Michael Clarke
迈克尔·克拉克
MD
Associate Director for Research, Stanford Cancer Institute; Karel H. Vesely Professor斯坦福癌症研究所研究副主任；卡雷尔·韦塞利教授
👥Biography 个人简介
Michael Clarke, MD at Stanford University co-discovered breast cancer stem cells in 2003, identifying a CD44+/CD24-/low population capable of tumor initiation in NOD/SCID mice. His lab studies tumor hierarchy, self-renewal pathways (Bmi1, Wnt), and how microenvironmental signals maintain CSC states. His work has shaped the therapeutic targeting of breast CSCs.
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
Identification of Breast Cancer Stem Cells
Co-authored the 2003 Cell paper demonstrating that as few as 100 CD44+/CD24-/low breast cancer cells could form tumors in NOD/SCID mice while tens of thousands of other cells could not, establishing functional breast CSCs.
Bmi1 and Self-Renewal in Cancer
Showed that the polycomb gene Bmi1 is essential for self-renewal of both normal mammary stem cells and breast CSCs, linking developmental stem cell programs to tumor maintenance.
Tumor Microenvironment and CSC Niche
Demonstrated that signals from the tumor microenvironment, including hypoxia and cytokines, dynamically regulate the CSC state, highlighting plasticity within the cancer hierarchy.
Representative Works 代表性著作
Prospective identification of tumorigenic breast cancer cells
PNAS (2003)
Landmark identification of CD44+/CD24-/low breast cancer cells with tumor-initiating capacity in NOD/SCID mice, founding breast CSC biology.
The cancer stem cell hypothesis: a work in progress
Laboratory Investigation (2010)
Comprehensive review refining the CSC model, addressing hierarchical vs. plastic states and implications for therapy.
Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells
Nature (2003)
Established Bmi1 as a key regulator of stem cell self-renewal, later shown to be critical in breast CSC maintenance.
🏆Awards & Recognition 奖项与荣誉
📄Data Sources 数据来源
Last updated: 2026-01-15 | All information from publicly available academic sources
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