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Review
. 2024 Apr 21;14(4):503.
doi: 10.3390/biom14040503.

Recent Findings on Therapeutic Cancer Vaccines: An Updated Review

Sara Sheikhlary  1 , David Humberto Lopez  2 , Sophia Moghimi  2 , Bo Sun  2
Affiliations
Review

Recent Findings on Therapeutic Cancer Vaccines: An Updated Review

Sara Sheikhlary et al. Biomolecules. .

Abstract

Cancer remains one of the global leading causes of death and various vaccines have been developed over the years against it, including cell-based, nucleic acid-based, and viral-based cancer vaccines. Although many vaccines have been effective in in vivo and clinical studies and some have been FDA-approved, there are major limitations to overcome: (1) developing one universal vaccine for a specific cancer is difficult, as tumors with different antigens are different for different individuals, (2) the tumor antigens may be similar to the body's own antigens, and (3) there is the possibility of cancer recurrence. Therefore, developing personalized cancer vaccines with the ability to distinguish between the tumor and the body's antigens is indispensable. This paper provides a comprehensive review of different types of cancer vaccines and highlights important factors necessary for developing efficient cancer vaccines. Moreover, the application of other technologies in cancer therapy is discussed. Finally, several insights and conclusions are presented, such as the possibility of using cold plasma and cancer stem cells in developing future cancer vaccines, to tackle the major limitations in the cancer vaccine developmental process.

Keywords: cancer vaccines; cold plasma; immunotherapy; stem cells.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 4
Figure 4
Cancer vaccine platforms and their mechanisms of action. All of the discussed vaccine platforms tend to be up taken by the antigen-presenting cells to finally induce and enhance the T cell-mediated pathways of killing cancer cells [404].
Figure 1
Figure 1
APC presentation mechanisms. tumor microenvironment and its components: TME contains a wide range of antigen cross-presentation processes that can be mediated by dendritic cells either through the canonical/cross-presentation pathways (A), or through the non-canonical/cross-dressing path (B). The cross-presentation mechanisms are mediated in two ways: cytosolic or proteosome degradation (A-1) and through the vacuolar pathway (A-2). In the cytosolic pathway, antigens that stem from either endosome or phagosome structures move toward the cytosol, forming acidic cytosolic proteosomes that cleave the antigens into shorter peptides. These peptides have two fates: (1) they are transported to the endoplasmic reticulum (ER) for further modifications. The modified antigenic peptides are then loaded on MHC class I molecules and move to the cell surface. (2) the cleaved peptides return to phagosomes/endosomes prior to loading on the MHC I and moving to the cell surface. In the vacuolar pathway, the aforementioned events related to antigen loading on MHC class I occur in the phagosomes or endosomes, which is followed by the moving of the antigen-loaded APCs (DCs) toward the secondary lymphoid organ (SLO) to activate T cells [13,41,49,50,51,52,53]. In the non-canonical/cross-dressing path, the antigen–MHC complex is formed on another cell and is then transformed to the APCs, such as DCs, and the DCs would finally be able to activate the related effector T cell via different pathways: trogocytosis (B-1), exosome uptake (B-2), and tunneling nanotubes (B-3) [59,60,64,65,66,67]. In Trogocytosis, the membrane patch, including the plasma membrane and cytosol from one cell (donor), is transformed to the other cell (trogocytic) [58,59]; exosome uptake by APCs depends on the ability of the exosomes (small membrane-based vesicles formed during the endocytosis process) to transfer particular materials (that can not only be further degraded and reprocessed by APCs for presentation on the MHC molecules, but can also be considered as functional MHC–peptide complexes [59,68]); the tunneling nanotubes are long protrusions derived from cell membranes that not only facilitate the exchange of cell surface molecules and cytoplasmic contents but also can mediate cross-dressing between remote DCs through the transferring of MHC molecules between distant cells [59,69].
Figure 2
Figure 2
Caner immune cycle phases and regulation. Cancer immune cycle phases are regulated by a wide spectrum of cytokines and chemokines, some of which stimulate the cancer immune cycle to kill the cancer cells, whereas some cytokines act as inhibitors and down regulate the processes. The stimulatory cytokines work together to mediate the T cell activation. Activated T cells go the TME and induce tumor killing. Each phase is regulated by a wide range of cytokines and other molecular factors, as shown in green for inducers and red as inhibitors.
Figure 3
Figure 3
Tumor antigen classifications. In general, tumor antigens are classified as tumor-specific and tumor-associated antigens, each divided into several categories. Each category is compared in terms of (1) tumor specificity (refers to the degree to which a particular immune response targets and interacts specifically with tumor cells or its antigens while sparing normal cells; hence, a high tumor specificity is desired), (2) central tolerance (mechanisms by which the immune system recognizes the self-antigens from cancer antigens and eliminates cancer cells during their development within the body without mounting immune responses against the self-antigens. Thus, a high central tolerance is desired, as it means that the immune system exhibits a strong level of tolerance towards self-antigens, including those present on normal cells and tissues, and can recognize them better), (3) immunogenicity (indicates the ability of cancer cells to stimulate an immune response from the host immune system. This immune response can involve the activation of immune cells, and the production of antibodies against tumor-specific or tumor-associated antigens; so, high immunogenicity is a desired factor), and (4) prevalence (this shows how common or rare the occurrence of tumor antigens is in patients) [25,26,54,93,94,95,96].
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This research was supported by the start-up fund from the College of Pharmacy at the University of Arizona.

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