echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Antitumor Therapy > FGFR1 mutation associated with internal bleeding in low-level glioma spontaneous tumors

    FGFR1 mutation associated with internal bleeding in low-level glioma spontaneous tumors

    • Last Update: 2020-05-30
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    It is rare for low-grade gliomas (low-grade gliomas, LGG) to develop spontaneous tumor internal bleeding; Therefore, it is of clinical significance to study the risk factors of internal bleeding in LGG spontaneous tumorsYukitomo Ishi of Hokkaido University School of Medicine in Japan and others found a higher incidence of mutations in LGG intrafibromyl growth factor receptor 1 (Fibroblast Growth Factor 1, FGFR1) of spontaneous tumor internal bleedingThe findings were published online in J Neurosurg in February 2020study methodsthe authors retrospectively analyzed 66 patients under 30 years of age who were pathologically diagnosed as WHO I or WHO IIAll cases were genetically tested to determine whether BRAF V600E, FGFR1 N546/K656, IDH1R132, IDH2 R172 and KIAA1549-BRAF (K-B) fusion gene mutations occurred and recorded spontaneous intra-tumor bleedingof the 66 patients, 39 were WHO Class I gliomas and 27 were WHO Class II gliomasDuring the follow-up, 5 cases (7.6%) had spontaneous tumor internal hemorrhage, including 4 cases of acute intra-tumor hemorrhage and 1 case of late-onset tumor internal hemorrhageThe incidence of spontaneous tumor stoma in WHO Class I and WHO Class II glioma was 5.1% and 11.1%, respectivelyFour haemorrhagic tumors are located in the middle line, including the hypothalamus and thalamusthe authors analyzed the BRAF, FGFR1, and IDH1/2 genes in 66 patientsThe K-B fusion gene mutation was detected in 18 patients (27.3%), braF V600E mutation was detected in 14 patients (21.2%), and braF V600E mutation was most common in WHO Class I gliomasEight (12.1%) IDH1/2 mutations were detected in all WHO Class II gliomas and 4 (6.1%) detected FGFR1 mutationsSpontaneous tumor internal hemorrhage occurred in 55.6% of patients with K-B fusion gene mutations and in patients with 100% of FGFR1 mutationsNone of braF mutations, IDH mutations, and wild BRAF/FGFR1/IDH patients developed spontaneous tumor internal bleedingSingle-factor analysis showed that there was a significant correlation between FGFR1 mutation and tumor double-sided distribution and internal bleeding in spontaneous tumors In 19 patients with tumors in the bilateral neural pathways, hypothalamus and thalamus, The FGFR1 mutation was significantly associated with internal bleeding in spontaneous tumors (p 0.001) conclusions
    the results of the study showed that the Mutation of FGFR1 was significantly associated with internal bleeding in patients with low-level gliomas under 30 years of age The specific mechanism is not clear, and further research is needed on the molecular mechanism of The Tumor Bleeding caused by the FGFR1 mutation.
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.