{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T23:01:33Z","timestamp":1778886093596,"version":"3.51.4"},"reference-count":29,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2003,8,18]],"date-time":"2003-08-18T00:00:00Z","timestamp":1061164800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The pathogenesis of Hodgkin lymphoma (HL) is still unclear. Previous investigations have demonstrated constitutive nuclear activity of the transcription factor NF kappa B (NF\u2010\u03baB) in Hodgkin\/Reed\u2013Sternberg (HRS) cells as an important prerequisite in protecting these cells from apoptosis. As a molecular mechanism leading to constitutive NF\u2010\u03baB activity in HRS cells, mutations of the NF\u2010\u03baB inhibitor I kappa B alpha (I\u03baB\u03b1) have recently been identified in classical (c) HL\u2010derived cell lines in a patient with cHL. In the present study, the NF\u2010\u03baB inhibitor I kappa B epsilon (I\u03baB\u03b5) has been analysed for somatic mutations in the same group of six patients already studied for I\u03baB\u03b1 mutations, as well as in cHL\u2010derived cell lines. In one cHL\u2010derived cell line (L428), a hemizygous frame\u2010shift mutation generating a pre\u2010terminal stop codon resulting in a severely truncated protein was found. Moreover, in the HRS cells of one patient, a hemizygous mutation affecting the 5\u2032\u2010splicing site of intron 1 of the I\u03baB\u03b5 gene was found. These results, in combination with recently described I\u03baB\u03b1 mutations, indicate that defective NF\u2010\u03baB inhibitors appear more frequent than previously thought and might explain the constitutive nuclear activity of NF\u2010\u03baB in a significant proportion of cHL cases. Copyright \u00a9 2003 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.1454","type":"journal-article","created":{"date-parts":[[2003,10,28]],"date-time":"2003-10-28T03:00:42Z","timestamp":1067310042000},"page":"413-420","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":128,"title":["Inactivating I kappa B epsilon mutations in Hodgkin\/Reed\u2013Sternberg 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