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    BIOMARKER:

    MYD88 L265P + CXCR4 mutation

    i
    Other names: CXCR4, CD184, D2S201E, fusin, HM89, HSY3RR, LESTR, NPY3R, NPYR, NPYY3R, Chemokine (C-X-C motif) receptor 4, MYD88, MYD88 Innate Immune Signal Transduction Adaptor, Myeloid Differentiation Primary Response Protein MyD88, Myeloid Differentiation Primary Response Gene (88), Myeloid Differentiation Primary Response 88, Mutant Myeloid Differentiation Primary Response 88, MYD88D
    Entrez ID:
    4615; 7852
    Related biomarkers:
    Expression
    Mutation
    Others
    5ms
    The Incidence, Clinical Application and Prognostic Significance of MYD88 and CXCR4 Mutation in Chinese Patients with Lymphoplasmacytic Lymphoma/ Waldenström Macroglobulinemia (ASH 2023)
    NGS was the most sensitive method for detecting CXCR4 mutation. MYD88 mutation had prognostic significance in BTKi-based therapy, while CXCR4 mutation indicated higher tumor burden and inferior survival in BTKi-based therapy.
    Clinical
    |
    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CXCR4 (Chemokine (C-X-C motif) receptor 4)
    |
    MYD88 mutation • MYD88 L265P • CXCR4 mutation • MYD88 mutation + CXCR4 mutation • MYD88 L265P + CXCR4 mutation • MYD88 wild-type
    6ms
    CD19-Targeting CAR T-Cell Therapy in Transformed Waldenström Macroglobulinemia/Lymphoplasmacytic Lymphoma: A Descar-T and US Collaborative Study (ASH 2023)
    We retrospectively identified patients with biopsy-proven transformed WM/lymphoplasmacytic lymphoma treated with axicabtagene ciloleucel (axi-cel) or tisagenlecleucel (tisa-cel) in the French DESCAR-T registry (NCT04328298) and 2 US centers. This study shows a high efficacy of anti-CD19 CAR T-cell therapy in R/R tWM with no unexpected toxicity. Longer follow-up is needed to confirm the long-term efficacy of CAR T-cells in tWM.
    CAR T-Cell Therapy • IO biomarker
    |
    CXCR4 (Chemokine (C-X-C motif) receptor 4)
    |
    MYD88 L265P • CXCR4 mutation • MYD88 L265P + CXCR4 mutation
    |
    Yescarta (axicabtagene ciloleucel) • Kymriah (tisagenlecleucel-T)
    1year
    Waldenström macroglobulinemia and non-IgM-type lymphoplasmacytic lymphoma are genetically similar. (PubMed, Acta Haematol)
    Most mutations detected by NGS were subclonal following MYD88 L265P, although one non-IgM-type LPL patient harbored only CXCR4 S338X mutation. Our NGS analyses reveal genetic characteristics in LPL patients and suggest genetic similarities between these two subsets of LPL, WM and non-IgM-type.
    Journal • PD(L)-1 Biomarker • IO biomarker
    |
    PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • ARID1A (AT-rich interaction domain 1A) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • KMT2D (Lysine Methyltransferase 2D) • CD79B (CD79b Molecule) • NOTCH2 (Notch 2) • PD-L2 (Programmed Cell Death 1 Ligand 2) • MLL2 (Myeloid/lymphoid or mixed-lineage leukemia 2) • PRDM1 (PR/SET Domain 1)
    |
    TP53 mutation • ARID1A mutation • KMT2D mutation • MYD88 L265P • CXCR4 mutation • CD79B mutation • CXCR4 S338X • MYD88 L265P + CXCR4 mutation
    over1year
    Long-Term Follow-up of Bendamustine Plus Rituximab Regimen in 69 Treatment Naïve (TN) Patients with Waldenström Macroglobulinemia, a Study on Behalf of the French Innovative Leukemia Organization (FILO) (ASH 2022)
    Eight patients received ibrutinib, and 6 chemo-immunotherapy. Conclusion This study demonstrates that the BR regimen is efficient in treatment naïve WM pts, yielding long-term responses. The occurrence of secondary cancers, including TRMN, should be closely monitored in these patients.
    Clinical • IO biomarker
    |
    TP53 (Tumor protein P53) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CXCR4 (Chemokine (C-X-C motif) receptor 4)
    |
    TP53 mutation • MYD88 mutation • MYD88 L265P • CXCR4 mutation • MYD88 mutation + CXCR4 mutation • MYD88 L265P + CXCR4 mutation • MYD88 wild-type
    |
    Imbruvica (ibrutinib) • Rituxan (rituximab) • bendamustine
    almost2years
    A MULTICENTER, INTERNATIONAL COLLABORATIVE STUDY EVALUATING FRONTLINE THERAPY WITH BENDAMUSTINE RITUXIMAB FOR WALDENSTRÖM MACROGLOBULINEMIA (EHA 2022)
    Conclusion Fixed-duration BR is a highly effective regimen for pts with previously untreated symptomatic WM, irrespective of the MYD88 L265P mutation status, although early POD, within 2 years of initiation of BR, is associated with inferior subsequent survival. Our preliminary analysis, suggesting that the presence of CXCR4 mutation confers resistance to BR, warrants confirmation in prospective studies.
    Clinical • IO biomarker
    |
    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CXCR4 (Chemokine (C-X-C motif) receptor 4)
    |
    MYD88 L265P • CXCR4 mutation • MYD88 L265P + CXCR4 mutation • MYD88 wild-type
    |
    Rituxan (rituximab) • bendamustine
    over2years
    IgM Plasma Cell Myeloma. (PubMed, Am J Clin Pathol)
    Distinguishing IgMPCM from other IgM-related disorders requires correlation with clinical, laboratory, and radiologic findings. Exclusion of MYD88 L265P and WHIM-like CXCR4 mutations may be useful to diagnose IgMPCM.
    Journal
    |
    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CCND1 (Cyclin D1) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • SDC1 (Syndecan 1)
    |
    Chr t(11;14) • MYD88 L265P • MET expression • CXCR4 mutation • CCND1 expression • SDC1 positive • Chr del(13)(q14) • MYD88 L265P + CXCR4 mutation