2018
DOI: 10.1158/1535-7163.mct-17-0789-atr
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Abstract: Inhibition of B-cell receptor (BCR) signaling through the BTK inhibitor, ibrutinib, has generated a remarkable response in mantle cell lymphoma (MCL). However, approximately one third of patients do not respond well to the drug, and disease relapse on ibrutinib is nearly universal. Alternative therapeutic strategies aimed to prevent and overcome ibrutinib resistance are needed. We compared and contrasted the effects of selinexor, a selective inhibitor of nuclear export, with ibrutinib in six MCL cell lines tha… Show more

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Cited by 35 publications
(25 citation statements)
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“…Consistent with previous studies of KPT-330 on acute myeloid leukemia, our studies of KPT-330 in NHL showed induction of G1 cell cycle arrest in MCL and TCL 9 . As was shown in sarcoma and MCL in previous studies, we also found that MCL cells have increased IkB localization in the nucleus with KPT-330 treatment 10,11 . In recent studies, it was found that bortezomib and DNA damaging agents such as gemcitabine impose a synergistic antitumor effect when combined with KPT-330 in solid tumors such as sarcoma and breast cancer, and hematologic malignancies such as AML, MM, and DLBCL [4][5][6]8,12 .…”
supporting
confidence: 88%
“…Consistent with previous studies of KPT-330 on acute myeloid leukemia, our studies of KPT-330 in NHL showed induction of G1 cell cycle arrest in MCL and TCL 9 . As was shown in sarcoma and MCL in previous studies, we also found that MCL cells have increased IkB localization in the nucleus with KPT-330 treatment 10,11 . In recent studies, it was found that bortezomib and DNA damaging agents such as gemcitabine impose a synergistic antitumor effect when combined with KPT-330 in solid tumors such as sarcoma and breast cancer, and hematologic malignancies such as AML, MM, and DLBCL [4][5][6]8,12 .…”
supporting
confidence: 88%
“…Overall, the advent of ibrutinib is a “great leap forward” in the treatment of MCL; however, problems with ibrutinib discontinuation, management of ibrutinib‐refractory disease, and mechanisms of ibrutinib resistance pose new challenges. In contrast with SLL/CLL, where the C481S mutation is commonly associated with ibrutinib resistance, this mutation is infrequent in ibrutinib‐resistant MCL, and other mechanisms of ibrutinib resistance and ways to overcome ibrutinib resistance must be explored. A detailed discussion about the molecular aspects of ibrutinib resistance is beyond the scope of the current article.…”
Section: Advances In the Treatment Of MCLmentioning
confidence: 99%
“…In addition, acquired resistance to ibrutinib has been repeatedly associated with enhanced activity of the PI3K-AKT pathway, caused, e.g., by downregulation of PTEN phosphatase and FOXO3a [127]. Notably, the AKT inhibitor MK2206 and the exportin 1 inhibitor selinexor both synergized with ibrutinib and were able to overcome the acquired resistance to ibrutinib [129,130]. Ibrutinib-resistant MCL cells also appear to be more dependent on BCL2 antiapoptotic signaling and the combination of ibrutinib and venetoclax has emerged as a highly promising combination [131].…”
Section: Resistance To Ibrutinib and Other Bruton Tyrosine-kinase Inhmentioning
confidence: 99%