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Shirong Liu

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Senior Scientist

Dana-Farber Cancer Institute

United States

Research Interests

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The role of fecal microRNA in CNS autoimmune inflammatory disease

Open Date: 2018-04-01

Close Date: 2021-04-01

Articles (19)

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Collaborators (6)

Millicent Ekwudo

Florey Institute of Neuroscience and Mental Health

AUSTRALIA

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Luke Schwerdtfeger

Assistant Professor

Colorado State University

UNITED STATES

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Davide Mangani

Senior Scientist

Institute for Research in Biomedicine

SWITZERLAND

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Giulia Escobar

Principal Investigator at the Cellular Immunotherapy Center

Massachusetts General Hospital

UNITED STATES

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Eugenio Morelli

Assistant Professor

Università degli Studi di Torino

ITALY

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Laura Cox

Assistant Professor

Brigham and Women's Hospital and Harvard Medical School

UNITED STATES

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Shirong Liu

Research Interests

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Recent Grants

Articles (19)

Chemoimmunotherapy‐associated CD20 (MS4A1) resistance mutations in Waldenström macroglobulinemia: Epitope disruption independent of expression with implications for CD20‐directed cellular therapies

Evolution of tumor subclones and T-cell dynamics underlie variable ibrutinib responses in Waldenström macroglobulinemia

Repurposing pacritinib to target MYD88‐mutated Waldenström macroglobulinaemia

Discovery and Characterization of a First-In-Class HCK/BTK PROTAC DFCI-002-06 for the Treatment of MYD88 Mutated B Cell Malignancies

Development and characterization of the novel <i>MYD88</i> mutated, 6q deleted BCWM.2 cell line for Waldenstrom macroglobulinaemia

Dietary protein modulates intestinal dendritic cells to establish mucosal homeostasis.

Identification of robust predictors for ibrutinib response by multiomics in MYD88-mutated Waldenström macroglobulinemia

Gamma-delta T cells modulate the microbiota and fecal micro-RNAs to maintain mucosal tolerance.

Ibrutinib and venetoclax as primary therapy in symptomatic treatment naïve Waldenström macroglobulinemia

Aberrant Expression of Spliced WNK2 Is an Early Event in MYD88 Mutated WM That Activates ERK1/2 and Supports Tumor Growth

Atypical Stem Cell, Pre-B-Cell, T-Cell and Myeloid Gene Expression Characterizes Early Waldenstrom's Macroglobulinemia Clones Which Diminishes with Advancing Disease and Has Therapeutic Implications

Changes in Methylation and Chromatin Accessibility Underlie Subtype Classification and Disease Evolution in Waldenstrom's Macroglobulinemia

Early Subclones Showing Aberrant Co-Expression of Stem Cell, T Cell and Myeloid Genes Can be Detected By Flow Cytometry in MYD88 Mutated Waldenstrom's Macroglobulinemia Patients

Establishment of the Bcwm.2 Cell Line As a BTK-Inhibitor Resistant, BCL2 Inhibitor Sensitive in Vitro and In Vivo Study Model for Waldenstrom's Macroglobulinemia

Ibrutinib and Venetoclax in Symptomatic, Treatment-Naive Patients with Waldenstrom Macroglobulinemia

Novel Isoforms Identified By Isoseq Analysis Drive Expression Differences in Key Genes That Delineate the Subtypes of Waldenstrom's Macroglobulinemia

Novel Protacs Demonstrate Dual Kinase Inhibition and Degradation of HCK and BTK, and Are Highly Active in MYD88 Mutated WM and ABC DLBCL Cells

Pacritinib Blocks Key Pro-Survival Signaling Related to Mutated MYD88, Produces High Levels of Apoptosis and Overcomes Mutated BTK Cys481 Related BTK-Inhibitor Resistance

Quantitative MYD88 L265P Analysis Represents a Powerful Tool for Assessing Disease Response and Evaluating Clinical Trial Performance in Waldenstrom's Macroglobulinemia

Collaborators (6)

Millicent Ekwudo

Luke Schwerdtfeger

Davide Mangani

Giulia Escobar

Eugenio Morelli

Laura Cox

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