William L. Carroll
威廉·卡罗尔
MD
Director, NYU Cancer Institute Pediatric Cancer Research Program; Professor of Pediatrics; Julius B. Richmond Professor of Children's Health纽约大学儿童癌症研究项目主任，儿科学教授
👥Biography 个人简介
William L. Carroll, MD is the Julius B. Richmond Professor of Children's Health and Director of the Pediatric Cancer Research Program at NYU Langone Health, widely regarded as a leading authority on the biology of relapsed childhood acute lymphoblastic leukemia (ALL). His research has focused on understanding why ALL, which is highly curable at diagnosis, relapses in approximately 15-20% of cases with far worse outcomes, using whole-genome and single-cell approaches to characterize clonal evolution, the acquisition of drug resistance mutations, and the contributions of the bone marrow microenvironment to treatment failure. He has made pivotal contributions to characterizing mutations in NRAS, KRAS, TP53, and NT5C2 that emerge at relapse, and has modeled these in isogenic systems to understand their functional consequences and to identify new therapeutic targets for relapsed disease.
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
Clonal Evolution and Resistance at ALL Relapse
Demonstrated through paired diagnosis-relapse sequencing that ALL relapse arises from outgrowth of minor subclones harboring pre-existing or newly acquired resistance mutations—including TP53 mutations and alterations in nucleotidase NT5C2—rather than solely de novo mutation, reframing the biology of treatment failure.
NT5C2 Mutations as a Mechanism of Thiopurine Resistance
Independently identified gain-of-function NT5C2 mutations as a dominant mechanism of 6-mercaptopurine resistance in relapsed ALL, a finding simultaneously reported with the Bhojwani group, revealing a critical vulnerability point for maintenance chemotherapy.
Microenvironment and Stromal Contributions to ALL Relapse
Characterized interactions between leukemic cells and bone marrow stromal niches—including adhesion-mediated drug resistance (CAM-DR)—identifying integrin signaling and stroma-derived cytokines as actionable therapeutic targets to prevent and overcome relapse.
Functional Genomics of Pre-B ALL
Performed systematic shRNA and CRISPR loss-of-function screens in pre-B ALL models to identify essential dependencies in the context of oncogenic pathway activation, producing a genomic atlas of drug-gene interactions relevant to relapsed ALL therapy.
Representative Works 代表性著作
Clonal evolution mechanisms in NT5C2 mutant-relapsed acute lymphoblastic leukaemia
Nature (2018)
Single-cell and bulk sequencing study revealing the clonal architecture of NT5C2-mutant ALL relapse and establishing that relapse-associated mutations arise from minor ancestral clones selected by thiopurine therapy.
Mutations of the dominant negative SH2-domain of RRAS2 cooperate with BCR-ABL to transform hematopoietic cells
Oncogene (2010)
Identified cooperating signaling mutations in Ph+ ALL relapse, demonstrating RAS pathway hyperactivation as a mechanism of resistance to imatinib therapy.
Relapsed pediatric ALL: current approaches and future directions
Blood (2020)
Comprehensive review of relapsed childhood ALL biology, prognostic classification, salvage therapy approaches, and emerging targets identified by genomic characterization of relapse.
🏆Awards & Recognition 奖项与荣誉
📄Data Sources 数据来源
Last updated: 2026-04-06 | All information from publicly available academic sources
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