刘霞｜湖南师范大学｜学者主页

2026

长征精神话语叙事的历史演进与发展逻辑

尤琳，刘霞

《河北师范大学学报(哲学社会科学版)》，Vol. 49, No. 5

2026

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

Hao Sun, R. Sklavenitis-Pistofidis, Shi-Rong Liu, Xia Liu, N. Tsakmaklis, J. Hatcher, M. Guerrera, A. Kofides, Andres Ramirez-Gamero, Abigail L. Peachey, Shuqiang Li, Derin B. Keskin, Vipheaviny A. Chea, Nawoo Kim, Haoxiang Lyu, Wesley S. Lu, K. Livak, K. Meid, A. Guijosa, C. Flynn, Dominic Pizzarella, Christopher J. Patterson, Mu Hao, Shu-Hua Yi, Wei-Ping Yuan, A. Branagan, Catherine J. Wu, I. Ghobrial, L. Qiu, S. Sarosiek, J. Castillo, Z. Hunter, S. Treon

Blood

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期刊论文

长征精神话语叙事的历史演进与发展逻辑

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

Zanubrutinib and pirtobrutinib show synergistic killing and suppression of BTK signaling in MYD88-mutated lymphoma cells

Quantitative MYD88L265P and CXCR4S338X analysis to assess clinical trial performance in Waldenstrom macroglobulinemia

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

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

Discovery of JH-XIII-05-01, a First-in-Class Dual IRAK1/IRAK4 Degrader for MYD88 Mutant Lymphomas.

Final Report of a Phase II Study of Ibrutinib and Venetoclax in Previously Untreated Waldenström Macroglobulinemia

WNK2 oncogenicity revealed by the discovery and functional characterization of novel gene isoforms in MYD88 mutated Waldenström’s Macroglobulinemia

Re-purposing pacritinib to target MYD88 mutated Waldenstrom’s Macroglobulinemia

Discovery of an undocumented pattern of intron retention that is abundant in healthy B-cells and circumvented in Waldenstrom's macroglobulinemia impacting genes driving cellular growth and survival

Regulatory network analysis identifies changes in ahr, TFAP4, and AP-1 transcription factors as top drivers of symptomatic disease progression in Waldenstrom's macroglobulinemia.

Final report of a phase II study of ibrutinib and venetoclax in previously untreated Waldenström macroglobulinemia

Novel mechanistic insights for IRAK1 and IRAK4 signaling provide a framework for the development of dual IRAK1 and IRAK4 protacs for MYD88 mutated lymphomas.

LOX1 expression identifies a population of polymorphonuclear myeloid-derived suppressor cells that are highly enriched in bone marrow samples of treatment-Naïve and BTKi-Relapsed/Refractory WM patients and show constitutive activation of BTK

Zanubrutinib and pirtobrutinib (ZAP) but not ibrutinib and pirtobrutinib (IAP) show synergistic tumor cell killing and suppression of BTK and downstream signaling in MYD88 mutated lymphoma cells.

Diverse signaling and vulnerabilities accompany distinct BTK mutations associated with clinical resistance to COVALENT, non-COVALENT and protacs targeting BTK in MYD88 mutated lymphomas.

Double-hit alterations of TP53 identify ultra high-risk disease in previously treated, MYD88 mutated waldenstrom macroglobulinemia.

CD20 (MS4A1) mutations are strongly associated with prior chemoimmunotherapy exposure in Waldenström macroglobulinemia and have predicted functional consequences for the development of CD20-directed cellular therapies.

Development and characterization of the novel MYD88 mutated, 6q deleted BCWM.2 cell line for Waldenström macroglobulinaemia

High VGPR/CR rates with pirtobrutinib plus venetoclax in previously treated Waldenström macroglobulinemia: Results from a multicenter phase II study

童年期家庭负性经历对青少年自伤行为的独立作用及累加效应

A Phase II Study of Pirtobrutinib and Venetoclax in Previously Treated Patients with Waldenström Macroglobulinemia: An Interim Analysis

Analysis of Alternative Splicing in Waldenstrom's Macroglobulinemia Reveals Novel Targets, Insights into IgM Production and Improved Gene Level Expression Estimates

Two-Year Follow-up after Ibrutinib and Venetoclax in Symptomatic, Treatment-Naive Patients with Waldenström Macroglobulinemia

Development and Evaluation of a Multiplex Digital PCR Assay for Detecting CXCR4 S338X Mutations in Waldenstrom's Macroglobulinemia

Development and Characterization of Novel Dual HCK/BTK Bifunctional Protacs That Potently Inhibit Kinase Function and Demonstrate Robust in Vitro and In Vivo Degradation of Targets for the Treatment of MYD88-Mutated B-Cell Malignancies

Multi-Omic Analysis Identifies Deletions in Chr17p and High ROR1 Expression, but Not TP53 Mutations As Predictors of Overall Survival in Patients with Untreated Waldenstrom's Macroglobulinemia (WM)

Development and Characterization of a Novel Bifunctional Protac Jh-XIII-05-1 That Shows Potent IRAK1 and IRAK4 Kinase Inhibition and Target Degradation and Is Highly Active in MYD88 Mutated B-Cell Lymphoma Cells Alone and in Combination with BTK- and BCL2- Inhibitors

Pacritinib Effectively Inhibits Pro-Survival Signaling and Overcomes BTKCys481Ser-Mediated Resistance in MYD88-Mutated B-Cell Malignancies

Establishment of a Novel Waldenström's Macroglobulinemia (WM) Cell Line Bcwm.2 with Del6q and Unique MYD88S243N, LYNI297N, SPI1Q227E Mutations and That Shows Robust In Vivo Engraftment in SCID NOD Mice

Discovery of Undocumented, Cancer-Specific and Pro-Inflammatory Isoforms of WNK2 That Are Highly Expressed in MYD88 Mutated Waldenström's Macroglobulinemia and Represent Novel Therapeutic Targets.

Single-Cell RNA Analysis of Bone Marrow Mononuclear Cells Reveals Abnormal Activation of T Cells and Monocytes, and Identifies CD35 As a Novel Biomarker and Therapeutic Target in Waldenstrom Macroglobulinemia

Genomic Evolution By Serial Single-Cell Sequencing Identifies High Tumor Expression of LYN As a Promoter of Resistance in Waldenstrom's Macroglobulinemia Undergoing Ibrutinib Monotherapy

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

面向新时代的生态道德教育

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

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

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

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

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

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

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

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

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

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

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

行动危机对大学生消极情绪的影响：认知融合的中介作用和自我抽离的调节作用

走向类存在：面对人类发展困境的道德教育

中小学教师育德能力及其培育

The ERK1/2 Regulator WNK2 Shows Novel Alternative Splicing Aberrations That Support Tumor Growth in MYD88 Mutated Waldenström's Macroglobulinemia

Ibrutinib and Venetoclax in Previously Untreated Waldenström Macroglobulinemia

Multi-Omic Analysis of 253 Untreated Patients with Waldenström's Macroglobulinemia Reveals Clinically and Genomically Distinct Disease Subtypes and a Model for Disease Progression

Identification of Robust Predictors for Ibrutinib Response By Multi-Omic Genomics in MYD88 Mutated Waldenstrom's Macroglobulinemia

A new role for the SRC family kinase HCK as a driver of SYK activation in MYD88 mutated lymphomas

双相抑郁与单相抑郁患者认知功能的比较

流动儿童主观社会经济地位与问题行为的关系：公正世界信念与社会自尊的作用

Phase I study of Ibrutinib and the CXCR4 antagonist Ulocuplumab in CXCR4 mutated Waldenstrom Macroglobulinemia.

The ERK1/2 Regulator WNK2 Shows Differential Expression and Isoform Usage, Primarily Driven By Aberrant Methylation, in MYD88 Mutated Waldenström's Macroglobulinemia

A New Role for the SRC Family Member HCK As a Driver of BCR/SYK Signaling in MYD88 Mutated Lymphomas

Diagnostic Next-generation Sequencing Frequently Fails to Detect MYD88L265P in Waldenström Macroglobulinemia

The HCK/BTK inhibitor KIN-8194 is active in MYD88 driven lymphomas and overcomes mutated BTKCys481 ibrutinib resistance.

Cell‐free DNA analysis for detection of MYD88L265P and CXCR4S338X mutations in Waldenström macroglobulinemia

Bone marrow involvement and subclonal diversity impairs detection of mutated CXCR4 by diagnostic next generation sequencing in Waldenström macroglobulinemia

Pirtobrutinib (LOXO-305) Is Active and Overcomes ERK Related Pro-Survival Signaling in Ibrutinib Resistant, BTK Cys481 Mutant Expressing WM and ABC DLBCL Lymphoma Cells Driven By Activating MYD88 Mutations

Venetoclax in Previously Treated Waldenström Macroglobulinemia

Long-term follow-up of ibrutinib monotherapy in treatment-naive patients with Waldenstrom macroglobulinemia

Response and survival predictors in a cohort of 319 patients with Waldenström macroglobulinemia treated with ibrutinib monotherapy

Natural history of Waldenström macroglobulinemia following acquired resistance to ibrutinib monotherapy

强化认知干预对脑卒中伴抑郁和焦虑患者认知功能和负性情绪的影响

人工智能时代师生关系的伦理审视

Response and Survival Outcomes to Ibrutinib Monotherapy for Patients With Waldenström Macroglobulinemia on and off Clinical Trials

A matched case-control study comparing features, treatment and outcomes between patients with non-IgM lymphoplasmacytic lymphoma and Waldenström macroglobulinemia

Ixazomib, dexamethasone, and rituximab in treatment-naive patients with Waldenström macroglobulinemia: long-term follow-up.

CXCR4 mutational status does not impact outcomes in patients with Waldenström macroglobulinemia treated with proteasome inhibitors

Expression of the prosurvival kinase HCK requires PAX5 and mutated MYD88 signaling in MYD88-driven B-cell lymphomas.

Partial response or better at 6 months is prognostic of superior progression-free survival in Waldenstrom macroglobulinemia patients treated with ibrutinib

Genomic Landscape of Waldenström Macroglobulinemia and Its Impact on Treatment Strategies.