15), Andrew H. Ko(13), Eric A. Collisson(13), Reyno Delrosario(12), Allan Balmain(12), Eve Kandyba(11), Kyle Halliwill(11), Leslie A. Lange(11), Quân Tran(10), Di Wu(9), Melissa Quino Reeves(9), S. M. Ashiqul Islam(9), Laura Riva(9), Erik N. Bergstrom(9), Kavya Achanta(9), John DiGiovanni(9), Ludmil B. Alexandrov(9), Heidi S. Feiler(8), Joe W. Gray(8)