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In addition to\n                    <jats:italic>HTLV-1 bZIP factor<\/jats:italic>\n                    (\n                    <jats:italic>HBZ<\/jats:italic>\n                    ), a leukemogenic antisense transcript of HTLV-1, abnormalities of genes involved in TCR-NF-\u03baB signaling, such as\n                    <jats:italic>CARD11<\/jats:italic>\n                    , are detected in about 90% of patients. Utilizing mice expressing CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell-specific CARD11(E626K) and\/or CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell-specific\n                    <jats:italic>HBZ<\/jats:italic>\n                    , namely CARD11(E626K)\n                    <jats:sup>\n                      <jats:italic>CD4<\/jats:italic>\n                      -Cre\n                    <\/jats:sup>\n                    mice,\n                    <jats:italic>HBZ<\/jats:italic>\n                    transgenic (Tg) mice, and CARD11(E626K)\n                    <jats:sup>\n                      <jats:italic>CD4<\/jats:italic>\n                      -Cre\n                    <\/jats:sup>\n                    ;\n                    <jats:italic>HBZ<\/jats:italic>\n                    Tg double transgenic mice, we clarify these genes\u2019 pathogenetic effects. CARD11(E626K)\n                    <jats:sup>\n                      <jats:italic>CD4<\/jats:italic>\n                      -Cre\n                    <\/jats:sup>\n                    and\n                    <jats:italic>HBZ<\/jats:italic>\n                    Tg mice exhibit lymphocytic invasion to many organs, including the lungs, and double transgenic mice develop lymphoproliferative disease and increase CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells in vivo. CARD11(E626K) and\n                    <jats:italic>HBZ<\/jats:italic>\n                    cooperatively activate the non-canonical NF-\u03baB pathway, IRF4 targets, BATF3\/IRF4\/HBZ transcriptional network, MYC targets, and E2F targets. Most KEGG and HALLMARK gene sets enriched in acute-type ATL are also enriched in double transgenic mice, indicating that these genes cooperatively contribute to ATL development.\n                  <\/jats:p>","DOI":"10.1038\/s42003-022-04284-x","type":"journal-article","created":{"date-parts":[[2022,11,29]],"date-time":"2022-11-29T05:03:27Z","timestamp":1669698207000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia\/lymphoma"],"prefix":"10.1038","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0100-1710","authenticated-orcid":false,"given":"Takuro","family":"Kameda","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kotaro","family":"Shide","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayako","family":"Kamiunten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1158-5131","authenticated-orcid":false,"given":"Yasunori","family":"Kogure","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisuke","family":"Morishita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junji","family":"Koya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Tahira","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiichi","family":"Akizuki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takako","family":"Yokomizo-Nakano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sho","family":"Kubota","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kosuke","family":"Marutsuka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaaki","family":"Sekine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomonori","family":"Hidaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoko","family":"Kubuki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuichi","family":"Kitai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tadashi","family":"Matsuda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akinori","family":"Yoda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1501-6430","authenticated-orcid":false,"given":"Takayuki","family":"Ohshima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Midori","family":"Sugiyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2318-5987","authenticated-orcid":false,"given":"Goro","family":"Sashida","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keisuke","family":"Kataoka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7778-5374","authenticated-orcid":false,"given":"Seishi","family":"Ogawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2555-8188","authenticated-orcid":false,"given":"Kazuya","family":"Shimoda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,11,29]]},"reference":[{"key":"4284_CR1","doi-asserted-by":"publisher","first-page":"481","DOI":"10.1182\/blood.V50.3.481.481","volume":"50","author":"T Uchiyama","year":"1977","unstructured":"Uchiyama, T., Yodoi, J., Sagawa, K., Takatsuki, K. & Uchino, H. 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Shimoda has received consulting fees from Novartis Pharma, Takeda Pharmaceutical, Bristol-Myers, Shire Japan, and Celgene, all outside the submitted work, and has received research grants from Perseus Proteomics, Pharma Essentia Japan KK, AbbVie GK, Astellas Pharma, MSD, Chugai Pharmaceutical, Kyowa Kirin, Pfizer, Novartis Pharma, Otsuka Pharmaceutical, Asahi Kasei Medical, all outside the submitted work. K.K. holds stock in Asahi Genomics, has a patent for genetic alterations as a biomarker in T-cell lymphomas, and has received research funding from Chordia Therapeutics outside the submitted work. The remaining authors declare no competing interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"1309"}}