Charles G. Mullighan
查尔斯·穆利根
MBBS(Hons), MD, PhD
Deputy Director; Member, Department of Pathology; Co-Director, Hematological Malignancies Program副院长;病理系研究员;血液恶性肿瘤项目联合主任
👥Biography 个人简介
Charles G. Mullighan, MBBS(Hons), MD, PhD is Deputy Director of St. Jude Children's Research Hospital and a world-leading authority on the genomic landscape of acute lymphoblastic leukemia. Born in Australia and trained at the University of Melbourne before joining St. Jude, Dr. Mullighan has been the defining force in understanding how genetic alterations drive ALL pathogenesis and how genomic subtypes should guide therapy. His foundational 2007 and 2009 Nature papers established that deletion of IKZF1 (encoding the Ikaros transcription factor) is a hallmark of BCR-ABL1-positive and BCR-ABL1-like ALL and a critical determinant of poor prognosis. He co-led the international effort to comprehensively characterize Ph-like ALL, identifying the full spectrum of kinase-activating alterations (CRLF2/JAK pathway, ABL-class fusions, RAS pathway mutations) and demonstrating this subtype comprises approximately 15% of pediatric B-ALL and up to 25-30% of adults. Dr. Mullighan's group has also defined the genomic features of B-ALL in children with Down syndrome, characterizing the unique biology of DS-ALL and elucidating why these patients are both highly sensitive to chemotherapy and at risk for treatment-related toxicities. His work integrating genomic data with clinical outcomes has reshaped ALL risk classification and directly enabled precision medicine trials.
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
Defining the Ph-like ALL Genomic Landscape
Co-led comprehensive genomic profiling studies that defined Ph-like ALL as a distinct high-risk subgroup with kinase-activating alterations including CRLF2 rearrangements (P2RY8-CRLF2, IGH-CRLF2), JAK1/2 mutations, and ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), providing the molecular basis for targeted therapy trials.
IKZF1 as a Key Prognostic Alteration in ALL
Discovered that IKZF1 deletions define BCR-ABL1-like ALL biology and are independently associated with poor outcome, establishing IKZF1 status as a critical prognostic biomarker now incorporated into clinical risk stratification across major ALL cooperative groups worldwide.
Genomic Characterization of Down Syndrome ALL
Led comprehensive characterization of the unique genomic features of ALL in children with Down syndrome, identifying high rates of CRLF2 overexpression, JAK mutations, and distinct mutational signatures that explain the unique clinical behavior and treatment sensitivity of DS-ALL.
Representative Works 代表性著作
Genomic Analysis of the Clonal Origins of Relapsed Acute Lymphoblastic Leukemia
Science (2008)
Landmark study demonstrating that ALL relapse can arise from ancestral pre-leukemic clones or from the dominant diagnosis clone, reshaping understanding of relapse biology.
BCR-ABL1-like Acute Lymphoblastic Leukemia
Journal of Clinical Oncology (2015)
Comprehensive characterization of Ph-like ALL genetic subtypes and therapeutic implications for targeted therapy integration.
🏆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
Related Experts 相关专家
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University of California San Diego, Ludwig Cancer Research
Cigall Kadoch
Dana-Farber Cancer Institute / Broad Institute of MIT and Harvard
Luciano Di Croce
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Alexander Meissner
Max Planck Institute for Molecular Genetics, Berlin
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