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Gupta, M.;  Wahi, A.;  Sharma, P.;  Nagpal, R.;  Raina, N.;  Kaurav, M.;  Bhattacharya, J.;  Oliveira, S.R.;  G.dolma, K.G.;  Paul, A.; et al. Current Vaccines  and Mechanisms of Cancer Vaccines. Encyclopedia. Available online: https://encyclopedia.pub/entry/38757 (accessed on 06 December 2025).
Gupta M,  Wahi A,  Sharma P,  Nagpal R,  Raina N,  Kaurav M, et al. Current Vaccines  and Mechanisms of Cancer Vaccines. Encyclopedia. Available at: https://encyclopedia.pub/entry/38757. Accessed December 06, 2025.
Gupta, Madhu, Abhishek Wahi, Priyanka Sharma, Riya Nagpal, Neha Raina, Monika Kaurav, Jaydeep Bhattacharya, Sonia Rodrigues Oliveira, Karma G. G.dolma, Alok Paul, et al. "Current Vaccines  and Mechanisms of Cancer Vaccines" Encyclopedia, https://encyclopedia.pub/entry/38757 (accessed December 06, 2025).
Gupta, M.,  Wahi, A.,  Sharma, P.,  Nagpal, R.,  Raina, N.,  Kaurav, M.,  Bhattacharya, J.,  Oliveira, S.R.,  G.dolma, K.G.,  Paul, A.,  Pereira, M.D.L.,  Wilairatana, P.,  Rahmatullah, M., & Nissapatorn, V. (2022, December 14). Current Vaccines  and Mechanisms of Cancer Vaccines. In Encyclopedia. https://encyclopedia.pub/entry/38757
Gupta, Madhu, et al. "Current Vaccines  and Mechanisms of Cancer Vaccines." Encyclopedia. Web. 14 December, 2022.
Current Vaccines  and Mechanisms of Cancer Vaccines
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This entry is adapted from the peer-reviewed paper 10.3390/vaccines10122011

A vaccine is created to develop specific immunity against a particular disease or infection. The purpose of cancer immunotherapy is to activate the immune system so that it can identify and eliminate cancer cells. Anticancer immunotherapies are classified as either “passive” or “active” based on their ability to (re-)activate the host immune system against malignant cells. Tumor-targeting monoclonal antibodies (mAbs) and adoptively transferred T-cells (among other approaches) are considered passive forms of immunotherapy because they have intrinsic anticancer activity. Antigen-specificity is an alternative classification of immunotherapeutic anticancer regimens. While tumor-targeting mAbs are widely regarded as antigen-specific interventions, immunostimulatory cytokines or checkpoint blockers activate anticancer immune responses with unknown (and generally broad) specificity.

cancer vaccines immunotherapy antigen

1. Current Vaccines and Antigens for Cancer Treatment

 Commonly used vaccines and antigens are listed in Table 1.

1.1. Antitumor Response of Therapeutic Vaccine

Although many primary tumors can be surgically removed and there is often a long period of time before the tumor recurs at metastatic sites, cancer vaccines have been proposed as a therapy to elicit and/or boost antitumor immunity in patients with minimal residual disease, thereby preventing or delaying recurrence. Few vaccines have been evaluated in this ideal clinical setting [1]. So far, the majority of phase I and II studies have been conducted in late-stage disease with a relatively large tumor burden following the failure of standard therapies. Even in the best of circumstances, the ability of the immune system to overcome tumor-induced, therapy-induced, or age-induced immunosuppression will be critical to the success of therapeutic vaccines. Another factor that influences the effectiveness of therapeutic vaccines is the growth of tumor cells, which can evade the immune response for various reasons (Figure 1). The development of vaccines for melanoma patients has yielded the most clinical results of any therapeutic vaccine effort. It began with the use of cell lysates from allogeneic tumor cell lines in combination with adjuvants [2][3] or protein products shed into such cell lines [4][5]. These studies included hundreds of patients with advanced stage III or IV melanoma, many of whom had metastatic disease and had failed chemotherapy. In the case of one of these vaccines, Melacine (Corixa Corporation, Seattle, WA, USA), phase I and II trials in stage IV patients revealed a 1020% response rate (clearing of some metastatic sites) and disease stabilization in another 1020% of patients (no progression of tumors that were growing for various periods of time). Melacine was compared to a four-drug chemotherapy regimen in a multi-center phase III study, and the response rates and survival rates were the same [6]. Melacine had an advantage over chemotherapy because it is non-toxic, allowing a higher quality of life when compared to chemotherapy. As a result, Melacine is now available on prescription in Canada and is awaiting approval in the United States. Canvaxin, a similar vaccine preparation, was tested in 1000 stage IV melanoma patients and compared to an equal number of patients who received surgery and chemotherapy but did not receive the vaccine during the same time period. In this single-institution study, the vaccinated group had a small but statistically significant increase in overall survival. A multi-center phase III randomized trial is now underway to evaluate the vaccine.
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Figure 1. Manipulation of antitumor immune responses by therapeutic vaccination. (a) Therapeutic vaccines are administered after the tumor is diagnosed, at the time of interactions between the tumor and the immune system that correspond to part (c). Therapeutic vaccines boost immunity against minimal residual disease and prevent the outgrowth of metastases shown in parts (b,c). A vaccine based on an autologous tumor was administered in an immunostimulatory preparation (with adjuvant) that can activate Langerhans cells—dendritic cells (DCs) that reside in the epidermis. Activated Langerhans cells take up the tumor antigens and traffic to the draining lymph node in which they present antigens to T-cells. B-cells are also activated, and the expected outcome is clonal expansion of tumor-specific T-cells and the production of tumor-specific antibodies. (b) Tumor-specific T-cells migrate to the sites of tumor metastases where they attempt to kill tumor cells that express antigens contained in the vaccine. (c) Metastases that continue to grow are composed of tumor cells that lack antigens recognized by T-cells and antibodies or are otherwise resistant to immune destruction.
DC-based vaccines [7] are the most recent advancement in cancer vaccine development. Autologous or allogeneic tumors [8], apoptotic bodies [9], tumor lysates [10], tumor RNA [11][12], and tumor DNA [13][14] can be loaded into DCs. Most of these preparations have been shown in animal models to be immunogenic and to have the potential for tumor rejection and are currently being evaluated in the clinic. Recently, the results of a phase I study of a vaccine composed of DCs loaded with messenger RNA encoding prostate-specific antigen (PSA) were published. Vaccination of prostate cancer patients with elevated levels of PSA expression induced T-cell responses against PSA in the majority of patients, and the log slope of PSA was temporarily decreased [15], possibly indicating that tumor growth was slowing.

1.2. Antitumor Response of Prophylactic Vaccine

Many of the potentially insurmountable issues that limit cancer vaccines’ therapeutic efficacy would not need to be addressed in the context of preventing cancer. An immune system that has been trained to recognize tumor antigens is predicted to damage the tumor before it becomes clinically visible, heterogeneous, and capable of suppressing and evading the immune response (Figure 2).
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Figure 2. Proposed mechanism of action of prophylactic vaccine. (a) Prophylactic vaccination is used to manipulate antitumor immune responses. Individuals who are at high risk of developing tumors or have been diagnosed with premalignant changes in target tissues would receive prophylactic vaccines prior to the occurrence of tumors. A vaccine based on antigens expected to be expressed by the anticipated tumor is administered in an immunostimulatory preparation (with adjuvant) that can activate Langerhans cells—epidermal dendritic cells (DCs). Activated Langerhans cells transport tumor antigens to the draining lymph node, where they present antigens to T-cells. B-cells are also activated, with the expected result of clonal expansion of tumor-specific T-cells and antibody production. This clonal expansion of effector cells is followed by the generation of a pool of memory cells specific for the tumor antigen/s over time. (b) If a tumor grows in the future, tumor antigens that reach the draining lymph node will reactivate tumor-specific memory cells and trigger a rapid secondary immune response. This response will be distinguished by a large number of effector T-cells, a high titer of antibodies, and continuous activation of DCs at the tumor site, allowing for continuous processing and presentation of tumor antigens and further immune amplification. (c) Since the incipient tumor has not grown large and heterogeneous, it is easily eliminated by the prepared immune response. Furthermore, the memory compartment is expanded by this tumor-mediated boost.
A prophylactic cancer vaccine aims to induce an adaptive primary immune response, enabling a quick and powerful secondary immune response in the event of carcinogenesis [16][17]. The first example of this approach is the Hepatitis B virus (HBV) vaccine, a virus that can lead to cirrhosis, liver cancer, and chronic hepatitis. According to early studies in Taiwanese children, the vaccination program against HBV reduced the risk of hepatocellular carcinoma by 70% [18]. The Human Papillomavirus (HPV) vaccine soon followed [18][19][20]. HPV is a family of carcinogenic, sexually transmitted viruses that can cause various neoplastic illnesses, from benign lesions to metastatic carcinomas. Furthermore, pre-approval trials have shown a very high level of vaccination efficacy (near 100%) [21]. These preventative vaccines work by eliciting an immune response to cells that have undergone malignant transformation through a process known as specific immunity to changed self-antigens [22][23]. When microbes and other foreign substances present in vaccination are administered, it alerts the host’s immune system through the display of damage-associated molecular patterns (DAMPs), which drives innate immune cells such as APCs to release cytokines required for activating T-cells [16]. A prophylactic vaccine can stimulate the development of memory T- and B-cells, which are necessary to prevent a subsequent attack or antigen exposure. When exposed again, the response is more substantial and quicker due to the proliferation of these memory cells [24]. However, many preventative vaccines require unnecessary exposure to cancer antigens, and these vaccines must be designed to ensure that antigens do not increase cancer risk [25]. Additionally, this can make it difficult for the general population to successfully accept and apply preventative cancer vaccines in medical settings. Moreover, there are safety concerns about off-target effects and toxicity of any vaccination components. Another challenge for prophylactic cancer vaccines is the immune system deterioration in aged people, as adaptive immunity is crucial to vaccine effectiveness. Hence, these issues must be addressed to develop a successful prophylactic vaccine [26].
Table 1. Current therapies as cancer vaccines and antigens [14].
Name of
Vaccine/
Antigens		 Type of Vaccine Targeted Site Combination/Route of Administration
Onyvax Anti-idiotype vaccine Colorectal
adenocarcinoma		 Either intramuscularly with the alum adjuvant or endemic with the BCG vaccine
OncoVAX A personalized vaccination/Autologous vaccine Stomach cancer Not in use
Cancer VAX Autologous vaccine Surgery for the management of patients with stage III melanoma Along with the BCG vaccine, another vaccine is administered
NY-ESO-1 Peptide vaccine Stage II to IV cancer displaying the NY-ESO-1, LAGE marker LAGE, or NY-ESO-1 antigens Endemic
11D10 Anti-idiotype vaccine Non-small cell lung cancer in stages II or IIIA (T1-3, N1-2, M0) Beginning 14 to 45 days following surgery
GP100 AND MART-1 GP100, MART-1, and tyrosinase peptides Stage III or IV ocular or mucosal melanoma, or stage IIB IIC, III, or IV cutaneous melanoma In addition to the alum adjuvant
ALVAC-CEA/B7.1 Virus antigens Metastatic colorectal cancer Provided together with treatment as soon as a condition is diagnosed
VG-1000 Vaccine Autologous therapy Carcinomas and melanomas First-line therapy for people with newly discovered malignancies
HSPPC-96, or Oncophage Antigens extracted from melanoma Autologous therapy Heat-shock protein
Sipuleucel-T Dendritic cell vaccine Metastases castrate-resistant cancer that is silent or barely symptomatic (hormone refractory) breast cancer Intramuscularly
HPV Vaccine
• Gardasil		 Human papillomavirus (HPV) Girl’s and women’s vulvar, vaginal, and cervical cancer Given intramuscularly in the greater posterolateral portion of the thigh or the deltoid portion of the right forearm
Cervarix Human papillomavirus (HPV) Types 16 and 18 of the carcinogenic human papillomaviruses (HPV) Three injections of 0.5 mL each into the muscle
Other drugs      
Thalidomide   Multiple myeloma It is advised to take 200 mg of Thalomid once daily (in 28-day treatment cycles) orally with water, ideally just before bed and at least an hour after dinner.
Lenalidomide   Multiple myeloma Administered orally
Bacillus
Calmette–Guérin		   Bladder cancer in its superficial stages, colon cancer, lung cancer, and melanoma There are several ways to deliver Bacillus Calmette–Guerin, including intravenously, subcutaneously, directly into some tumors, intranasally, pharyngeally, or as an inhalation spray into the lungs.
Novel insights into the mechanisms and physiological processes by which the human body can identify and eliminate pre-cancerous and cancerous cells spontaneously, as well as in reaction to certain therapeutic interventions, have been reported in recent years [27][28]. Furthermore, pure, transgenic, or synthesized markers have been used in peptide-based antitumor vaccines to immunize only against a particular set of tumor-associated antigens (TAAs) and then to trigger an immune or inflammatory response against these markers. A variety of methods have been employed in recent years to discover effective antitumor immunotherapies [29][30][31][32] ranging from immunomodulatory monoclonal antibodies (mAbs), which attack CD4+ and CD8+ T-cells protein receptor cytotoxic T-lymphocyte-associated antigen (CTLA-4, also known as CD152), and the transmembrane ligand/receptor axis PD-1/PD-L1 (programmed cell death protein 1 (or CD279)/programmed cell death ligand 1), to vaccine adjuvants and precision delivery based on biomimetic formulations. Additionally, many of these immuno-technologies also activate co-stimulatory receptors found on immunological effector cell surfaces and neutralize substances generated in the TME, such as transforming growth factor β1 [33][34]. In a cancer treatment that includes immunotherapies such as immunostimulatory cell damage (ICD) causative agents, immunostimulatory cytokines are known to activate the immune system of cancer patients, which has been an important treatment modality. In this context, interferon alpha (IFNα) was approved for adjuvant treatment of completely resected high-risk melanoma patients and several refractory malignancies, and high-dose interleukin-2 (HDIL-2) was approved for treatment of metastatic renal cell cancer and melanoma [35]. Some of the marketed cancer immunotherapies are listed in Table 2 [36][37]. Major histocompatibility complex (MHC) components coupled to antibodies are expressed in high quantities by APCs, and have the capacity to take up and handle antigens [38]. Innate defense cells known as oligodendrocytes (DCs) were initially identified and described by Ralph Steinman in 1973 [39]. Due to their distinct characteristics and functions, DCs are by far the most significant APCs working at the juncture of innate and adaptive immunity, which causes the body to activate immunological responses. Different DC subsets have distinct differences in history and transmitter activation [40].
Table 2. Immunotherapies for cancer currently on the market [37].
Paradigm Example Approved * Target
mAbs that target tumors Herceptin Yes Herceptin is approved for the treatment of early-stage breast cancer that is human epidermal growth factor receptor 2-positive (HER2+).
Transfer of adoptive cells Vemurafenib No Vemurafenib is used to slow the growth of certain types of cancer cells.
Oncolytic viruses RIGVIR, Oncorine, and T-VEC Yes The treatment, which is injected into tumors, was engineered to produce a protein that stimulates the production of immune cells in the body and to reduce the risk of causing herpes.
DC-based therapies _ No Targeted treatment that involves extracting and manipulating components of a patient’s immune system (the dendritic cells) to boost its chances of eliminating unnoticed cancer cells.
Vaccinations based on peptides TAS0314 Yes Dramatically suppressed tumor growth.
Immunomodulatory mAbs Rituximab (Rituxan) Yes It specifically targets the CD20 protein. B-cells, a type of white blood cell, have CD20, and it is indicated in patients for non-Hodgkin’s lymphoma and chronic lymphocytic leukemia.
Immunostimulatory cytokines IFN-α Yes Approved for the treatment of some hematological malignancies and AIDS-related Kaposi sarcoma.
Immunosuppressive metabolism inhibitors Rapamycin No Decrease the risk of organ transplant patients to develop cancer.
PRR agonists Imiquimod Yes To achieve the purpose of regulating immunity and treating tumors.
ICD inducers Radiation Yes The best-characterized inducer of immunogenic cell death.
* In one of its forms for use in cancer patients, by the US Food and Drug Administration or an equivalent regulatory agency worldwide.

2. Mechanisms of Cancer Vaccines

For a therapeutic cancer vaccine, it is a prerequisite that it triggers a strong immunological reaction, precisely recognizes, and gets rid of tumor cells (primary and secondary), is antigen-specific, has minimal systemic side effects, and does not generate autoimmune responses [41]. Another consideration is that the vaccine must induce a robust immunological recall to counteract cancer cells, which is critical to attain long-term disease resolution [42]. In reality, relapses, rather than the primary tumor, have been largely blamed for the high cancer mortality rate [43]. The aim of immunotherapy-based cancer vaccines is to activate the endogenous cellular- or humoral-acquired immune system against cancer. Mostly, cancer vaccines induce the production of cancer-specific CD8+ T-cells that specifically recognize and kill cancer cells [44]. Tumor antigen-specific cytotoxic T lymphocytes (CTLs) recognize cancer antigen epitopes by binding to their T-cell receptor (TCR). Furthermore, CTLs via several TCR signaling pathways, such as degranulation (release of perforin/serine protease), or via upregulation of cluster of differentiation ligand (CD95L) or TNF-related apoptosis-inducing ligand (TRAIL), induce cancer cell death. For effective use, CTLs need to be trained by tumor dendritic cells (DCs). Type 1 conventional CD103+ migrating DCs are antigen-presenting cells (APCs) that elucidate CTLs before cancer cell detection via three different mechanisms: cancer antigen adhered to MHC-I, co-stimulatory molecules (CD80/86 and CD28/152), and pro-inflammatory cytokines (IL-12 and TNF-α) [45]. CTLs and CD4C Th cells develop certain characteristics upon activation that greatly influence the subsequent efficiency of CTL cytotoxic responses [46]. In addition, cytokine-mediated DC licensing activates and supports CD4+ Th cells [46]. APCs also activate CD4+ T-cells similarly to CD8+ T-cells, except that the tumor antigen epitope is displayed on MHC-II rather than MHC-I. CTLs and CD4C Th cells develop certain characteristics after activation, that greatly influence the subsequent efficiency of CTL cytotoxic responses [47]. CTL phenotypes are commonly defined by the cytokine cocktail that is released via a cytotoxic mechanism to promote cell death. Many studies have demonstrated that CTL-mediated production of IFN-ϒ and TNF-α corresponds to good tumor reduction potential and improved patient endurance [48]. Other investigations have shown that when CD4C Th cells adopt a Th1 phenotype, characterized by the release of IFN-ϒ, TNF-α, and IL-2, patient endurance improves. Although more debatable [49], it has been demonstrated that combining the Th1 response with a Th17 inclination, as defined by IL-17 production, may be even more advantageous. As each T-cell has a unique TCR that recognizes just one antigenic epitope, immunological responses that create a broad measure of antitumor T-cell levels (many T-cell clones) are stronger [47]. The optimum immune response to immunization may vary amongst malignancies. Cancer vaccination can also harness antibody-mediated cytotoxic pathways to limit cancer progression [50] (Figure 3). Antibody-mediated cytotoxicity and antibody-mediated phagocytosis [51] can be used to kill cancer cells when they bind to antibodies. Cancer vaccines based on humoral immunotherapy, aiming to elicit anticancer antibodies in the patient´s body, have mainly used these techniques for passive immunotherapy [52]. Immunological cells responsible for innate immunity (natural killer cells, macrophages, and neutrophils) can identify the attached antibody Fc receptors and drive cell lysis or phagocytosis, once antibodies recognize epitopes on cancer cell surfaces [53].
Vaccines 10 02011 g003 550
Figure 3. Mechanism of action of cancer vaccines (created with biorender.com).
Finally, coactivation of other innate immunity systems, such as T-cells, can help to enhance the adaptive immune response that is sought by cancer vaccinations. The innate lymphoid cells (ILCs), for example, NK cells or invariant NK T-cells (iNKT), offer complementary abilities to CTLs in terms of cancer cell control. To avoid T-cell identification, cancer cells that downregulate MHC-I or overstimulate NK cell-activating receptors (e.g., NKG2D, 4-1BB) can be lysed by NK cells, which have cytotoxic capabilities [54]. When iNKT cells are activated, they secrete cytokines such as Th1 or Th2 in the surroundings and enhance the expression of CD40L. The importance of iNKT cells in influencing adaptive immune responses has been demonstrated by their ability to aggressively boost DC and B-cell maturation, as well as indirectly promoting T-cell responses [55]. Despite this, cancer vaccinations generally fail to target NK or iNKT cells because they do not bear epitopes.

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Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Madhu Gupta , Abhishek Wahi , Priyanka Sharma , Riya Nagpal , Neha Raina , Monika Kaurav ,
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