Abstract
Cancer vaccines are a type of immune therapy that seeks to modulate the host’s immune system to induce durable and protective immune responses against cancer-related antigens. The little clinical success of therapeutic cancer vaccines is generally attributed to the immunosuppressive tumor microenvironment at late-stage diseases. The administration of cancer-preventive vaccination at early stages, such as pre-malignant lesions or even in healthy individuals at high cancer risk could increase clinical efficacy by potentiating immune surveillance and pre-existing specific immune responses, thus eliminating de novo appearing lesions or maintaining equilibrium. Indeed, research focus has begun to shift to these approaches and some of them are yielding encouraging outcomes.
Highlights
The idea of cancer vaccines is not new
We review the previous work on cancer therapies and how to implement them into cancer prevention, giving emphasis to the recently neoantigenbased vaccines and proposing Lynch Syndrome patients as an ideal clinical model to study these approaches
Vaccine efficacy could be enhanced depending on the carriers and/or adjuvants during manufacturing; for example, in vaccines based on dendritic cells, these can be separately saturated with a certain peptide to avoid competition amongst different human leukocyte antigen (HLA) binding affinities, ensuring that all epitopes included in the vaccine will be presented [96]
Summary
The idea of cancer vaccines is not new. it has been studied intermittently over the last four decades. The first antitumoral vaccine clinical trials focused on the identification and targeting of tumor-associated antigens (TAAs) in therapeutic settings, either with synthetic peptides [1,2,3] or with whole tumor cells or cell lysates [4] These approaches elicited minimal impact on overall survival [5], efforts to develop such therapies have persevered over the years due to the high potential of immunotherapeutic vaccines to elicit and amplify antigen-specific immune responses. The idea of CPV against non-viral cancers has been associated with a high risk of autoimmunity because in the vast majority of clinical trials the targeted antigens were TAAs, which generally derive from self-antigens that are selectively or overexpressed in tumor cells or involved in tissue differentiation such as the transmembrane glycoprotein Mucin 1 (MUC1) [20]. We review the previous work on cancer therapies and how to implement them into cancer prevention, giving emphasis to the recently neoantigenbased vaccines and proposing Lynch Syndrome patients as an ideal clinical model to study these approaches
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