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Block 7 Week 1 > Cancer immunology-Hudig > Flashcards

Cancer immunology-Hudig Flashcards

1
Q

What is the immunotherapy for advanced melanoma?

A

adoptive transfer of tumor infiltrationg lymphocytes (TILs) CD8 CTLs

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2
Q

Why are TILs so awesome?!!?!?

A

because they affect only the tumor and it lasts a lifetime (immunological memory)

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3
Q

Why is not awesome about TILs?

A

immune response to tumor is limited because tumor is similiar to self (few antigens. tolerance)

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4
Q

What about a tumor makes it hard to be recognized as foreign?

A

low amount of antigen, lack of microbial ‘patterns’ to activate defenses, lack of inflammation at oncogenic site, immunosuppresion inside the tumor

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5
Q

What do microbial patterns activate?

A

APCs, generate IL-1, and TNF alpha cytokines and signal 2

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6
Q

What are the 2 types of immunotherapies?

A

passive

enhancing active immunity

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7
Q

Tumor immunity is (blank)

A

weak

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8
Q

Tumor antigens are tolerated as (blank)

A

self

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9
Q

Persistent immune responses to tumors leads to T cell (blank)

A

exhaustion

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10
Q

The tumor (blank) is suppressive

A

environment

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11
Q

Why is tumor immunity weak?

A

tumorgenesis induces T cell anergy- resulting in lack of inflammation and “signal 2”

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12
Q

Progression from normal to malignant is a multi-step mutational process that takes (blank)

A

years

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13
Q

Explain the path to get colorectal cancer

A

normal epithelium-> tumor supressor gene (APC) lost-> excessive epithelial proliferation-> oncogene (RAS) activated-> small benign tumor -> tumor suppressor gene (DCC) lost-> large tumor-> tumor becomes invasive-> rapid accumulation of mutations-> metastasis

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14
Q

The (blank) indirectly regulates transcription of a number of critical cell proliferation genes, through its interaction with the transcription factor beta catenin.

A

APC gene product

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15
Q

APC itself stabilizes

blank

A

microtubules

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16
Q

WHen unbound to netrin 1, (blank) activates apoptosis, so considred a “conditional tumor supressor”

A

DCC

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17
Q

In colorectal cancer, by regulating apoptosis in the absence in netrin-1, DCC is a conditional tumor suppressor. In normal conditions, DCC induced apoptosis limits cellular lifespan in the intestineal crypt and thereby inhibits the initiation of malignant transformation.
T or F

A

T

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18
Q

Absent (blank) expression is a strong predictor of poor survival in stage II and stage III CRCs

A

DCC

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19
Q

If p53 is autosomal what is the least number of mutational hits would it take to inactive p53.

A

2

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20
Q

T or F

very few tumors are caused by viruses

A

T (otherwise we could just go after the virus antigens)

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21
Q

Where are passive immunotherapies made?

A

fermenters

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22
Q

Where are active immunotherapies made?

A

CTLS in a person

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23
Q

If p53 is autosomal what is the least number of mutational hits would it take to inactivate p53

A

2 mutations

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24
Q

How many “hits” are illustrated here for colorectal carcinoma?

A

6 mutations and 1 oncogene (dominant)

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25
Q

What are the 3Es of tumor immunity?

A

Elimination; immunosurveillance of highly antigenic neoplasma
Equilibrium between tumor growth and immune killing
Escape; tumor loses antigens, secretes inhibitory factors, grows fast, recruits Tregs, etc…

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26
Q

When do you usually diagnose cancer?

A

after “escape”

want to re-create elimination or restore equilibrium

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27
Q

tumor is a (blank) arising from on cell

A

clone

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28
Q

What is the elimination phase of tumor immunity?

A

when tumor arise in tissue, a number of immune cells can recognize and eliminate them

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29
Q

What is the equilibrium phase of tumor immunity?

A

variant tumor cells arise that are more resistant to being killed
Over time a variety of different tumor varients develop

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30
Q

What is the escape phase of tumor immunity?

A

eventually, one variant may escape the killing mechanism or recruit regulatory cells to protect it, and so spread unchallenged

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31
Q

Transplantable tumors in syngeneic mice indicated (blank)

A

tumor immunity

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32
Q

Everyones tumor antigens will be (blank)

A

different

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33
Q

Research and recent clinical success have verified that some human tumors are recognized and can be killed by immunity… which ones?

A

melanoma, renal carcinoma, non-small lung carcinoma

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34
Q

Normal cells presents self peptides bound to MHC molecules. A poitn mutation in a self protein allows binding of a (blank) peptide to MHC molecules and creates a new (blank) for recognition by T cells

A

new

epitope

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35
Q

How can you get a tumor antigen?

A 
by changing an amino acid in a self protein 
(middle of polypeptide binds to t cell receptor so 2 ways to make a tumor antigen)
1) point mutation in center of self peptide causes it to be recognized as foreign by T cell receptor
2) point mutation at end causing foreign recognition by MHC class I
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36
Q

What happens if you get a change in the amino acid of a self protein at the end of the 9-11 amino acid?

A

You will get a new peptide that will anchor into the MHC class I that is still seen as self to the T cell receptor but was not normally presented :) and is now seen as foreign cuz of the irregular attachment at the end

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37
Q

To get a CTL response, what other cells and antigens are needed?

A

T helper cells and MHC2 tumor peptide antigens and CTL

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38
Q

Where do you find tumor specific antigens (TSA)?

A
  • on tumor cells but not on normal cells

- unique or shared (oncogenic viral ag’s)

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39
Q

What are some examples of TSA?

A

Ras mutant peptides in MHC 1;

Papilloma viral antigens in MHCI

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40
Q

What are tumor associated antigens (TAA)?

A

on tumor and normal cells

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41
Q

What are some examples of TAA?

A

melanoma MAGE
HER2 on breast carcinomas
Carinoembyronic antigen (CEA) on colon cancers, prostate specific antigens

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42
Q

(Blank) are products of mutated oncogenes and other tumor suppressor genes.

A

Tumor specific antigens

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43
Q

What are some tumor specific antigens?

A
  • RAS mutations
  • P210 product of Bcr/Abl (kinase)
  • Mutated p53 tumor suppressor protein
  • Viral antigens of EBV-associated tumors
  • Unique Ig receptors on B cell lymphomas
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44
Q

(blank) mutations are in 10% of human carcinomas

A

Ras

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45
Q

(blank) rearrangements are common in chronic myelogenous leukemia (CML)

A

P210 product of Bcr/Abl

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46
Q

Mutated (blank) proteins are found in 50% of human tumors.

A

p53

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47
Q

(blank), (blank), (blank) in melanomas (normally expressed in melanocytes) are tumor associated antigens

A

tyrosinase, gp100, MART

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48
Q

(blank), (blank), (blank) proteisn expressed in melanoma and many other carcinomas, proteins that are normally only expressed in the testis and placenta. These are tumor associated antigens.

A

MAGE, BAGE, GAGE

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49
Q

(blank) are on some breast cancer cells. These are tumor associated antigens.

A

HER2

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50
Q

(blank) are higher on tumor cells. This is a tumor associated antigen.

A

Muc-1

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51
Q

(blank) factor and (blank) receptor are higher in cancer cells. This is a tumor associated antigen.

A

Epidermal growth factor (EGF) and EGFR

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52
Q

(blank) is an epithelial membrane antigen the is elevated in colon, breast, ovarian, lung and pancreatic cancers.

A

Muc-1 (mucin)

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53
Q

There are (blank) classes of tumor rejection antigens

A

7

54
Q 
What class of antigen do these belong to:
Cycline-dependent kinase 4
Beta-catenin
Caspase 8
Surface Ig/idiotype
A

TUmor-Specific

(mutated oncogene or tumor suppressor, unique to one cell, not in normal tissues_

55
Q

What is the antigen that is found in melanoma and is a cell-cycle regultor?

A

cyclin-dpenedent kinase 4

56
Q

What is the antigen that is found in melanoma and is a relay in signal transduction pathway?

A

beta-catenin

57
Q

What is the antigen that is found in squamos cell carcinoma and is a regulator of apoptosis?

A

Caspase 8

58
Q

What is the antigen that is found in lymphoma and is a specific antibody after gene rearrangements in B-cell clone

A

Surface Ig/idiotype

59
Q

What class of antigen does this belong to:
Mage-1
Mage-3
NY-ESO-1

A

cancer-testis antigens

60
Q

What antigen is this:

found in melanoma, breast, gilioma and are normal testicular proteins?

A

MAGE-1
Mage-3
Ny-ESO-1

61
Q

What is the best class of antigen to develop drugs for?

A

tumor-specific

62
Q

What class of antigen does tyrosinase and alpha fetoprotein belong to?

A

differentiation

63
Q

What does tyrosinase and alpha fetoprotein do?

A

enzyme in pathway of melanin synthesis

64
Q

What is the tumor type that tyrosinase and alpha fetoprotein are antigens for?

A

melanoma and hepatoma

65
Q 
What is the antigen and what class does it belong to:
a receptor tyrosine kinase that is found on breast and ovary tumors
A 
Her-2 neu 
(class is abnormal gene expression)
66
Q

(blank) is a set of antigen-binding sites that characterizes the antibodies produced by a particular clone of antibody-producing cells.

A

idiotype

67
Q

What is the most desirable tumor for anti tumor drugs?

A

melanoma

68
Q 
what is this antigen and what class of antigen does it belong to:
works on leukemia and is a transcription factor;
A

wilm’s tumor-(class is abnormal gene expression

69
Q 
what is this antigen and what class of antigen does it belong to:
works on breast and pancrease tumors, underglycosylated mucin
A 
Muc-1
(class is abnormal post-translational modification)
70
Q 
what is this antigen and what class of antigen does it belong to:
Works on melanoma, retention of introns in the mRNA
A

gP100 and TRP2 (abnormal post-transcriptional modification class)

71
Q 
What is the antigen and what class of antigen does it belong to:
Viral transforming gene product that is found on cervical carcinoma and burkitt's lymphoma
A

HPV type 16. E6 and E7 proteins and EBV

72
Q

There are 5 antigens found within melanom, this is why melanoma is most desirable tumor for anti-tumor immunity. t or f

A

t

73
Q

What are the 5 cell types active in tumor immunity?

A 
Th1 T
Macrophages
Cytotoxic T lymphocytes
NK cells
Tregs
74
Q

How can you get TH1 T helper cells (CD4 ) cells to recognize a tumor?

A

the tumor needs to die to be presenting by MHC class II

75
Q

DTH and TH1 activates (blank)

A

macrophages

76
Q

Activated macrophages are (blank)

A

toxic/cytostatic

77
Q

cytotoxic T lymphocytes kill tumors via tumor antigens in (blank) proteins

A

MHC1

78
Q

What do this:
in immunosurveillance, to stress proteins
-late stage if tumors lose MHC class I’s
-active in ADCC if anti-tumor ab’s present

A

NK cells

79
Q

What does this:

reduces CTL and NK function (baand THd)

A

Tregs

80
Q

Tumors that lose (blank) expression can be killed by NK cells

A

MHC 1 expression

81
Q

Are NK cells T cells?

A

no

82
Q

(blank) are CD3-, use perforin and granzymes.

A

NK lymphocytes

83
Q

What do NK and LAK (lymphokine-activated killer) cells do?

A

selectively kill virally infected cells and MHC I-negative cells

84
Q

What makes up 15% of all peripheral blood lymphocytes (PBLs) in all people?

A

NK and LAK cells

85
Q

How do Nk and LAK cells manage their killing?

A

have complex “on-off” receptors to “kill” and “inhibit killing”

86
Q

Activating NK receptors such as NKG2 say (off/on) for killing

A

On

87
Q

MHC i signals “off” through (blank) receptors on NK cells.

A

KIR

88
Q

In the “on/off” balance of activation of NK and LAK cells, the balance usually favors (blank)

A

off

89
Q

If you lose MHC I signals what happens to your killing balance?

A

NK cells stay on and kill

90
Q

Control of NK cells is very well regulated. T or F

A

T

91
Q

NK cells will not kill solid tumors, however if you activate them with (blank) you can activate them to kill.

A

IL-2 or IL-21

92
Q

Tumor antigens take up and presented by APCs in absence of co-stimulation will be treated as (blank)

A

self

93
Q

What are the five mechanisms where by tumors avoid immune recognition?

A
  • low immunogenicity
  • tumor treated as self antigen
  • antigenic modulation
  • tumor-induced immune suppression
  • tumor-induced privileged site
94
Q

What is antigenic modulation that can lead to avoidance of tumor recognition by immune system?

A

antibody against tumor cell-surface antigens can induce endocytosis and degredation of the antigen. Immune selection of antigen-loss variants.

95
Q

How do you get tumor-induced immune suppression?

A

factors (ie TGF-beta, IL-10, IDO) secreted by tumor cells inhibit T cells and induce regulatory T cells (ie suppress immune response)

96
Q

What are tumor-induced priveleged sites?

A

factors secreted by tumor cells create a physical barrier to immune system

97
Q

The tumor microenvironment represents peristent antigens, what are they?

A

CTLA-4 down regulation of T cell division

Immune exhaustion of CTLs

98
Q

(blank), also known as CD152 (cluster of differentiation 152), is a protein receptor that downregulates the immune system. It is found on the surface of T cells, which lead the cellular immune attack on antigens. The T cell attack can be turned on by stimulating the CD28 receptor on the T cell. The T cell attack can be turned off by stimulating the (blank) receptor, which acts as an “off” switch.

A

CTLA-4
CTLA-4
awesome anticancer target*

99
Q

What are the types of immunotherapies?

A
  • Passive mAb

- Enhancing active immunity

100
Q

How do you get passive mAb?

A

blocking growth factor receptors

supporting ADCC

101
Q

How do you get enhanced active immunity?

A
  • increase weak anti-tumor immunity
  • adoptive transfer of activated LAKs
  • adoptive transfer of CTLs
  • Vaccines to boost immunity
102
Q

What is the monoclonal anti-HER2 for breast cancer ?

A

herceptin

103
Q

What is the monoclonal anti-EGF for colon cancer?

A

Erbitux (cetuximab)

104
Q

What is the monoclonal anti-CD20 for non-hodgkins lymphoma?

A

Rituxan (rituximab)

105
Q

(blank) is the major effector mechanism for the major Mab’s for anti tumor associated antibodies.

A

ADCC

106
Q

The alleles of CD16 which are F/F (used in ADCC) allow for more or less affinity with monoclonal therapies. If you have a F/F allele type rather than an F/O allele type, will you respond better or worse to rituxan

A

worse

107
Q

what is the percent of F/F people in the general population?

A

32%

108
Q

Her2, a receptor of EFG receptor family, is expressed on both normal tissue and 20-30% of all (blank)

A

breast carcinomas

109
Q

What are the three breakthroughs of 2013?

A
  • specific anti-tumor responses enhanced
  • durable anti-tumor responses maintained
  • responses persist without continual therapy
110
Q

Anti-CTLA-4 (CD153) increases (blank)

A

tumor-specific T cells

111
Q

Anti-programmed death receptor 1 (PD-1, CD279) to keep (blank) and (blank) alive and functional.

A

T helper

CTL

112
Q

PD-1 receptor on T cell encounters PD-1 ligand and the (blank) dies

A

T cell

therefore you want to block PD-1

113
Q

(blank) is co-stimulatory molecule with B7

A

CD28

114
Q

What are the 2 Mabs to increase T cell activities?

A

Mab anti-CTLA-4 (CD 152)

Mab anti-PD-1 (CD279)

115
Q

(blank) ipilimumab (YervoyR) IgG1 & tremelimumab IgG2; block one T cell checkpoint and support proliferation.

A

Mab anti-CTLA-4

116
Q

(blank) nivolumab (?R) IgG4; pembrolizumab (KeytrudaR); lambrolizumab blocks programmed death receptor

A

Mab anti-PD-1

117
Q

Which is better IgG1 or IgG4?

A

IgG4 because it does nto kill the cell (short half life)

igG1 has long half life

118
Q

(blank) and (blank) block program cell death as a Mab anti-PD-1?

A

pembrolizumab

lambrozilumab

119
Q

(blank) is an IgG1 and (blank) is an IgG2 blocks one T cell checkpoint and supports proliferation as a Mab anti-CTLA-4 (CD152).

A

Ipilimumab

tremelimumab

120
Q

anit-melanoma, bladder, carcinoma, renal carcinoma, and nonsmall cell ung carcinoma responds to (blank) and (Blank) durably for greater than 2 years after 4 rounds of 2 mAbs every 3 weeks.

A

nivolumab

ipiimumab

121
Q

What is a tumor vaccine?

A

to boosts patient’s active immunity.

Vaccine is autologous tumor transfected with genes for cytokines or other proteins.

122
Q

What are the components of the tumor vaccine?

A

IL-2, gamma IFN, IL-12, TNFapha genes and B7 gene

123
Q

What does the B7 gene do?

A

provides T cell costimulation

124
Q

How do you make a tumor vaccine?

A

put genes into bacterial plasmid w/ strong promotor. Transfect individual patients tumor w/ plasmid and grow transfected autologous tumor and use as immunogen (good in mice, yet to work well in people)

125
Q

Most tumor rejection antigens are unique to a specific (blank), so tumor vaccines may need to be customized for each patient.

A

cancer

126
Q

To overcome (blank), individuals tumor can be transfected with B7 co-stimulatory molecules and used to re-stimulate T cells.

A

anergy

127
Q

(blank) is the absence of the normal immune response to a particular antigen or allergen.

A

anergy

128
Q

Malignant tumor cells expressing Tumor related antigens (TRA) but no co-stimulatory molecules. Naive CD8 T cells specific for TRA cannot be activated by the tumor cells and may be rendered (blank). If you transfect tumor cells with B7. Tumor cells expressing B7 can activate TRA-specific (blank) cells and activate them which can eliminate tumors.

A

anergic

CD8 T cells

129
Q

tumors have (Blank) but most tumors are weakly immunogenic

A

tumor-specific antigens

130
Q

Tumors evade immune detection and immune effectors. (blank) immunotherapies are in use against tumor associated antigens.

A

mAb

Block 7 Week 1 (10 decks)

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