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    Home > Biochemistry News > Biotechnology News > BRCA: 30 Years of Wind and Rain from Gene Identification to Targeted Therapy

    BRCA: 30 Years of Wind and Rain from Gene Identification to Targeted Therapy

    • Last Update: 2022-04-17
    • Source: Internet
    • Author: User
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    Article source: Medicine Rubik's Cube Med

    Author: Zisu

    The discovery and research of oncogenes and tumor suppressor genes is an epoch-making beginning in the history of tumor research, and it is also an important sign that people begin to understand tumors at the molecular level


    King has been researching the heritability of breast cancer since 1974.


    BRCA: Timeline from gene identification to targeted cancer therapy [7]

    After the susceptibility genes for breast and ovarian cancer were identified in 1991, multiple laboratories began to join the BRCA1/2 positional cloning competition


    From genetic identification to cancer prevention

    From genetic identification to cancer prevention

    Subsequent studies have improved our understanding of the complex roles and functions of BRCA1/2


    Primary product encoded by BRCA1 and BRCA2 genes[6]

    Genetic testing and counseling for BRCA1/2 mutations is now part of routine breast and ovarian cancer prevention and treatment


    There have been many new technologies for early cancer screening for hereditary breast or ovarian cancer.


    From cancer prevention to targeted therapy

    From cancer prevention to targeted therapy

    The greatness of science lies not only in its perseverance, but sometimes in its rich imagination


    Molecular mechanism behind the anticancer effect of PARP inhibitors[10]

    However, so far, no PARP inhibitors have been approved for use in combination with chemotherapy or radiation


    The synthetic lethal mechanism hypothesis states that a synthetic lethal effect occurs when a combination of defects in the expression of two or more genes causes cell death, whereas it does not occur when only one of these genes is defective


    This approach has been incredibly successful and has resulted in substantial increases in progression-free and overall survival in ovarian and prostate cancer patients


    We believe that the potential of PARP inhibitors to treat many different diseases will continue to be fully explored, bringing new options to more patients, especially those lacking effective treatment options


    Note: The original text has been deleted

    References:

    [1] Hall JM, Lee MK, Newman B, et al.


    [2] Narod SA, Feunteun J, Lynch HT, et al.


    [3] King MC.


    [4] Miki Y, Swensen J, Shattuck-Eidens D, et al.


    [5] Wooster R, Bignell G, Lancaster J, et al.


    [6] O'Donovan PJ, Livingston DM.
    BRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair.
    Carcinogenesis.
    2010;31(6):961-967.
    doi:10.
    1093/carcin /bgq069

    [7] Grinda T, Delaloge S.
    BRCA2: a 25-year journey from gene identification to targeted cancer treatment.
    Lancet Oncol.
    2021;22(6):763-764.
    doi:10.
    1016/S1470-2045(21)00272- 2

    [8] Kriege M, Brekelmans CT, Boetes C, et al.
    Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition.
    N Engl J Med.
    2004;351(5):427-437.
    doi:10.
    1056/NEJMoa031759

    [9] Domchek SM, Friebel TM, Neuhausen SL, et al.
    Mortality after bilateral salpingo-oophorectomy in BRCA1 and BRCA2 mutation carriers: a prospective cohort study.
    Lancet Oncol.
    2006;7(3):223-229.
    doi:10.
    1016 /S1470-2045(06)70585-X

    [10] Curtin NJ, Szabo C.
    Poly(ADP-ribose) polymerase inhibition: past, present and future.
    Nat Rev Drug Discov.
    2020;19(10):711-736.
    doi:10.
    1038/s41573-020-0076- 6

    [11] Bryant HE, Schultz N, Thomas HD, et al.
    Specific killing of BRCA2-deficient tumors with inhibitors of poly(ADP-ribose) polymerase [published correction appears in Nature.
    2007 May 17;447(7142):346] .
    Nature.
    2005;434(7035):913-917.
    doi:10.
    1038/nature03443

    [12] Farmer H, McCabe N, Lord CJ, et al.
    Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy.
    Nature.
    2005;434(7035):917-921.
    doi:10.
    1038/nature03445

    [13] Fong PC, Boss DS, Yap TA, et al.
    Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers.
    N Engl J Med.
    2009;361(2):123-134.
    doi:10.
    1056 /NEJMoa0900212

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