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Block 7 Week 1 Colt > Tumor Immunology - Hudig > Flashcards

Tumor Immunology - Hudig Flashcards

(73 cards)

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1
Q

The immune response to tumors is limited because they have few Ags which are similar to (blank)

A

self

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2
Q

Tumors lack microbial (blanks) to activate APCs

A

patterns

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3
Q

The lack of activation of APCs by a tumor leads to an insufficiency of what two cytokines necessary to create an inflammatory response?

A

IL1 and TNFa

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4
Q

The lack of activation of APCs via (blank) by tumors leads to anergy

A

signal 2

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5
Q

T/F: tumors employ active immunosuppresion

A

true

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6
Q

What are the three E’s of tumor avoidance of the immune system?

A

Elimination
Equilibrium
Escape

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7
Q

Describe the elimination phase of tumor growth?

A

This is good: immunosurveillance actually kills highly antigenic neoplasms

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8
Q

Describe the equilibrium phase of tumor growth?

A

Better than actively growing, more like stasis. Balance between tumor growth and killing of tumor cells

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9
Q

describe the escape phase of tumor growth?

A

tumor loses Ags, secretes inhibitory factors, and recruits Tregs to protect it

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10
Q

What two genetic changes favor tumor equilibrium or escape?

A

translocations and polyploidy

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11
Q

At which of the three E’s do we normally make a clinical diagnosis?

A

escape

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12
Q

The goal of tumor tx is the restore which of the two Es?

A

elimination or equilibrium

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13
Q

tumor cells express MHC (1/2), but do not express the other which is necessary to stimualte CD4 T helper cells to activate CTLs

A

express MHCI but not II

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14
Q

If tumor cells don’t express both MHC I and II, how are they at all recognized by the immune system?

A

DC cells engulf the tumor cells whole then express the tumor MHC I and II on their own surface

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15
Q

the process of DCs presenting tumor ags on their surface is the same process as it is for (viruses/bacteria) that infect cells other than DCs

A

viruses

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16
Q

The reason that DC cells are able to activate CTLs after ingesting a tumor cell is because they are able to create a (blank) for the T cell to prevent anergy

A

costimulatory signal 2

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17
Q

What is a tumor specific ag?

A

on a tumor cell but not on a normal cell

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18
Q

T/F: tumor specific ags can be shared via oncogenic viral antigens

A

true

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19
Q

RAS MHC I peptides and MHCI papilloma viral antigens are examples of (blank) viral antigens

A

oncogenic

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20
Q

Tumor specific antigens are the products of oncogenes or mutated (blank)

A

tumor suppressor genes

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21
Q

P210, the product the BCR-ABL fusion, is a tumor specific Ag seen in (blank)

A

CML

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22
Q

RAS is seen in 10% of (sarcoma/carcinoma)

A

carcinoma

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23
Q

p53 mutations occur in what percent of all tumors?

A

50%

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24
Q

(EBV/HSV) can cause tumors

A

ebv

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25
T/F: unique Ig receptors on B cells can lead to lyphoma
true
26
What is a tumor associated ag?
seen on both tumor cells and normal cells
27
the melonma MAGE, HER2 receptor, CEA on colon cancer, PSA, Muc-1, and EGF(R) are all examples of tumor (specific/associated) ags
associated
28
Tumor (specific/associated) ags are over expressed or abnormally (expression at the wrong time) expressed proteins
assocaited, that's why they are in normal cells, they're normally used in housekeeping
29
What are the five cell types that participate in tumor surveillance?
1. Th1 2. Activated macrophages 3. NK cells 4. CTLs 5. Tregs
30
What is the role of TH1 cells in tumor surveillance?
delayed type hypersensitivity responses and activation of macrophages
31
What is the role of the activated macrophages in tumor surveillance?
toxic or cytostatic effects
32
What are the roles of NK and LAK cells in tumor surveillance?
immunosurveillance of stress proteins | Active in ADCC if anti-tumor mAbs are present
33
NK cells use what two compounds to lyse tumor cells?
perforins and granzymes
34
NK cells selectively kill virally infected cells and MHC 1 (neg/pos) cells
negative
35
The NKG2D receptor on cells signals for (OFF/ON) killing
ON
36
The KIR receptor via MHC I signals for (OFF/ON) killing
off
37
How does a lack of MHCI signal for death via NK cells?
no off signal for killing so they constitutively kill cells lacking MHCI
38
Cells killed by NK cells die by (apoptosis/necrosis)
apoptosis
39
What are the roles of the CTLs in tumor surveillance?
recognize tumor MHC I tumor ags
40
What are the roles of the Tregs in tumor surveillance?
they help to activate the CTLs
41
Late stage tumors lose MHC (I/II) expression
I
42
NK cells are CD3 (neg/pos)
negative
43
When are NK cells active in ADCC?
when antitumor mAbs are present
44
Describe the process of a CTL CD8 cell becoming sensitized to particular tumor?
1. Ingestion of tumor cell by DC 2. CD8 attaches to MHCI on DC 3. Thelper CD4 attaches to MHCII on DC 4. Thelper induces activation of CD8 into CDL
45
What are the three ways in which a tumor cell evades the immune system?
1. low immunogenicity 2. treated as self ag 3. tumor induced immune suppression
46
Low immunogenicity of tumors is accomplished by lacking the (blank) ligand, and what two classes of molecules?
MHC ligand and a lack of adhesion and costimulatory molecules
47
What three cytokines do tumors release to actively inhibit T cells?
TGF-b, IL10, and IDO
48
What do tumor cells do to indirectly inactivate t cells?
induce Tregs to protect them
49
The tumor microenvironment persistently supplies the immune system with antigen leading to the downregulation of (blank) causing lower T cell division an the exhaustion of (blank) cells from Ag overstimulation
downregulation of CTLA-4 | exhaustion of cTLS
50
Herceptin acts on the (blank) receptor and is used for breast cancer
HER2`
51
Eribtux acts on the (blank) receptor and is used for colon cancer
Anti-EGFR
52
Rituximab is anti-CD20 and is used in (non/hodgkin) lymphom
NON hodgkin's
53
What is the major effector mechanism for all mAb therapy?
ADCC
54
158 V/V is anti (blank) with high affinity for IgG1
anti-CD16A
55
158 F/F is a (low/high) affinity receptor for IgG1
low
56
HER2, antiEGFR, and anti-CD20 are all used when a patient has (weak/absent) antitumor immunity
absent
57
Anti-CTLA-4 and PD1/CD279 are used when a patient has (weak/absent) antitumor immunity
weak
58
(Anti-CTLA4 / PD1-CD279) blocks a t cell checkpoint and supports proliferation
AntiCTLA4
59
(Anti-CTLA4 / PD1-CD279) is an anti-programmed cell death receptor to keep T helper cells and CTLs alive
PD1 CD279
60
The Her2 receptor pathway is inhibited by mAbs via:
inhibition of Her2 signaling and ADCC
61
antiEGFRs are effective via:
inhibition of EGF signaling
62
Anti-CD20 mAbs are effective via:
ADCC, direct induction of apoptosis, complement dependent cytoxicity
63
T/F: Adoptive transfer of TILs including T helpers and CTLs is an effective treatment option
true, but super fucking expensive, gotta personalize it to each pt
64
In tumor vaccine immunotherapy, autologous tumor cells are transfected with genes for three cytokines including:
IL2, IFNg, and TNFa
65
The (blank) gene in tumor vaccine immunotherapy causes T cell costimulation
B7
66
With no costimulation, T cells become (blank)
anergic
67
What three types of cancer can be killed by host immunity?
Melanoma, carcinoma, and NSCLC
68
Cyclin dependent kinase 4, B-catenin, and Surface Ig idiotypes are tumor (specific/associated) ags
specific
69
eBV can be related to the formation of what type of lyphoma?
Burkitt's Lymphoma
70
t/f: antigenic modulation and the creation of physical barriers to immune cells are common methods that tumors evade the immune system
false; antigenic modulation is questionable and the formation of physical barriers is seen in rodents
71
In antitumor therapy, (blank) antitumor responses are enhanced
specific
72
In antitumor therapy, (blank) antitumor responses are maintained
durable
73
In antitumor therapy, antitumor responses persist (with/without) continual therapy
without!

Block 7 Week 1 Colt (9 decks)

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