Lecture 29 terms Flashcards
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a type of hypothesis that takes multiple damaging events to cause neoplastic transformation
Multi-hit hypothesis
antigens which are expressed by both normal and tumor cells expressed at the wrong time, place or level
tumor associated antigens
antigens expressed only by tumor cells not expressed by healthy cells
tumor specific antigens
antigens that serve as normal host molecules that are abnormally expressed and include a wide variety of substances
tumor associated antigens (TAA)
antigens that are abnormal molecules like protein and carbs which are not expressed by healthy cells
tumor specific antigens (TSA)
proteins and carbs make up this type of TSA
mutated self molecules
proteins of oncogenic viruses make up this type of TSA
foreign molecules
well defined stages in tumor progression and each stage is accompanied by changes in immunoregulation
tumorigenesis and immunology
activation of growth factors, inhibition of apoptosis
dysplasia
enzyme production (MMPs, uPA) by local inflammatory cells
invasion
increased production of angiogenic cytokines (VEGF, FGF, PDGF)
angiogenesis
altered expression of cell adhesion molecules, chemokines, and chemokine receptors
metastasis
the process by which the immune system protects against cancer growth and the development of tumor immunogenicity
The Model of Cancer Immunoediting
innate immune cells that monitor for presence of neoplastic cells, then innate and adaptive immunity eliminates them
elimination or immunosurveillance
adaptive immunity works to control tumor growth, a tug of war as adaptive immune response and cancer cell fight for supremacy
equilibrium
tumor escapes adaptive immune control by either altering its antigens or immunoevasion or by turning off host immunity immunosuppression; disease becomes apparent
escape
innate and adaptive immune responses participate in control of cancer
NK, MACs, CD8, cytolytic mechanisms, IL-12, IFN-gamma
elimination or immunosurveillance
a stalemate in the tug of war between immune response and cancer
CD8, CD4, IFN-gamma, IL-12, cytotoxic mechanisms
equilibrium
plasticity of host immunity allows for continual editing to increase the specificity and affinity of the response
affinity maturation of Ab, selection of high affinity TCR bearing T cells
immunoediting
genetically unstable neoplastic cells adapt to immune pressure and continually change to increase chances of escape and survival
cancer editing
if cancer editing is successful, neoplastic cells leave immune system control and grow to a clinically observable mass
escape
the neoplastic cell changes itself until it is not recognized by host immune responses
immune evasion
the neoplastic cell changes the host immune response so it can no longer effectively kills cancer cells
immune suppression
the goal of this therapy is to facilitate DC maturation and Ag processing to generate a DC that can rapidly and efficiently activate CD8 CTL
DC based immunotherapy
a new subset of Ab based drugs that serve as immune checkpoint inhibitors, the target is PD-1 and the mechanism removes block on T cell effector function; binds PD-1 on tumor specific t cell before the t cell can bind PD-L1/PD-L2 on tumor cell and become inactivated
Nivolumab (OPDIVO)