{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T03:23:42Z","timestamp":1791343422404,"version":"4.3.1"},"reference-count":61,"publisher":"Rockefeller University Press","issue":"6","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,6,2]]},"abstract":"<jats:p>Leukemic stem cells (LSCs) isolated from acute myeloid leukemia (AML) patients are more sensitive to nuclear factor \u03baB (NF-\u03baB) inhibition-induced cell death when compared with hematopoietic stem and progenitor cells (HSPCs) in in vitro culture. However, inadequate anti-leukemic activity of NF-\u03baB inhibition in vivo suggests the presence of additional survival\/proliferative signals that can compensate for NF-\u03baB inhibition. AML subtypes M3, M4, and M5 cells produce endogenous tumor necrosis factor \u03b1 (TNF). Although stimulating HSPC with TNF promotes necroptosis and apoptosis, similar treatment with AML cells (leukemic cells, LCs) results in an increase in survival and proliferation. We determined that TNF stimulation drives the JNK\u2013AP1 pathway in a manner parallel to NF-\u03baB, leading to the up-regulation of anti-apoptotic genes in LC. We found that we can significantly sensitize LC to NF-\u03baB inhibitor treatment by blocking the TNF\u2013JNK\u2013AP1 signaling pathway. Our data suggest that co-inhibition of both TNF\u2013JNK\u2013AP1 and NF-\u03baB signals may provide a more comprehensive treatment paradigm for AML patients with TNF-expressing LC.<\/jats:p>","DOI":"10.1084\/jem.20130990","type":"journal-article","created":{"date-parts":[[2014,5,20]],"date-time":"2014-05-20T07:37:44Z","timestamp":1400571464000},"page":"1093-1108","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":91,"title":["Co-inhibition of NF-\u03baB and JNK is synergistic in TNF-expressing human AML"],"prefix":"10.1084","volume":"211","author":[{"given":"Andrew","family":"Volk","sequence":"first","affiliation":[{"name":"Molecular Biology Program 1 , 2"},{"name":"Department of Biology, Loyola University Chicago, Chicago, IL 60660 1 , 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Biology, College of Life and Environment Science, Shanghai Normal University, Shanghai 200234, People\u2019s Republic of China 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junping","family":"Xin","sequence":"additional","affiliation":[{"name":"Oncology Institute, Cardinal Bernardin Cancer Center, Department of Pathology 4 ; 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