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

Tumor Immunology - Hudig Flashcards

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
Q

T/F: unique Ig receptors on B cells can lead to lyphoma

A

true

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26
Q

What is a tumor associated ag?

A

seen on both tumor cells and normal cells

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27
Q

the melonma MAGE, HER2 receptor, CEA on colon cancer, PSA, Muc-1, and EGF(R) are all examples of tumor (specific/associated) ags

A

associated

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28
Q

Tumor (specific/associated) ags are over expressed or abnormally (expression at the wrong time) expressed proteins

A

assocaited, that’s why they are in normal cells, they’re normally used in housekeeping

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29
Q

What are the five cell types that participate in tumor surveillance?

A
  1. Th1
  2. Activated macrophages
  3. NK cells
  4. CTLs
  5. Tregs
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30
Q

What is the role of TH1 cells in tumor surveillance?

A

delayed type hypersensitivity responses and activation of macrophages

31
Q

What is the role of the activated macrophages in tumor surveillance?

A

toxic or cytostatic effects

32
Q

What are the roles of NK and LAK cells in tumor surveillance?

A

immunosurveillance of stress proteins

Active in ADCC if anti-tumor mAbs are present

33
Q

NK cells use what two compounds to lyse tumor cells?

A

perforins and granzymes

34
Q

NK cells selectively kill virally infected cells and MHC 1 (neg/pos) cells

A

negative

35
Q

The NKG2D receptor on cells signals for (OFF/ON) killing

A

ON

36
Q

The KIR receptor via MHC I signals for (OFF/ON) killing

A

off

37
Q

How does a lack of MHCI signal for death via NK cells?

A

no off signal for killing so they constitutively kill cells lacking MHCI

38
Q

Cells killed by NK cells die by (apoptosis/necrosis)

A

apoptosis

39
Q

What are the roles of the CTLs in tumor surveillance?

A

recognize tumor MHC I tumor ags

40
Q

What are the roles of the Tregs in tumor surveillance?

A

they help to activate the CTLs

41
Q

Late stage tumors lose MHC (I/II) expression

A

I

42
Q

NK cells are CD3 (neg/pos)

A

negative

43
Q

When are NK cells active in ADCC?

A

when antitumor mAbs are present

44
Q

Describe the process of a CTL CD8 cell becoming sensitized to particular tumor?

A
  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
Q

What are the three ways in which a tumor cell evades the immune system?

A
  1. low immunogenicity
  2. treated as self ag
  3. tumor induced immune suppression
46
Q

Low immunogenicity of tumors is accomplished by lacking the (blank) ligand, and what two classes of molecules?

A

MHC ligand and a lack of adhesion and costimulatory molecules

47
Q

What three cytokines do tumors release to actively inhibit T cells?

A

TGF-b, IL10, and IDO

48
Q

What do tumor cells do to indirectly inactivate t cells?

A

induce Tregs to protect them

49
Q

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

A

downregulation of CTLA-4

exhaustion of cTLS

50
Q

Herceptin acts on the (blank) receptor and is used for breast cancer

A

HER2`

51
Q

Eribtux acts on the (blank) receptor and is used for colon cancer

A

Anti-EGFR

52
Q

Rituximab is anti-CD20 and is used in (non/hodgkin) lymphom

A

NON hodgkin’s

53
Q

What is the major effector mechanism for all mAb therapy?

A

ADCC

54
Q

158 V/V is anti (blank) with high affinity for IgG1

A

anti-CD16A

55
Q

158 F/F is a (low/high) affinity receptor for IgG1

A

low

56
Q

HER2, antiEGFR, and anti-CD20 are all used when a patient has (weak/absent) antitumor immunity

A

absent

57
Q

Anti-CTLA-4 and PD1/CD279 are used when a patient has (weak/absent) antitumor immunity

A

weak

58
Q

(Anti-CTLA4 / PD1-CD279) blocks a t cell checkpoint and supports proliferation

A

AntiCTLA4

59
Q

(Anti-CTLA4 / PD1-CD279) is an anti-programmed cell death receptor to keep T helper cells and CTLs alive

A

PD1 CD279

60
Q

The Her2 receptor pathway is inhibited by mAbs via:

A

inhibition of Her2 signaling and ADCC

61
Q

antiEGFRs are effective via:

A

inhibition of EGF signaling

62
Q

Anti-CD20 mAbs are effective via:

A

ADCC, direct induction of apoptosis, complement dependent cytoxicity

63
Q

T/F: Adoptive transfer of TILs including T helpers and CTLs is an effective treatment option

A

true, but super fucking expensive, gotta personalize it to each pt

64
Q

In tumor vaccine immunotherapy, autologous tumor cells are transfected with genes for three cytokines including:

A

IL2, IFNg, and TNFa

65
Q

The (blank) gene in tumor vaccine immunotherapy causes T cell costimulation

A

B7

66
Q

With no costimulation, T cells become (blank)

A

anergic

67
Q

What three types of cancer can be killed by host immunity?

A

Melanoma, carcinoma, and NSCLC

68
Q

Cyclin dependent kinase 4, B-catenin, and Surface Ig idiotypes are tumor (specific/associated) ags

A

specific

69
Q

eBV can be related to the formation of what type of lyphoma?

A

Burkitt’s Lymphoma

70
Q

t/f: antigenic modulation and the creation of physical barriers to immune cells are common methods that tumors evade the immune system

A

false; antigenic modulation is questionable and the formation of physical barriers is seen in rodents

71
Q

In antitumor therapy, (blank) antitumor responses are enhanced

A

specific

72
Q

In antitumor therapy, (blank) antitumor responses are maintained

A

durable

73
Q

In antitumor therapy, antitumor responses persist (with/without) continual therapy

A

without!

Block 7 Week 1 Colt (9 decks)

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