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However, the molecular mechanisms underlying this tumorigenic process are poorly understood. We previously reported the presence of a biological link between the expression of CD30, which serves as a marker for ATL progression, and the actively proliferating fraction of human T\u2010cell leukemia virus type 1 (HTLV\u20101)\u2010infected cells that display polylobulation. Here, we demonstrated that CD30 signaling induced chromosomal instability with clonal expansion through DNA double\u2010strand breaks (DSBs) via an increase of intracellular reactive oxygen species. CD30<jats:sup>+<\/jats:sup>ATL cells were composed of subclones with additional genomic aberrations compared with CD30<jats:sup>\u2212<\/jats:sup>ATL cells in ATL patients. Furthermore, we found an accumulation of copy number loss of DSB repair\u2010related genes as the disease progressed. Taken together, CD30 expression on ATL cells appears to be correlated with genomic instability, suggesting that CD30 signaling is one of the oncogenic factors of ATL progression with clonal evolution. This study provides new insight into the biological roles of CD30 signaling and could improve our understanding of tumorigenic processes of HTLV\u20101\u2010infected cells.<\/jats:p>","DOI":"10.1111\/cas.15706","type":"journal-article","created":{"date-parts":[[2022,12,21]],"date-time":"2022-12-21T12:06:20Z","timestamp":1671624380000},"page":"1556-1568","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The oncogenic driving force of <scp>CD30<\/scp> signaling\u2010induced chromosomal instability in adult T\u2010cell leukemia\/lymphoma"],"prefix":"10.1111","volume":"114","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9843-9040","authenticated-orcid":false,"given":"Makoto","family":"Nakashima","sequence":"first","affiliation":[{"name":"Laboratory of Tumor Cell Biology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences University of Tokyo  Tokyo 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