Articles | Open Access
Vol. 2 No. 4 (2015)
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1Dept. of Immunology and Infectious Disease, Shinshu University Graduate School of Medicine, 2Horiuchi Ladies Clinic, 3Dept. of Laboratory Medicine, Shinshu University Hospital, 4,Pathology Division, National Cancer Center Research Institute. 5Dept. of Obstetrics and Gynecology, Osaka City University Graduate School of Medicine, 6Dept. of Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, 7Dept. of Obstetrics and Gynecology, Shinshu University, School of Medicine, 7The Cancer System Laboratory, Research Center for Advanced Science and Technology, The University of Tokyo, 8Dept. of Obstetrics and Gynecology, Kyoto University Graduate School of Medicine, 9Promoting Business using Advanced Technology, Japan Science and Technology Agency (JST), and 10The International Human Epigenome Consortium (IHEC) and CREST, Japan Science and Technology Agency (JST). Email: yoyoyo224@hotmail.com
Abstract
Human uterine leiomyosarcoma (Ut-LMS) is neoplastic malignancy that typically arises in tissues of mesenchymal origin. The identification of novel molecular mechanism leading to human UtLMS formation and the establishment of new therapies has been hampered by several critical points. We earlier reported that mice with a homozygous deficiency for proteasome subunit beta type (PSMB) 9, an interferon (IFN)-g inducible factor, spontaneously develop Ut-LMS. The use of research findings of the experiment with mouse model has been successful in increasing our knowledge and understanding of how alterations, in relevant oncogenic, tumor suppressive, and signaling pathways directly impact sarcomagenesis. The IFN-g signaling pathway is important for control of tumor growth and invasion and has been implicated in several malignant tumors. In this study, experiments with human tissues revealed a defective expression of PSMB9 in human Ut-LMS that was traced to the IFN-g signal cascade and the significant effect of somatic mutations of Janus kinase (JAK) 1 molecule or PSMB9 gene promoter region on the PSMB9 gene transcriptional activation. Understanding the molecular mechanisms of human Ut-LMS may lead to identification of new diagnostic candidates or therapeutic targets in human Ut-LMS.
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Copyright © 2015
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Takuma Hayashi , Akiko Horiuchi , Kenji Sano , Nobuyoshi Hiraoka Tomoyuki Ichimura , Osamu Ishiko,,
Yae Kanai , Nobuo Yaegashi , Hiroyuki Aburatani , and Ikuo Konishi, this is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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