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    Home > Active Ingredient News > Antitumor Therapy > Science: Add to this evidence that Bai Fan/Xu Tao of Peking University has found that horse bell acid is a cancer-causing mutagent.

    Science: Add to this evidence that Bai Fan/Xu Tao of Peking University has found that horse bell acid is a cancer-causing mutagent.

    • Last Update: 2020-10-12
    • Source: Internet
    • Author: User
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    There is still a lack of understanding of the accumulation of so many mutations in normal cells, which is essential to understanding the occurrence and development of cancer.
    October 2, 2020, Bai Fan and Xu Tao of Peking University jointly published a research paper entitled "Macroscopic somatic clonal expansion in morphologically normal human urothelium" on Science Online, which investigated somatic cell cloning events in normal human urethra (MNU;
    AA is a natural herbal-derived compound that is the main mutant driver in MNU.
    AA greatly accelerates mutation accumulation and enhances clone amplification.
    MNU mutations have been widely observed in chromatin remodeling genes such as KMT2D and KDM6A, but are rare in TP53, PIK3CA and FGFR3.
    found that KMT2D mutations are common in urethra endocrine cells, regardless of whether they experience exposure to extroverts.
    changes in the number of copies are rare and are largely confined to a small area, as well as the loss of copy-neutral hybridity.
    AA-related individual clones in MNU to a few square centimeters.
    , 2 October 2020, wellcome Sanger Institute, UK. The igo Martincorena team published a research paper online in Science entitled "Wide heterogeneity in somatic mutation and selection in humanbladder", which sequenced 2,097 bladder biopsies from 20 individuals using targeting (n s 1914 biopsies), full exon groups (n s 655) and whole genome sequencing from 20 individuals.
    the study found a wide range of positive options in 17 genes.
    chromosomal remodeling genes are often mutated, but not in several major bladder cancer genes.
    a wide range of individual choices, with different driving genes dominating the cloning pattern between individuals.
    mutation characteristics are heterogeneous between clones and individuals, indicating different levels of exposure to mutagenic agents in the urine.
    found evidence of APOBEC mutation in 22 percent of biopsy tissues.
    study sheds light on the richness of mutation processes and choices in the normal urethra, and there is a great deal of heterogeneity between cloning and the individual.
    2, 2020, Steven G. Rozen published a review article in Science entitled "Mutational selection in normal urothelium", which systematically reviewed both studies.
    throughout the life cycle, cells inevitably obtain soy cell mutations, which are mainly caused by unresoled or incorrectly repaired DNA replication errors during cell division.
    Although most somatic cell mutations in normal cells have no esoteric consequences, mutations that affect essential genes, especially those associated with cell proliferation and death, may trigger mutation cloning amplification.
    a recognized example of human cancer, where the gradual accumulation of soy cell mutations drives the amplification of clones and the eventual malignant transformation of cells.
    Although genome sequencing of various human malignancies has revolutionized our understanding of the molecular and genetic basis of cancer occurrence and development, little is known about the patterns and drivers of so many soytic cell mutations in normal cells prior to malignant transformation.
    Recent research has revealed mutations in different normal tissues, including skin epithelial, esodural tissue, colorectal tissue, liver, endometrial epithelial, bronchial epithelial, brain, embryonic tissue, and blood cells, helping us understand mutation rates in normal cells, driving genes and mutagenic drivers.
    , previous studies have highlighted the key role of aging-related endogenic mutation processes in normal cells, as evidenced by the positive correlation between the amount of mutation and age.
    , UV rays are reported to be an exogenous mutageng factor that triggers normal skin cell mutagengs and induces skin cancer attacks.
    other potential mutation processes, both endogenated and exogente, play an early role in normal cells and deserve further study.
    the upper urethra is the upper cortitis lined with the bladder and ureter.
    it is classified as transition skin because its properties are somewhere between a layered scaly skin and a simple non-layered skin.
    it has a high regenerative capacity for damage, thus ensuring its barrier function.
    Because the urethra skin is in direct contact with the urine, the urethra skin remains exposed to a range of potentially carcinogenic metabolites and environmental factors that can cause tissue damage and genetic toxicity to the urethra skin cells.
    these conditions, the urethra skin may accumulate soy cell mutations through repeated cell renewal.
    In this study, in combination with laser capture microanatomy and exosome sequencing, 120 cases of normal urethra endocrine (MNU) soymic cell mutant cloning in patients with UCC were systematically studied.
    AA is a natural herbal-derived compound that is the main mutant driver in MNU.
    AA greatly accelerates mutation accumulation and enhances clone amplification.
    MNU mutations have been widely observed in chromatin remodeling genes such as KMT2D and KDM6A, but are rare in TP53, PIK3CA and FGFR3.
    found that KMT2D mutations are common in urethra endocrine cells, regardless of whether they experience exposure to extroverts.
    changes in the number of copies are rare and are largely confined to a small area, as well as the loss of copy-neutral hybridity.
    AA-related individual clones in MNU to a few square centimeters.
    .
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