KR-102962919-B1 - Composition for preventing or treating cancer and method for producing the same
Abstract
The present invention relates to a composition for preventing or treating cancer, comprising as an active ingredient a supernatant of heat-treated cancer cells or a carrier thereof. Accordingly, by inducing IgE activity to suppress cancer activity and significantly activating an anti-tumor immune response, it can suppress tumor development and metastasis and be usefully utilized as a vaccine composition or an immunotherapeutic composition for an immune response against tumors.
Inventors
- 윤택준
Assignees
- 주식회사 두젠바이오
Dates
- Publication Date
- 20260512
- Application Date
- 20240216
Claims (11)
- It comprises heat-treated cancer cells or the supernatant of a carrier thereof as an active ingredient, and The above cancer cells or carriers are heat-treated for 20 minutes under conditions of a temperature of 121°C and a pressure of 0.15 MPa, and A composition for preventing or treating cancer, wherein the supernatant above is HMGB-1 removed.
- In paragraph 1, A composition for preventing or treating cancer, wherein the cancer cells are isolated from within an individual or cultured outside an individual.
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- In paragraph 1, The above composition is a composition for preventing or treating cancer that inhibits cancer activity by inducing the promotion of TNF-α production, the promotion of IL-6 production, the promotion of IL-12 production, the promotion of IgE production, or the inhibition of IL-10 production in immune cells.
- In paragraph 5, A composition for preventing or treating cancer, wherein the immune cells are selected from the group consisting of natural killer cells, T-cells, B-cells, macrophages, and dendritic cells.
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- In paragraph 1, A composition for preventing or treating cancer, wherein the cancer cells are contained at a concentration of 1 x 10⁵ to 1 x 10⁹ cells/ml.
- In any one of paragraphs 1, 2, 5, 6, and 8, A composition for preventing or treating cancer, wherein the cancer is selected from the group consisting of pancreatic cancer, breast cancer, ovarian cancer, cervical cancer, esophageal cancer, stomach cancer, liver cancer, lung cancer, nasopharyngeal cancer, oral cancer, thyroid cancer, prostate cancer, kidney cancer, gallbladder cancer, bile duct cancer, blood cancer, and melanoma.
- A step of heating cancer cells or a carrier thereof; and The method includes the step of centrifuging the heated cancer cells or carriers thereof to recover the supernatant, The cancer cells or carriers thereof in the heating step are heat-treated for 20 minutes under conditions of a temperature of 121°C and a pressure of 0.15 MPa, and A method for preparing a composition for preventing or treating cancer, wherein the supernatant above is one from which HMGB-1 has been removed.
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Description
Composition for preventing or treating cancer and method for producing the same The present invention relates to a composition for preventing or treating cancer and a method for preparing the same, and more specifically, to a composition capable of preventing or treating cancer by including an upper layer obtained from cancer cells or a carrier thereof as an active ingredient. The most critical characteristic of malignant tumors is uncontrolled proliferation. Immunoediting and immune regression mechanisms (evidence for cancer cell escape) are involved in the malignancy of cancer in vivo and present therapeutic limitations. Meanwhile, it has been confirmed that the risk of cancer development increases in immunosuppressive states, suggesting that immunotherapy could be the most promising method for cancer prevention and treatment. Since cancer cells present the whole array of mutated epitopes to CD8+ and CD4+ T cells, there is a possibility that their immune evasion capabilities can be neutralized. For tumor vaccines to achieve clinical success, effective methods for inducing tumor antigens that trigger an immune response must precede, and methods to reverse the immunosuppressive mechanisms caused by cancer are required. Ultimately, tumor vaccines must possess the ability to enhance the function of macrophages and NK cells against cancer, thereby effectively amplifying the T cell response and enabling activated T cells to successfully reach the tumor site without resistance caused by immunosuppressive mechanisms. In this regard, research results related to tumor vaccines manufactured from whole tumor cells to overcome cancer are ongoing. Immunogenic cell death (ICD), one of the methods by which cancer cells die, is a concept that plays a very important role in cancer treatment and prevention because it induces an immune response through specific signals and releases that activate the immune system during the process of cancer cell death. Since the definition of ICD was first proposed in 2005, cancer treatment through the activation of the host immune system has reached a new dimension. Unlike apoptosis, in which the plasma membrane does not rupture, cell death induced by ICD induces the release of damage-associated molecular patterns (DAMPs) and intracellular organelles; consequently, these are recognized by immune cells comprising the innate and acquired immune systems, triggering an immune response. Therefore, although DAMPs are not visible in living cells, they are generated during the process of cell death following exposure to stress, thereby exhibiting an immune-stimulating effect. DAMPs expressed by cancer cells exposed to ICD can be divided into three classes: (1) cell surface DAMPs such as CRT, HSP 70, and HSP 90; (2) extracellularly released DAMPs such as HMGB1, uric acid, and pro-inflammatory cytokines; and (3) end-stage degradation factors such as ATP, DNA, and RNA. DAMPs are recognized by TLRs (toll-like receptors), NLRs (NOD-like receptors), RIG-I-like receptors (retinoic acid-inducible gene-I-like receptors), and RLRs (RIG-I-like receptors). Important DAMPs include calreticulin, HMGB1 (High Mobility Group Box 1), ATP, HSP 70 and 90, type 1 interferon, and Annexin A1. Chronic exposure to these DAMPs interacts with receptors and ligands on dendritic cells (DCs), activating immature DCs to convert them into DCs with a mature phenotype and ultimately accelerating the capture of antigenic components by promoting their phagocytic capacity. In this process, DCs that have captured cancer antigens utilize MHC molecules to present antigen peptides to T cells in the lymph nodes, inducing the generation of effector T cells that migrate to sites of infection, inflammation, or injury. IFN-γ and GM-CSF are key cytokines involved in the maturation of DCs and the activation of macrophages. Upon recognizing an antigen, DCs sequentially release cytokines such as IL-6, IL-12, or TNF, which activate natural killer (NK) and T cell responses. DCs initiate an adaptive immune response by stimulating αβT and γδT cell responses that have the function of killing more cancer cells through antigen presentation, and eventually reach the peak of the immune response with the establishment of a CTL-mediated anticancer immune response capable of killing resistant cancer cells through an IFN-γ-dependent mechanism. Representative methods of ICD currently under study are as follows. Apoptosis induced by high hydrostatic pressure (HHP) treatment affects biomolecules, cellular processes, and viability, which form the basis of antitumor effects. Specifically, apoptosis of cancer cells induced by HHP treatment leads to the expression of immunogenic molecules such as HSP70, HSP90, and CRT, the release of HMGB1 from the nucleus, and an increase in extracellular ATP levels. Another type II ICD process, photodynamic therapy (PDT), induces apoptosis by using laser light on a chemical (hypericin) used as a photosensitizer. PDT preferentially