Mechanisms of B-cell lymphoma pathogenesis
By Ralf Küppers. Nature Reviews. Cancer, 2005
1,011 citations recorded by the source corpus.
Subfields: Genetics, Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/7f0a772820e83583ea926b037819e47f1cf57e52
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Citations in the corpus
- Germinal Centers (2017, methodology): “To visualize and track NP-specific plasma cells, use B1–8 Jκ / mice crossed onto Blimp1:GFP reporter mice, which indicates plasma cell differentiation [3, 4].”
- The biology of Hodgkin's lymphoma (2009, background): “Deregulated transcription factor networks B-cell lymphomas and leukaemias usually retain key phenotypical and functional features of the B cells they derive fro”
- The Bruton tyrosine kinase inhibitor PCI-32765 blocks B-cell activation and is efficacious in models of autoimmune disease and B-cell malignancy (2010, background): “Validation of this probe in dogs with spontaneous NHL and the agreement between Btk occupancy in PBMC and tumor biopsies supports the current use of PCI-33380 as a pharmacodynamic marker in PBMCs in ongoing human clinical trials.”
- Bruton tyrosine kinase inhibitor ibrutinib (PCI-32765) has significant activity in patients with relapsed/refractory B-cell malignancies. (2013, background): “been hypothesized that functional BCR signaling is essential for the survival and proliferation of the malignant cell.(5) BTK has been shown to be an essential component of chronic active BCR signaling, which is a key survival pathway in the activated B-cell subtype of DLBCL, because genetic knockdo”
- EuroFlow antibody panels for standardized n-dimensional flow cytometric immunophenotyping of normal, reactive and malignant leukocytes (2012, background): “Clonogenic events lead to the expansion and accumulation of matureappearing lymphocytes, which carry a proliferative and/or survival advantage over their normal counterparts (3, 74, 75).”
- From pathogenesis to treatment of chronic lymphocytic leukaemia (2010, background): “Functional BCRs are expressed in most B cell lymphomas but BCR surface expression is usually weak in CLL (reviewed in Ref”
- Germinal centres: role in B-cell physiology and malignancy (2008, background): “Chromosomal translocations associated with GC-derived non-Hodgkin lymphomas frequently involve the immunoglobulin locus, with the breakpoints either in the switch region or in the target region for SH”