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    Home > Active Ingredient News > Blood System > Blood: Who is the carrier of the mutation driven by Langehans cell tissue cell growth?

    Blood: Who is the carrier of the mutation driven by Langehans cell tissue cell growth?

    • Last Update: 2020-10-02
    • Source: Internet
    • Author: User
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    Langehans Cell Tissue Cell Growth (LCH) is a myelin tumor driven by occasional activation mutations in the MAPK path path.
    The "misleading myelin dextry cells (DC)" model suggests that high-risk, multi-system, and dangerous organ-positive (MS-RO-plus) LCH is caused by a drive mutation in multi-potential hemastogenous progenitor cells that reside in the bone marrow (BM), while low-risk, MS-RO-and single-system (SS) LCH is caused by pregenuity cells (DC) that reside in circulation or tissue.
    study looked at the possibility that CD34-c-Kit-FLT3-FLT3-myelin ancestral cell groups were potential carriers of mutations in all LCH disease manifestations.
    this group consists of monocytes (Mo)/macrophages (MF), bone-breaking cells (OC), and degeneration progeny cells of degeneration cells (DC).
    CD34-c-Kit-FLT3-plus cells from the bone marrow source of MS-RO-LCH patients, Langerhans cells (LCs)-like cells can be produced in-body.
    LC samples and DC descendants of the progeny's source carry BRAF mutations, confirming their common origin.
    in patients with high-risk and low-risk LCH, the percentage of CD34-c-Kit-FLT3-plus ancestral cells in the blood was higher than that of healthy blood donors.
    in 1 case of MS-RO-LCH, the percentage of CD34-c-Kit-FLT3-plus cells in the blood and their BRAF-mutated offspring all changed with chemotherapy.
    In-body, CD34-c-Kit-FLT3-plus ancestral cells from exosome blood sources in high- and low-risk LCH patients can produce DC and LC-like cells, but their drive mutations are not easily detected, possibly due to a low percentage of mutated ancestral cells.
    , the researchers also found mutated BRAF allotopes in lesions Mo/MF, DC, LC and/or OC-like cells in multiple low-risk patients, as well as in blood Mo and DC.
    , the researchers speculated that in both high- and low-risk LCH patients, drive mutations are present in myelin pregenitic cells that reside in BM, which can be mobilized into the bloodstream.
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