Tumor immunology consists of two essential concepts: immune surveillance, w
hich specifies the host immune reactions against tumor cells, and tumor imm
une escape, which refers to the tumor-cell evasion process against the host
immune system. Effective antitumor immunity by the host immune surveillanc
e is supposed to be dependent on the identification of tumor antigens. In t
he process of malignant transformation, genetic mutations with aberrant exp
ression of cancer-related genes and protein products are potentially immuno
genic, which may serve as rejection antigens. Several scenarios are propose
d to be responsible for tumor immune-escape mechanisms. The elucidation of
the immune deficit against cancer progression has been a difficult task and
no solitary mechanism explains the complicated cancer-host immune interact
ions. Cancer cells may overcome immune surveillance through a common but ef
fective pathway, either by changing the polarity of effector cells, thus do
wn-regulating the proliferation of tumor-specific cytotoxic T cells, or alt
ering the effector compositions of immune cells within the tumor milieu, or
both. Understanding the interaction between cancer cells and host immune c
ells within the tumor milieu is of importance for further clinical applicat
ions of immunotherapy in cancer treatment.