Description:
<jats:title>Abstract</jats:title>
<jats:p>Cancer Immunoediting is the process by which the immune system controls and shapes cancer. We originally envisaged that cancer immunoediting would occur in three phases: Elimination (also known as cancer immunosurveillance, the host protective phase of the process), Equilibrium (the phase in which tumor cells that survive immune elimination remain under immunologic growth control resulting in a state of functional tumor dormancy) and Escape (the phase where clinically apparent tumors emerge because immune sculpting of the tumor cells has produced variants that display either reduced immunogenicity or enhanced immunosuppressive activity). Strong experimental data has now been obtained using mouse models of cancer to demonstrate the existence of each phase of the cancer immunoediting process and compelling clinical data suggests that a similar process may also occur during the evolution of certain types of human cancer. Our efforts now focus on elucidating the molecular and cellular mechanisms that underlie each phase of cancer immunoediting and identifying the critical checkpoints that regulate progression from one phase of the process to the next. This approach has led to the discovery of a new mouse cancer model that shows remarkable developmental, molecular and functional similarity to human estrogen receptor alpha positive (ERα+) luminal breast cancer. We have found that the cancers in our mice arise as a result of dysfunctional JAK-STAT pathway signaling and, interestingly, this observation has led to the discovery of a heretofore-unrecognized similar phenotype in a subset of human ERα+ luminal breast cancers. The therapeutic implications of our work will be discussed.</jats:p>
<jats:p>Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr BS3-1.</jats:p>