Lecture 29 terms Flashcards Preview

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Flashcards in Lecture 29 terms Deck (25)
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1
Q

a type of hypothesis that takes multiple damaging events to cause neoplastic transformation

A

Multi-hit hypothesis

2
Q

antigens which are expressed by both normal and tumor cells expressed at the wrong time, place or level

A

tumor associated antigens

3
Q

antigens expressed only by tumor cells not expressed by healthy cells

A

tumor specific antigens

4
Q

antigens that serve as normal host molecules that are abnormally expressed and include a wide variety of substances

A

tumor associated antigens (TAA)

5
Q

antigens that are abnormal molecules like protein and carbs which are not expressed by healthy cells

A

tumor specific antigens (TSA)

6
Q

proteins and carbs make up this type of TSA

A

mutated self molecules

7
Q

proteins of oncogenic viruses make up this type of TSA

A

foreign molecules

8
Q

well defined stages in tumor progression and each stage is accompanied by changes in immunoregulation

A

tumorigenesis and immunology

9
Q

activation of growth factors, inhibition of apoptosis

A

dysplasia

10
Q

enzyme production (MMPs, uPA) by local inflammatory cells

A

invasion

11
Q

increased production of angiogenic cytokines (VEGF, FGF, PDGF)

A

angiogenesis

12
Q

altered expression of cell adhesion molecules, chemokines, and chemokine receptors

A

metastasis

13
Q

the process by which the immune system protects against cancer growth and the development of tumor immunogenicity

A

The Model of Cancer Immunoediting

14
Q

innate immune cells that monitor for presence of neoplastic cells, then innate and adaptive immunity eliminates them

A

elimination or immunosurveillance

15
Q

adaptive immunity works to control tumor growth, a tug of war as adaptive immune response and cancer cell fight for supremacy

A

equilibrium

16
Q

tumor escapes adaptive immune control by either altering its antigens or immunoevasion or by turning off host immunity immunosuppression; disease becomes apparent

A

escape

17
Q

innate and adaptive immune responses participate in control of cancer

NK, MACs, CD8, cytolytic mechanisms, IL-12, IFN-gamma

A

elimination or immunosurveillance

18
Q

a stalemate in the tug of war between immune response and cancer

CD8, CD4, IFN-gamma, IL-12, cytotoxic mechanisms

A

equilibrium

19
Q

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

A

immunoediting

20
Q

genetically unstable neoplastic cells adapt to immune pressure and continually change to increase chances of escape and survival

A

cancer editing

21
Q

if cancer editing is successful, neoplastic cells leave immune system control and grow to a clinically observable mass

A

escape

22
Q

the neoplastic cell changes itself until it is not recognized by host immune responses

A

immune evasion

23
Q

the neoplastic cell changes the host immune response so it can no longer effectively kills cancer cells

A

immune suppression

24
Q

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

A

DC based immunotherapy

25
Q

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

A

Nivolumab (OPDIVO)