Stanford University

Quan TranMD

MD · Stanford

Residency · Internal Medicine Residency, Stanford University

ORCID 0000-0002-5769-3480

publications

first author

median RCR

7.51

citations

Publications

2026
CD39+CD49a+CD103+ cytotoxic tissue-resident natural killer cells infiltrate and control solid epithelial tumor growth in mice
Science Translational Medicine
2026
Effect of race and sex on lupus diagnosis in primary care: A randomized factorial survey study.
PloS one0 citesPMID 41650210
2025
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
2025
Data from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
2025
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
2025
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
2025
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
2025
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
2025
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
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
2025
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
2025
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
2025
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
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
2025
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
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
2024
TeleHelp Ukraine: A distributed international telemedicine response to the ongoing war.
Journal of global healthRCR 0.964 citesPMID 39451063
2023
Oral cavity cancer in young, non-smoking, and non-drinking patients: a contemporary review.
Critical reviews in oncology/hematologyRCR 7.5150 citesPMID 37633348
2021
Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells
Nature Communications
2021
Humanized Mouse Models for the Advancement of Innate Lymphoid Cell-Based Cancer Immunotherapies
Frontiers in Immunology
2017
DGAT1-Dependent Lipid Droplet Biogenesis Protects Mitochondrial Function during Starvation-Induced Autophagy
Developmental Cell

Compiled from public program rosters and open scholarly data (PubMed, OpenAlex, ORCID) with field-normalized impact (NIH iCite RCR). Publication attribution is being actively improved; counts shown are conservative.