As the overwhelming majority of the mutations in cancer cells are unrelated to malignancy, the mutation-generated epitopes shall be specific for each individual tumor, and constitute the antigenic fingerprint of each tumor. These calculations highlight the benefits for personalization of immunotherapy of human cancer, and in view of the substantial pre-existing antigenic repertoire of tumors, emphasize the enormous potential of therapies that modulate the anti-cancer immune response by liberating it from inhibitory influences.
–Srivastava N, Srivastava PK (2009)
Modeling the Repertoire of True Tumor-Specific MHC I Epitopes in a Human Tumor.
PLoS ONE 4(7): e6094. doi:10.1371/journal.pone.0006094
(My emphasis)
(See many of my previous posts here for more information)
This is probably a dumb question, but ISTM that most of the mutations in cancer cells are not going to have any functional importance (that is, not something like knocking out a tumor suppressor gene or clobbering p53 or turning a proto-oncogene into an oncogene.) But the functionally important ones, especially when a mutation makes/turns on an oncogene, seem like they should be rather similar for lots of different tumors. Wouldn’t those be a consistent target for an immune response?
But the functionally important ones, especially when a mutation makes/turns on an oncogene, seem like they should be rather similar for lots of different tumors. Wouldn’t those be a consistent target for an immune response?
Yes, definitely, that would be useful. Unfortunately the number of known targets mapping to such essential, common genes are relatively small, so it’s been hard to take advantage of them. If you check out the Tumor Epitope Database, for example, you can get a sense of the number of known shared epitopes vs those that are relatively random (I believe this database actually omits a lot of one-off epitopes, too, so it’s even overstating the proportion of potential targets).