Drugging the unfolded protein response in acute leukemias
Kharabi Masouleh, Behzad
Bruemmendorf, Tim H.
MetadataShow full item record
This item's downloads: 0 (view details)
Cited 19 times in Scopus (view citations)
Kharabi Masouleh, Behzad; Chevet, Eric; Panse, Jens; Jost, Edgar; O’Dwyer, Michael; Bruemmendorf, Tim H. Samali, Afshin (2015). Drugging the unfolded protein response in acute leukemias. Journal of Hematology & Oncology 8 ,
The unfolded protein response (UPR), an endoplasmic reticulum (ER) stress-induced signaling cascade, is mediated by three major stress sensors IRE-1 alpha, PERK, and ATF6 alpha. Studies described the UPR as a critical network in selection, adaptation, and survival of cancer cells. While previous reviews focused mainly on solid cancer cells, in this review, we summarize the recent findings focusing on acute leukemias. We take into account the impact of the underlying genetic alterations of acute leukemia cells, the leukemia stem cell pool, and provide an outline on the current genetic, clinical, and therapeutic findings. Furthermore, we shed light on the important oncogene-specific regulation of individual UPR signaling branches and the therapeutic relevance of this information to answer the question if the UPR could be an attractive novel target in acute leukemias.
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Ireland
Showing items related by title, author, creator and subject.
Deregulated expression of the hsp40 family members auxilin-1 and -2 is indicative of proteostasis imbalance and predicts patient outcome in ph+ leukemia Vieri, Margherita; Geng, Huimin; Patterson, John B.; Panse, Jens; Wilop, Stefan; Samali, Afshin; Chevet, Eric; Masouleh, Behzad Kharabi (Springer Nature, 2015-12-01)Background: Proteostasis is defined by the orchestrated control of anabolic and catabolic protein pathways. Disruption of proteostasis results in cell stress and adaptation to proteostasis imbalance is mediated by adaptive ...
The impact of clonal evolution on response to imatinib mesylate (sti571) in accelerated phase cml O'Dwyer, M. E. (American Society of Hematology, 2002-05-13)
Nilotinib in patients with ph+ chronic myeloid leukemia in accelerated phase following imatinib resistance or intolerance: 24-month follow-up results le Coutre, P D; Giles, F J; Hochhaus, A; Apperley, J F; Ossenkoppele, G J; Blakesley, R; Shou, Y; Gallagher, N J; Baccarani, M; Cortes, J; Kantarjian, H M (Springer Nature, 2011-11-11)Nilotinib (Tasigna) is a potent and selective BCR-ABL inhibitor approved for use in patients with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CML-CP) and in patients with CML-CP and accelerated phase ...