The somatic mutations in Interferon-γ signal molecules in human uterine leiomyosarcoma
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BGG-2-126.pdf
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480.92 KB
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Checksum (MD5)
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Author(s)
Hayashi, Takuma
Ichimura, Tomoyuki
Kasai, Mari
Ando, Hirofumi
Ida, Koichi
Kawano, Miki
Shiozawa, Tanri
Tonegawa, Susumu
Kanai, Yae
Aburatani, Hiroyuki
Date Issued
April 2017
Journal
Biomedical Genetics and Genomics
Publisher
Open Access Text Pvt, Ltd
Citation
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
Version
Final published version
Abstract
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.
MIT Department
Picower Institute for Learning and Memory
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Creative Commons Attribution 4.0 International License
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DOI of Published Version
https://doi.org/10.15761/BGG.1000126
