echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Study of Nervous System > Acta Neuropathologica: CDKN2A deficiency in on-screen membrane chamber spacing tumors with RELA changes is a sign of poor post-mention: a retrospective analysis of HIT chamber spacer tumor trials.

    Acta Neuropathologica: CDKN2A deficiency in on-screen membrane chamber spacing tumors with RELA changes is a sign of poor post-mention: a retrospective analysis of HIT chamber spacer tumor trials.

    • Last Update: 2020-10-05
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    ReLA-EP has been identified as a unique new tumor entity.
    fusion between C11orf95 and RELA is pathologically activated by the accumulation of p65-RelA indicated by the NF-B signal path.
    the authors assessed the frequency and effect on prognosmence of CDKN2A deficiency in 54 children treated under the HIT2000-E protocol.
    high-resolution genome-wide copy spectrum through molecular probe (MIP) analysis.
    chromosome fractures corresponding to fusion transcripts were found in the C11orf95 and RELA genes (Figure 1a, d).
    cases showed that the pathological accumulation of p65-RelA was a hallmark of RELA-EP (Figure 1f).
    9 out of 54 cases (16.7%) detected CDKN2A purity deficiency (total loss) (Figure 1c);
    in one case, few tumor cells expressed the p16 protein, indicating that the CDKN2A alletic gene was retained in a single cell.
    14 cases (25.9%) with CDKN2A semi-combined sub-missing.
    in these samples, p16 protein retention was found in 92.9% of the cases tested - only one case lacked p16 protein expression, indicating that the second allegory was insealed through other mechanisms.
    31 (57.4%) of the 54 cases reported that CDKN2A was not missing.
    all of them show p16 protein expression (Figure 1h).
    , p16 immunologic tissue chemistry can be used as an alternative indicator of complete CDKN2A deficiency, but it cannot distinguish between hemislyceration states.
    as previously described in IDH mutant gliomas, there is no statistical link between CDKN2A deficiency and filamentation activity.
    the presence of CDKN2A deficiency (pure or semi-joint) is associated with a higher age at diagnosis, CDKN2A deficiency may also be a secondary event in tumor progression.
    in order to identify possible differences between RELA-EP at the transcription level and without CDKN2A missing, 12 RELA-EP differential expression genes were analyzed by RNA sequencing.
    after several tests and corrections, five genes were found to have been significantly downgraded, including CDKN2A and CDKN2B, as well as their adjacent genes MTAP (S-methyl-5'-sulfur adenosine phosphatase) located in the missing area.
    MTAP is the key enzyme in the methionine pathway.
    its absence leads to dependence on the activity of the methyl transferase PRMT5, which can be blocked by PRMT5 inhibitors as a new treatment in MTAP-missing tumors.
    , KIF7 (15q26) encoded with cerum hair-related proteins and ZNF536 (19q12) labeled with coding neuron markers were found to be downgraded.
    found that GABRA2 (4p12), which encodes the gamma-amino butyric acid subject sub-alpha-2, was increased in height in tumors missing from CDKN2A.
    Kaplan-Meier analysis shows a significant correlation between CDKN2A deficiency and overall survival status (OS).
    groups: (1) pure CDKN2A missing and semi-combined CDKN2A missing, and tumors with two reserved alleth genes (p s 0.009); The absence of pure or semi-joint CDKN2A is separated from all three layers (p s 0.034) and (3) of tumors with two reserved allethic genes (p s 0.017).
    the absence of pure and semi-lying children did not show a prognosmative correlation with EFS.
    the main transparent cell morphology of histological characteristics is a good prognostic indicator of OS (p s 0.039), and the high silky division activity (sgt; 17 mitoses / 10HPF) is a predictor of tumor recurrence (p s 0.004) and OS (p s 0.007).
    multivariate analysis confirms that silk splitting activity is an independent prognosmation indicator of EFS.
    authors, the absence of CDKN2A represents the objective parameters of risk strat ion in RELA-EP.
    that the molecular probe method represents a sensitive and quantitative tool for CDKN2A evaluation in FFPE materials.
    In addition to cytoblastoma, CDKN2A's purity deficiency has recently been described as a poor prognostic marker for other central nervous system tumors, including mesolytic IDH mutant gliomas and low-level gliomas with BRAF mutations.
    /inactivation of CDKN2A may cause pathological activation of cell cycle protein-dependent kinases targeted by specific inhibitors such as palbociclib.
    , CDKN2A ineration in RELA-chamber meningioma may represent a potential therapeutic target.
    MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Originals" are owned by Mets Medicine and are not authorized to be reproduced by any media, website or individual, and are authorized to be reproduced with the words "Source: Mets Medicine".
    all reprinted articles on this website are for the purpose of transmitting more information and clearly indicate the source and author, and media or individuals who do not wish to be reproduced may contact us and we will delete them immediately.
    reproduce content at the same time does not represent the position of this site.
    leave a message here.
    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.