Abstract
The Identification Of Somatic Mutations In Interferon-g Signal Molecules In Human Uterine Leiomyosarcoma
Highlights
Uterine mesenchymal tumours have been traditionally divided into benign tumour leiomyomas (LMA) and malignant tumour leiomyosarcomas (LMS) based on cytological atypia, mitotic activity and other criteria
As the importance and involvement of the IFN-g signal pathway in the transcriptional regulation of the transporter associated with antigen processing (TAP1) and proteasome beta subunit 9 (PSMB9)/b1i promoter have been established, it is demonstrated that the defective PSMB9/b1i expression was attributable to G871E somatic mutation in the ATPbinding region of Janus-activated kinase 1 (JAK1) molecule in SKN cell line, which is established from patient with uterine LMS
The immunohistochemistry (IHC) experiments revealed a serious loss in the ability to induce expression of PSMB9/b1i in human uterine LMS tissues in comparison with normal myometrium tissues located in same tissue sections and other 4 mesenchymal tumour types (Figure 1)
Summary
Uterine mesenchymal tumours have been traditionally divided into benign tumour leiomyomas (LMA) and malignant tumour leiomyosarcomas (LMS) based on cytological atypia, mitotic activity and other criteria. As the importance and involvement of the IFN-g signal pathway in the transcriptional regulation of the transporter associated with antigen processing (TAP1) and PSMB9/b1i promoter have been established, it is demonstrated that the defective PSMB9/b1i expression was attributable to G871E somatic mutation in the ATPbinding region of JAK1 molecule in SKN cell line, which is established from patient with uterine LMS. Continued improvement of our knowledge of the molecular biology of uterine LMS may lead to novel therapies and improved outcome
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
