6 results match your criteria: "Bing Center for Waldenström's Macroglobulinemia and.[Affiliation]"
Autologous and Allogeneic Stem-Cell Transplantation for Transformed Waldenström Macroglobulinemia.
Am J Hematol
February 2025
Department of Hematology, University Hospital of Reims and UFR Médecine, Reims, France.
Biomarker analysis of the ASPEN study comparing zanubrutinib with ibrutinib for patients with Waldenström macroglobulinemia.
Blood Adv
April 2024
Department of Clinical Therapeutics, National and Kapodistrian University of Athens, Athens, Greece.
Article Synopsis
- The phase 3 ASPEN trial compared the effectiveness of two BTK inhibitors, zanubrutinib and ibrutinib, in treating Waldenström macroglobulinemia, analyzing genetic mutations' impact on treatment response.
- The study found that patients with mutations in CXCR4 and TP53 had poorer responses and survival rates but those treated with zanubrutinib generally showed better outcomes than those given ibrutinib.
- Overall, the research indicated that zanubrutinib offers improved clinical outcomes for patients with specific mutations compared to ibrutinib, highlighting the importance of genetic testing in treatment decision-making.
Effect of ibrutinib treatment on hemolytic anemia and acrocyanosis in cold agglutinin disease/cold agglutinin syndrome.
Blood
November 2021
Department of Hematology, Amsterdam University Medical Center (UMC), University of Amsterdam, Amsterdam, The Netherlands.
Hematopoietic cell kinase (HCK) is an SRC family member that is aberrantly upregulated in B-cell neoplasms dependent on MYD88-activating mutations and supports their growth and survival. We showed herein that activation of Toll-like receptor (TLR) signaling in MYD88 wild-type B cells also triggered HCK expression, denoting on path regulatory function for HCK by MYD88. To clarify the signaling cascades responsible for aberrant HCK expression in MYD88-mutated B-cell lymphomas, we performed promoter-binding transcription factor (TF) profiling, PROMO weighted TF consensus binding motif analysis, and chromatin immunoprecipitation studies.
View Article and Find Full Text PDFInhibition of the Bruton Tyrosine Kinase Pathway in B-Cell Lymphoproliferative Disorders.
Cancer J
November 2016
From the Bing Center for Waldenström's Macroglobulinemia and Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Activation of the Bruton tyrosine kinase (BTK) pathway plays an important role in the pathophysiology of a number of B-cell lymphoproliferative disorders (LPDs). A number of preclinical studies support inhibiting BTK as a mechanism to treat LPDs. Clinically, BTK inhibitors, specifically ibrutinib, have shown to be safe and effective on treating patients with indolent B-cell lymphomas and chronic lymphocytic leukemia (CLL).
View Article and Find Full Text PDFExpression of regulatory genes for lymphoplasmacytic cell differentiation in Waldenstrom Macroglobulinemia.
Br J Haematol
April 2009
Bing Center for Waldenstrom's Macroglobulinemia and Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Article Synopsis
- Waldenstrom Macroglobulinemia (WM) is a type of cancer involving the abnormal accumulation of lymphoplasmacytic cells in the bone marrow due to a failure in B-cell differentiation.
- A study analyzed gene expressions related to B-cell differentiation, focusing on PRDM1, PAX5, XBP1, and ERN1 in bone marrow samples from 31 WM patients and 6 healthy donors.
- Results indicated that 80% of patients exhibited high levels of XBP1 spliced mRNA and ERN1alpha, revealing a complex expression pattern of the studied genes and suggesting that XBP1-ERN1alpha may play a significant role in the development of WM.