The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma
Human uterine leiomyosarcoma (U-LMS) is neoplastic malignancy that typically arises in tissues of mesenchymal origin. The identification of novel molecular mechanism leading to human U-LMS formation and the establishment of new therapies has been hampered by several critical points. We earlier repor...
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2018
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Online Access: | http://hdl.handle.net/1721.1/116869 https://orcid.org/0000-0003-2839-8228 |
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author | Hayashi, Takuma Ichimura, Tomoyuki Kasai, Mari Ando, Hirofumi Ida, Koichi Kawano, Miki Shiozawa, Tanri Tonegawa, Susumu Kanai, Yae Aburatani, Hiroyuki Yaegashi, Nobuo Konishi, Ikuo |
author2 | Picower Institute for Learning and Memory |
author_facet | Picower Institute for Learning and Memory Hayashi, Takuma Ichimura, Tomoyuki Kasai, Mari Ando, Hirofumi Ida, Koichi Kawano, Miki Shiozawa, Tanri Tonegawa, Susumu Kanai, Yae Aburatani, Hiroyuki Yaegashi, Nobuo Konishi, Ikuo |
author_sort | Hayashi, Takuma |
collection | MIT |
description | Human uterine leiomyosarcoma (U-LMS) is neoplastic malignancy that typically arises in tissues of mesenchymal origin. The identification of novel molecular mechanism leading to human U-LMS 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 beta subunit 9 (Psmb9)/β1i, an interferon (IFN)-γ inducible factor, spontaneously develop U-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, tumour suppressive, and signaling pathways directly impact sarcomagenesis. The IFN-γ pathway is important for control of tumour growth and invasion and has been implicated in several malignant tumours. In this study, experiments with human tissues revealed a defective expression of PSMB9/β1i in human U-LMS that was traced to the IFN-γ pathway and the specific effect of somatic mutations of JANUS KINASE (JAK) 1 molecule or promoter region on the locus cording PSMB9/β1i gene. Understanding the molecular mechanisms of human U-LMS may lead to identification of new diagnostic candidates or therapeutic targets against human U-LMS. |
first_indexed | 2024-09-23T12:55:23Z |
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id | mit-1721.1/116869 |
institution | Massachusetts Institute of Technology |
last_indexed | 2024-09-23T12:55:23Z |
publishDate | 2018 |
publisher | Open Access Text Pvt, Ltd |
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spelling | mit-1721.1/1168692022-10-01T11:56:37Z The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma Hayashi, Takuma Ichimura, Tomoyuki Kasai, Mari Ando, Hirofumi Ida, Koichi Kawano, Miki Shiozawa, Tanri Tonegawa, Susumu Kanai, Yae Aburatani, Hiroyuki Yaegashi, Nobuo Konishi, Ikuo Picower Institute for Learning and Memory Tonegawa, Susumu Human uterine leiomyosarcoma (U-LMS) is neoplastic malignancy that typically arises in tissues of mesenchymal origin. The identification of novel molecular mechanism leading to human U-LMS 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 beta subunit 9 (Psmb9)/β1i, an interferon (IFN)-γ inducible factor, spontaneously develop U-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, tumour suppressive, and signaling pathways directly impact sarcomagenesis. The IFN-γ pathway is important for control of tumour growth and invasion and has been implicated in several malignant tumours. In this study, experiments with human tissues revealed a defective expression of PSMB9/β1i in human U-LMS that was traced to the IFN-γ pathway and the specific effect of somatic mutations of JANUS KINASE (JAK) 1 molecule or promoter region on the locus cording PSMB9/β1i gene. Understanding the molecular mechanisms of human U-LMS may lead to identification of new diagnostic candidates or therapeutic targets against human U-LMS. 2018-07-10T15:31:49Z 2018-07-10T15:31:49Z 2017-04 2017-02 2018-07-10T14:27:41Z Article http://purl.org/eprint/type/JournalArticle 2398-5399 http://hdl.handle.net/1721.1/116869 Hayashi, Takuma et al. “The Somatic Mutations in Interferon-γ Signal Molecules in Human Uterine Leiomyosarcoma.” Biomedical Genetics and Genomics 2, 1 (2017): 1-5 https://orcid.org/0000-0003-2839-8228 http://dx.doi.org/10.15761/BGG.1000126 Biomedical Genetics and Genomics Creative Commons Attribution 4.0 International License http://creativecommons.org/licenses/by/4.0/ application/pdf Open Access Text Pvt, Ltd Biomedical Genetics and Genomics |
spellingShingle | Hayashi, Takuma Ichimura, Tomoyuki Kasai, Mari Ando, Hirofumi Ida, Koichi Kawano, Miki Shiozawa, Tanri Tonegawa, Susumu Kanai, Yae Aburatani, Hiroyuki Yaegashi, Nobuo Konishi, Ikuo The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma |
title | The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma |
title_full | The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma |
title_fullStr | The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma |
title_full_unstemmed | The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma |
title_short | The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma |
title_sort | somatic mutations in interferon γ signal molecules in human uterine leiomyosarcoma |
url | http://hdl.handle.net/1721.1/116869 https://orcid.org/0000-0003-2839-8228 |
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