Normal or healthy cells have a natural ability to avoid being attacked by the immune system. So if a cancer cell has all inherited 'strategies' for avoiding the immune system (that are from their earlier pre-cancerous states) does this make them hard to detect or be affected by the immune system.
The development of cancer has various reasons. For example in more than 50% of tumors, p53 is mutated. p53 among other things regulates mitosis and forces the cell to arrest in a specific growth state if other systems detected a mutation in the DNA.
But in your special case we have to look at major histocompatibility complexes (MHCs) and NLRC5. There are two types of MHC, namely MHC class I and class II. MHC II presents mostly bacterial peptides to CD4+ T cells causing a immune response. However, MHC I presents viral peptides and peptides from your own body. These peptides are detected by CD8+ T cells which are cytotoxic T cells initializing apoptosis. Without these own peptides natural killer (NK) cells are activated because of a missing-self signal causing apoptosis, too.
Watson et al. (figure 1, Watson et al., Int.J.Cancer, 2006) showed that patients with high MHC I expression or an absent MHC I expression have a higher survival than patients with low MHC I expression. If patients express high levels of MHC I, the chance that these proteins present cancer peptides is higher than patients expressing low levels of MHC I and therefore cancerous cells get killed by cytotoxic T cells probably more often. Without MHC class I, NK cells will initiate apoptosis and cancerous cells will die, too. Patients with low MHC class I expression won´t present so much peptides to cytotoxic T cells and therefore less cancer peptides are presented. But as they have MHC I, NK cells keep inactive. So the cancer finds an escape mechanism in tricking the immune system.
NLRC5 is the biggest member of the NOD-like receptors (NLRs). Expression of NLRC5 can be enhanced by IFN-gamma which activates the JAK/STAT signaling pathway. STAT 1 enhances the expression of NLRC5 and NLRC5 itself can build an enhanceosome with RFX. This enhanceosome raises the expression of MHC class I! NLRC5 is often mutated for example in colorectal cancer. Research now has to focus on how to enhance NLRC5 and therefore MHC class I expression in different cancer types and out of these results to develop an efficient cancer treatment.
I hope that I could help you. Further literature especially on NLRC5 you can find in following paper.
Kobayashi et al., Nat. Rev. Immunology, 2012
Meissner et al., PNAS, 2010
Neerincx et al. (different paper, just google it ;) )
Staehli et al., J. of Immunology, 2015
Yao et al., Protein&Cell, 2012
Of course there are even more, but I think, these paper show a nice overview about this field.