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Gastrointestinal (GI) malignancies are the most common types of human cancers.

Tumour reduction cannot, however, be measured in minimal residual disease when cancer vaccines are most likely to be of clinical benefit.

Serum tumour markers for GI malignancies remain an unvalidated endpoint [43].

Analysis of micrometastasis in bone-marrow or peripheral blood before and after vaccination might be a promising surrogate marker in minimal residual disease [44].

Biodegradable microshperes, virus-like particles, heat-shock proteins (HSPs), and various oil- or lipid-based chemical adjuvants (such as liposomes, ISCOMs, QS21 or AF) promote cross-presentation of the antigen.

Attenuated viral vectors also belong to this category. tetanus toxoid) may also be useful in enhancing and skewing immunity towards a Th1 response [32, 36].

The review comprises a description of the immunogenicity of GI malignancies, various types of tumour antigens and mechanisms of action of cancer vaccines.

Tumour escape from immune surveillance, vaccine strategies and adjuvants are also described.Moreover, tumour response does not always correlate with an improved progression-free or overall survival.It is also difficult to interpret time-to-progression in patients with slow growing malignancies.Gemcitabine treatment for metastatic pancreatic carcinoma is only associated with a marginal survival benefit [3].The 5-year survival for patients with CRC following surgery varies between 80–90% for stage I, 70–75% for stage II, 35–50% for stage III and expanded DCs pulsed with tumour antigens are powerful immunogens.The majority of cancer vaccine studies in GI malignancies have been phase I or II non-randomised trials, which have not primarily been designed to address clinical efficacy.

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