Inhibition of the Bruton Tyrosine Kinase Pathway in B-Cell Lymphoproliferative Disorders

@article{Castillo2016InhibitionOT,
  title={Inhibition of the Bruton Tyrosine Kinase Pathway in B-Cell Lymphoproliferative Disorders},
  author={Jorge J. Castillo and Steven P P Treon and Matthew S. Davids},
  journal={The Cancer Journal},
  year={2016},
  volume={22},
  pages={34–39}
}
AbstractActivation 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). Ibrutinib has recently gained approval for the treatment of… 
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The clinical development of novel BTK inhibitors, ACP-196 (acalabrutinib), ONO/GS-4059, and BGB-3111 are summarized.
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Evidence is summarized indicating how CK2 embodies most of the features of a cancer growth-promoting non-oncogene, focusing on lymphoid tumors, which hold the promise to be additional options in novel drug combinations for the therapy of lymphoid and plasmacellular malignancies.
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The common and different features of the four lymphomas will be summarized to show how normal B lymphocytes can be subverted to generate tumours, how these tumours evolve and how their weaknesses can be attacked by targeted therapies.
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There is convincing evidence to show that kinase TAK1 is a druggable target in DLBCL, and it is found that MAP 3K7 (TAK1) is required forDLBCL survival.
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TLDR
Understanding of the PD-1/PD-L1 axis in Hodgkin lymphoma is summarized, recent clinical studies of anti-PD-1 monotherapy and promising combination immunotherapy in the pipeline are summarized.
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TLDR
In conclusion, this case showed that ibrutinib can be safely used in patients with severe renal failure under close renal function monitoring and suggests that additional renal function deterioration caused by disease progression is suggested.
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TLDR
As lectin interaction with the BCR is critical for FL and probably for some other lymphomas, targeting this interaction is considered to be an interesting therapeutic strategy and agents for blockade of lectin–BCR interaction may include antibodies against high-mannose glycans and mannose-based oligosaccharide mimics or non-carbohydrate glycomimetics.
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