Allan Balmain

University of California, San Francisco

Full Professor(heuristic)

Cancer-related Molecular Pathways · Oncology

h-index73

i10-index191

Publications337

Citations24,666

Grants

50 total · 4 active

NIH #2R35CA210018-08A1

Systems genetics analysis of tumor evolution in the mouse

Active

Amount: $817K
Period: 2017-06-01 → 2032-07-31
PIs: 1
Est. capacity / PI: ~5 students

NIH #4R01CA285426-03

A network approach to interrogate cellular plasticity and drug resistance in cancer

Active

Amount: $2.0M
Period: 2024-06-15 → 2029-05-31
PIs: 2
Est. capacity / PI: ~9 students

NIH #1R01CA285426-01A1

A network approach to interrogate cellular plasticity and drug resistance in cancer

Active

Amount: $672K
Period: 2024-06-15 → 2029-05-31
PIs: 2
Est. capacity / PI: ~3 students

Student capacity is a rough estimate from remaining award size, split equally among PIs. Actual funding decisions vary.

Lab Funding Health

Find elsewhere

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In-Field Influence

0.0015

PageRank within Oncology co-authorship network

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Admission Signals

New paper: Chemically induced skin tumors arise from long-lived stem cells of the upper hair follicle (Science)2026-06-11
New preprint: Cross-Species and Tissue-Agnostic Prediction of Human Cancer Treatment Response using AI-Powered Cellular Morphometric Biomarkers from a Genetically Diverse Erbb2 Mouse Model2025-09-15
New NIH award: $2,038K — A network approach to interrogate cellular plasticity and drug resistance in cancer2024-06-15
New NIH award: $672K — A network approach to interrogate cellular plasticity and drug resistance in cancer2024-06-15
New NIH award: $1,264K — PROMINENT - UCSF2022-06-22
New NIH award: $817K — Systems genetics analysis of tumor evolution in the mouse2017-06-01

Data Freshness

Publications as of 2026-07-01
Grants as of 2026-06-30

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ORCID: 0000-0001-6549-7861

Career Trajectory

Research Cluster Map

Direct collaborators. Node size = influence, colour = community, dashed = past collaboration.

Potential Collaborators

Recent Publications

Last 2 years · showing 20 of 21

Chemically induced skin tumors arise from long-lived stem cells of the upper hair follicle
Science · 2026-06-11
Tumour promotion through the lens of evolution
Nature · 2026-04-15 · 3 citations
Cross-Species and Tissue-Agnostic Prediction of Human Cancer Treatment Response using AI-Powered Cellular Morphometric Biomarkers from a Genetically Diverse Erbb2 Mouse ModelPreprint
medRxiv · 2025-09-15
0887 Long-lived and genetically-diverse skin organoids derived from murine adult hair follicle stem cells
Journal of Investigative Dermatology · 2025-07-21 · 1 citations
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 DamagePreprint
2025-06-03
Data from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
Supplementary Dataset from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue DamagePreprint
2025-06-03
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
2025-06-03
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
2025-06-03
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 DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
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 DamagePreprint
2025-06-03
Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Cancer Discovery · 2025-03-12 · 13 citations
Implementing Mutational Epidemiology on a Global Scale: Lessons from Mutographs
Cancer Discovery · 2025-01-13 · 15 citations
An AI-Powered tissue-agnostic cellular morphometrics biomarker for risk assessment in patients with pan-gastrointestinal precancerous lesions and cancersPreprint
medRxiv · 2024-11-15

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