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    Home > Active Ingredient News > Antitumor Therapy > Nat Commun: Inhibits special immunomodulation signaling path pathps in breast cancer or is expected to promote the body's efficient anti-tumor immune response

    Nat Commun: Inhibits special immunomodulation signaling path pathps in breast cancer or is expected to promote the body's efficient anti-tumor immune response

    • Last Update: 2020-12-26
    • Source: Internet
    • Author: User
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    December 17, 2020 // -- Despite the current success of immunotherapy in treating cancers such as lung cancer and melanoma, it is still not effective in treating breast cancer because of the low rate of immunocellular immersion in breast cancer (which is also known as a "cold" tumor due to its low immersion rate).
    tumor cells avoid immune surveillance by reducing the immersion or attraction of immune-suppressing cells that attack their cells, a strategy that may promote poor prognostication and make them unresponsive to immunotherapy in young breast cancer patients.
    For this reason, identifying a treatment that converts immune "cold" tumors into "hot" tumors may hopefully increase the effectiveness of immunotherapy in treating breast cancer because it attacks tumor cells based on reactivation of immune cells in host bodies.
    In a recent study published in the international journal Nature Communications, scientists from institutions such as Spain's National Cancer Research Centre found that RANK signaling paths may be a key candidate to help regulate the immune response in breast tumors;
    : CC0 Public Domain researchers say inhibiting rank proteins may promote the recruitment of immune cells in mouse models and body tumors in breast cancer patients.
    In addition, when the RANK signaling pathway in tumor cells is suppressed, tumors appear to become more sensitive to immunotherapy, and studies have shown that RANK protein plays a key role in the communication between tumor cells and immune cells, and that rank pathways may also serve as a possible escape route for cancer cells against immunotherapy.
    When researchers conducted clinical trials on patients with early pre menotinal breast cancer, they found that patients showed tolerance to monoclonal antibodies that inhibitRANK, which increased the immersion of immune cells in tumors, and identified specific biomarkers that could help select groups of patients who benefited from the therapy.
    the advantages of this study lie in two independent studies, a clinical trial and a preclinical study, which concluded that inhibiting the RANK signaling pathline may enhance the body's anti-tumor immune response. The monoclonal antibodies used in this study are commonly used to treat bone diseases, such as osteoporosis and bone metastasis, but are not used in cancer treatment, and this study supports the use of antibodies in combination with immunotherapy to treat breast cancer, a strategy that can convert immune "cold" tumors into tumors sensitive to immune system activity, said
    researcher González-Suárez.
    tumor's immune monitoring body's immune system recognizes foreign microorganisms, such as viruses and bacteria, and also produces a reaction to destroy pathogens, which play a key role in protecting the body against cancer, and cancer cells often express abnormal proteins that can be identified by the immune system because they act as labels to allow the host body's immune system to recognize and act as a disruptive force.
    presence of immune cells in tumors (so-called immuno-immersion) is directly related to whether the patient's prognostics are good.
    However, tumors have special mechanisms that help cancer cells avoid the immune response that usually inhibits malignant tumors, which means that immunotherapy may not always be effective in treating multiple types of cancer, and studies such as this one may help develop more new cancer therapies.
    () Original source: Gómez-Aleza, C., Nguyen, B., Yoldi, G. et al. Inhibition of RANK signaling in breast cancer induces an anti-tumor immune response orchestrated by CD8+ T cells. Nat Commun 11, 6335 (2020). doi:10.1038/s41467-020-20138-8。
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