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1.
Med Oncol ; 41(7): 175, 2024 Jun 14.
Article in English | MEDLINE | ID: mdl-38874788

ABSTRACT

The immune system plays a pivotal role in the battle against cancer, serving as a formidable guardian in the ongoing fight against malignant cells. To combat these malignant cells, immunotherapy has emerged as a prevalent approach leveraging antibodies and peptides such as anti-PD-1, anti-PD-L1, and anti-CTLA-4 to inhibit immune checkpoints and activate T lymphocytes. The optimization of gut microbiota plays a significant role in modulating the defense system in the body. This study explores the potential of certain gut-resident bacteria to amplify the impact of immunotherapy. Contemporary antibiotic treatments, which can impair gut flora, may diminish the efficacy of immune checkpoint blockers. Conversely, probiotics or fecal microbiota transplantation can help re-establish intestinal microflora equilibrium. Additionally, the gut microbiome has been implicated in various strategies to counteract immune resistance, thereby enhancing the success of cancer immunotherapy. This paper also acknowledges cutting-edge technologies such as nanotechnology, CAR-T therapy, ACT therapy, and oncolytic viruses in modulating gut microbiota. Thus, an exhaustive review of literature was performed to uncover the elusive link that could potentiate the gut microbiome's role in augmenting the success of cancer immunotherapy.


Subject(s)
Gastrointestinal Microbiome , Immunotherapy , Neoplasms , Gastrointestinal Microbiome/immunology , Humans , Immunotherapy/methods , Neoplasms/therapy , Neoplasms/immunology , Fecal Microbiota Transplantation/methods , Immune Checkpoint Inhibitors/therapeutic use , Probiotics/therapeutic use
2.
Biochim Biophys Acta Rev Cancer ; 1879(4): 189110, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38754793

ABSTRACT

Oncolytic viruses (OVs) are increasingly recognized as potent tools in cancer therapy, effectively targeting and eradicating oncogenic conditions while sparing healthy cells. They enhance antitumor immunity by triggering various immune responses throughout the cancer cycle. Genetically engineered OVs swiftly destroy cancerous tissues and activate the immune system by releasing soluble antigens like danger signals and interferons. Their ability to stimulate both innate and adaptive immunity makes them particularly attractive in cancer immunotherapy. Recent advancements involve combining OVs with other immune therapies, yielding promising results. Transgenic OVs, designed to enhance immunostimulation and specifically target cancer cells, further improve immune responses. This review highlights the intrinsic mechanisms of OVs and underscores their synergistic potential with other immunotherapies. It also proposes strategies for optimizing armed OVs to bolster immunity against tumors.


Subject(s)
Immunotherapy , Neoplasms , Oncolytic Virotherapy , Oncolytic Viruses , Humans , Neoplasms/therapy , Neoplasms/immunology , Oncolytic Viruses/immunology , Oncolytic Viruses/genetics , Oncolytic Virotherapy/methods , Immunotherapy/methods , Animals
3.
Immunology ; 172(4): 547-565, 2024 Aug.
Article in English | MEDLINE | ID: mdl-38566448

ABSTRACT

Ferroptosis, a necrotic, iron-dependent controlled cell death mechanism, is distinguished by the development of lipid peroxides to fatal proportions. Malignant tumours, influenced by iron to promote fast development, are vulnerable to ferroptosis. Based upon mounting evidence it has been observed that ferroptosis may be immunogenic and hence may complement immunotherapies. A new approach includes iron oxide-loaded nano-vaccines (IONVs), having supremacy for the traits of the tumour microenvironment (TME) to deliver specific antigens through improving the immunostimulatory capacity by molecular disintegration and reversible covalent bonds that target the tumour cells and induce ferroptosis. Apart from IONVs, another newer approach to induce ferroptosis in tumour cells is through oncolytic virus (OVs). One such oncolytic virus is the Newcastle Disease Virus (NDV), which can only multiply in cancer cells through the p53-SLC7A11-GPX4 pathway that leads to elevated levels of lipid peroxide and intracellular reactive oxygen species leading to the induction of ferroptosis that induce ferritinophagy.


Subject(s)
Ferroptosis , Immunotherapy , Neoplasms , Tumor Microenvironment , Humans , Neoplasms/immunology , Neoplasms/therapy , Immunotherapy/methods , Animals , Tumor Microenvironment/immunology , Reactive Oxygen Species/metabolism , Cancer Vaccines/immunology , Oncolytic Viruses/immunology , Oncolytic Virotherapy/methods
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