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Foundations 9 > Tumor Immunology > Flashcards

Tumor Immunology Flashcards

1
Q

Cancer and evolution

A

Relatively new problem

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2
Q

Benign tumors

A

Fibrous capsule facilitates removal

Clear margins

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3
Q

Malignant tumors

A

undefined and spreads
Can find CTCs in the blood
Break off and spread

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4
Q

Last place cancer spread

A

Bone and brain

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5
Q

Melanoma goes to

Colon goes to

A

Lung and liver

Liver

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6
Q

Evidence for anti-tumor immunity

A

Spontaneous regression of certain tumors (melanoma)
Infiltration of solid tumors with immune cells
Tumor specific ABs in circulation of cancer pts
Tumors occur more in young and old
Tumors more in immunosuppressed

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7
Q

Solid tumor makeup

A

Fibroblast for structure
Endothelial for vasculature
Host leukocytes
Tumor cells

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8
Q

Innate stimulators of cancer

A

Neutrophils
M2 macrophages
MDSCs

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9
Q

Innate inhibitors of cancer

A

Dendritic (some)

M1 macrophages

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10
Q

Adaptive stimulators of cancer

A

Th2CD4 T cells
CD4 Tregs
B lymphos

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11
Q

Adaptive inhibitors of cancer

A

CD8 cells
Th1CD4 T cells
Th17CD4 T cells

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12
Q

Th1 to Th2 ratio in cancer patients (which is good)

A

Th1 tipped is better for prognosis

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13
Q

NEcessary characteristics of cancer cells

A 
Stimulate own growht
ignore growth inhibiting signals 
Avoid death by apoptosis
Angiogenesis
Metastasis
Replicate constantly
Evade and outrun immune response
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14
Q

Tumor micro-environment

A

Central core of living and necrotic tissue which has outgrown blood supply
Outer living tissue getting blood supply

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15
Q

Differences between tumor cells in micro-environment

A

Metabolic and antigenic differences

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16
Q

Vasculture of tumor cells

A

Sinusoidal
VEGFs are important growth factors
Creates problems for chemotherapy delivery because you don’t know if you’re hitting all cells

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17
Q

Tumor mechanisms of evasion

A 
Down regulate MHC 1 
Down regulate tumor associated antigens 
Release suppressive cytokines (TGF-beta and IL-10)
Stimulate host to release suppressive
Attract or stimulate Tregs and MDSCs
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18
Q

Effect of TGF-beta and IL-10

A

TGF-beta inhibits CTLs, Th1s and increases Tregs

IL-10 inhibits Th1s

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19
Q

Do tumor cells express MHC 1?

A

Some down regulate but yes

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20
Q

Do tumor cells express MHC 2?

A

Only by dendritic, B, and macro normally but can be present sometimes

21
Q

Do tumor cells express costim

A

Should not but sometimes

22
Q

Do tumor cells release cytokineas and chemokines

A

Yes

23
Q

Do tumor cells secrete antibodies

A

Sometimes

24
Q

WHat do you need in order to treat cancer?

A

Acquired immune response

25
Q

Good inflammation of cancer

A

Acute…following chemo or radiation treatments

Can provide precursors to anti-tumor immunity

26
Q

Bad inflammation of cancer

A

Chronic
Neutrohpils release proteolytic enzymes
Cytokines

27
Q

Basic immune response to tumor

A 
Inflammation and capture by DC 
DCs and T cells to draining nodes
Effector cells primed in node
Effect cells go to tumor site
Effector cells function at site of tumor
28
Q

Innate mechs of tumor immune response

A

Complement - inflammatory and MAC
NK cells - both ADCC and decrease in MHC 1
Macrophage - NO mediated macrophage toxicity

29
Q

Antibodies and tumor immune response

A

CDC - complement
ADCC - NK cells
Growth inhibition - block growth factor receptors
Prevent metastasis - block receptors for endothelium

30
Q

Acquired immunity and immune tumor response

A

MHC - Class 2 initiates and class 1 distinguishes self
TCR - Mimicry of pathogen
Effector cells - Cytokine release(IL-2), cytotoxicity, and suppressors

31
Q

Antigen uptake summary

A

DC has CD80/86 binds CD28 of CD8 while MHC 1 binds TCR…CD8 goes to tumor cell and binds MHC1 and kills without costim
DC has CD40 that binds CD40L of CD4 while MHC 2 binds TCR

32
Q

Clona proliferation

A

Th1 and CD8 cells undergo using IL-2 from Th1 cells

NEED costim

33
Q

NK and CTL killing

A

CTL kills if MHC 1 present…if not, then NK cell

34
Q

TAAs

A

Expressed on both tumor and to a degree normal cells
Re-expressed embryonic antigens
Over-expressed low abundance self protein

35
Q

Neo-antigens

A

Mutated gene products specific to tumor cells

Oncogenic viral antigens

36
Q

Self antigen recognition

A

Typically expressed at inappropriate time or over-expressed to point
Recognition hampered and needs to be re-educated

37
Q

CLT mediated anti-tumor response breakdwon

A

50% against shared

50% against neo

38
Q

CEA

A

Carcinoembryonic antigen
Shared
Colon, lung, and breast cancer
CD4 and CD8 have receptors but can’t recognize
Must break tolerance using adjuvant to treat

39
Q

Tyrosinase

A

Expressed by melanocytes

Peripheral tolerance means you need to stimulate

40
Q

Mechs by which tumors evade response table

A 
Low immunogenicity - no peptide/MHC ligand, no adhesion molecules, no costim 
Tumor treated as self antigen 
Antigenic modulation 
Tumor-induced immune suppression
Tumor-induced privileged site
41
Q

MDSC cels

A

Impair differentiation of cells and result in defective antigen presentation

42
Q

Treg cells

A

Impaired activation of CTLs and secretion of suppressive cytokineas

43
Q

Macrophage

A

M2 differentiation

Lack of costim for T cells

44
Q

Dendritiic cells

A

IDO expression and inductionof Tregs

Lack of costim for T cells

45
Q

2 types of MDSC cells

A

Monocytic and granulocytic
Monocytic should become macro or dendritic
Granulocyte release arginase

46
Q

M1 functions

A 
Cytokines
Chemokines
Tumor cell lysis
ROS and RNS 
MMPs
47
Q

M2 functions

A 
pro-angiogenic cytokines and enzymes
ROS and RNS 
Cytokines 
Tissue factor 
MMPs 
Chemokines
48
Q

Three Es of immuno-editing

A

Elimination - immune sys prevailes
Equilibrium - co-exaist
Escape - tumor prevails

49
Q

HIV and cancer relation

A

Txs have developed and now chronic disease…could this happen for cancer?

Foundations 9 (6 decks)

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