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mTOR signaling as a driver of Castleman disease
Journal article   Open access   Peer reviewed

mTOR signaling as a driver of Castleman disease

John D. Colgan
Blood, Vol.135(19), pp.1614-1615
05/07/2020
DOI: 10.1182/blood.2020005361
PMID: 32379877
url
https://doi.org/10.1182/blood.2020005361View
Published (Version of record) Open Access

Abstract

In this issue of Blood, Arenas et al(1) report that a group of patients suffering from idiopathic multicentric Castleman disease (iMCD) display heightened activation of the mTOR signaling pathway, suggesting a much-needed new treatment strategy for this disease. iMCD is a rare but deadly hematologic disorder characterized by a slew of abnormalities, including cytokine-driven lymphoproliferation and lymph node enlargement, systemic inflammation, cytopenias, and multiorgan dysfunction.(2,3) The most severe cases of iMCD, known collectively as the TAFRO subtype, also display thrombocytopenia, widespread edema, fever, and organomegaly.(4) The causes of iMCD and what propagates the disease remain largely unknown, leaving patients with few treatment options. An important advance was the identification of the proinflammatory cytokine interleukin-6 (IL-6) as a driver of iMCD.(5) This observation led to the approval and use of biologics that block IL-6 signaling as a treatment of iMCD. Although targeting IL-6 has met with some success, similar to 60% of iMCD patients treated with antagonizers of IL-6 signaling failed to respond for reasons that remain unknown.6 These findings suggest mechanisms in addition to or beyond IL-6 signaling drive the etiology and pathogenesis of iMCD. Identification of such mechanisms is a critical need, as it could lead to new and more effective treatments for iMCD.
 Hematology Life Sciences & Biomedicine Science & Technology

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