Tyler Jacks
泰勒·杰克斯
PhD
David H. Koch Professor of Biology; Former Director, Koch Institute for Integrative Cancer Research大卫·科赫生物学教授；科赫综合癌症研究所前任主任
👥Biography 个人简介
Tyler Jacks is a world leader in cancer mouse modeling and tumor suppressor biology. His laboratory created foundational genetically engineered mouse models for p53, RB1, NF1, and KRAS-driven lung cancer, transforming preclinical oncology research. His Kras/p53 lung adenocarcinoma model remains the most widely used NSCLC preclinical platform globally.
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
p53 Knockout Mouse Model
Generated the first p53-null mouse demonstrating spontaneous tumor development, providing the gold-standard in vivo model for studying p53's tumor suppressive functions and therapeutic targeting.
KRAS/p53 Conditional Lung Cancer Mouse Model
Developed the Kras(G12D); Trp53(fl/fl) conditional mouse model recapitulating human lung adenocarcinoma, enabling mechanistic studies of KRAS oncogenesis and preclinical therapeutic testing.
RB1 and Cell Cycle Control in Cancer
Created Rb heterozygous knockout mice that develop pituitary and thyroid tumors, defining RB's essential role in cell cycle checkpoint control and establishing the two-hit hypothesis in vivo.
Representative Works 代表性著作
Tumour predisposition in mice heterozygous for a targeted mutation in Nf1
Nature Genetics (1994)
Demonstrated NF1 heterozygous mice develop myeloid leukemia and other tumors, validating the NF1 tumor suppressor role in vivo and modeling neurofibromatosis-associated malignancies.
Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal myeloproliferative disorder
Journal of Experimental Medicine (2004)
Showed conditional Kras activation in hematopoietic precursors drives fatal myeloproliferative disease, establishing KRAS as a direct driver in hematologic cancers.
A doxycycline-inducible system for studying p53 restoration in vivo
Cell (2007)
Demonstrated that p53 restoration in established tumors induces senescence or apoptosis depending on tumor type, providing key rationale for p53 reactivation therapies.
🏆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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