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Translational Medicine / 转化医学Cancer Epigenomics

Kristian Helin

克里斯蒂安·赫林

PhD

🏢Memorial Sloan Kettering Cancer Center(纪念斯隆-凯特琳癌症中心)🌐USA

Chair, Cell Biology Program; Director, Center for Epigenetics Research细胞生物学项目主席;表观遗传学研究中心主任

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h-index
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Key Papers
4
Awards
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Key Contributions

👥Biography 个人简介

Kristian Helin is a pioneering figure in cancer epigenetics, having made seminal contributions to understanding EZH2 and Polycomb Repressive Complex 2 (PRC2) as oncogenic drivers. His work at MSK has defined multiple epigenetic vulnerabilities in cancer and advanced the development of several epigenetic drugs now in clinical use.

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🧪Research Fields 研究领域

EZH2 and PRC2 in CancerEZH2与PRC2在癌症中的作用
Epigenetic Drug Targets表观遗传药物靶点
Histone Demethylases组蛋白去甲基化酶
Cell Cycle Epigenetics细胞周期表观遗传学
Chromatin and Cancer Therapy染色质与癌症治疗

🎓Key Contributions 主要贡献

EZH2 as an Oncogenic Driver

Demonstrated that EZH2 overexpression drives cancer by silencing tumor suppressor genes via H3K27me3, and that EZH2 gain-of-function mutations create neomorphic activity targeting specific loci to promote lymphomagenesis.

Histone Demethylase Function in Cancer

Discovered and characterized KDM family histone demethylases as tumor suppressors and oncoproteins, establishing that dynamic regulation of histone methylation is critical for maintaining normal gene expression programs.

Epigenetic Drug Target Validation

Systematically validated EZH2, LSD1, and JARID1 family members as drug targets using genetic and chemical tools, providing the mechanistic foundation for ongoing clinical trials of epigenetic inhibitors.

Representative Works 代表性著作

[1]

EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation

Cancer Cell (2013)

Demonstrated that EZH2 is essential for germinal center B cells and that lymphoma-associated gain-of-function mutations promote transformation.

[2]

KDM2B links the Polycomb repressive complex 1 to recognition of CpG islands

Nature Genetics (2012)

Revealed that FBXL10/KDM2B recruits variant PRC1 to unmethylated CpG islands, establishing a methylation-sensing mechanism for Polycomb targeting.

[3]

The histone H3 lysine 27 demethylase JMJD3 links inflammation to inhibition of Polycomb-mediated gene silencing

Cell (2007)

Identified JMJD3 as the H3K27me3 demethylase linking inflammatory signals to activation of Polycomb-silenced genes.

🏆Awards & Recognition 奖项与荣誉

🏆AACR Award for Outstanding Achievement in Cancer Research
🏆Danish Cancer Society Honorary Award
🏆European Research Council Advanced Grant
🏆EMBO Member

📄Data Sources 数据来源

Last updated: 2026-01-15 | All information from publicly available academic sources

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