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4II3 > Pre-Exam > Flashcards

Pre-Exam Flashcards

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1
Q

what are some hallmarks of cancer

A

sustained angiogenesis, inflammatory microenvironment, limitless cell division, evasion of apoptosis, metastasis

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2
Q

most important elements in defense against tumours

A

T cells and IFNy, though immune function as a whole is important

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3
Q

what are some traits selected for in tumours that help them evade T cells

A

mutating tumour-specific antigens, loss of MHC I, expression of PD-1

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4
Q

two main checkpoint inhibitors expressed by tumour cells

A

CTLA-4 and PD-1

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5
Q

some coinhibitory molecules

A

CTLA-4, PD-1, CD80, BTLA, TIM3

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6
Q

tumour-associated macrophages

A

M2-like macrophages, pro-tumour, downregulate M1 cells

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7
Q

Oncostatin M (OSM)

A

elevated in lungs of smokers, expressed by alveolar macrophages, promotes tumour growth

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8
Q

what cells express OSM receptor

A

pretty much every cell except hematopoietic

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9
Q

effect of OSM on Th and macrophage response

A

skews towards Th2 and M2

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10
Q

M1 and M2 macrophage markers, respectively

A

iNOS (nitric oxide synthase), Arginase

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11
Q

does OSM act directly on tumours?

A

no, in vivo experiments increase tumour size but culturing cancer cell lines with OSM doesn’t result in increased growth

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12
Q

does overexpression of IL-6 increase tumour burden in lung?

A

no

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13
Q

N1 v N2 neutrophils

A

N1 = inflammatory/anti-tumour, N2 = protumour

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14
Q

which cytokine promotes switch from N1 to N2 in neutrophils

A

TGFB, IFNB to go the other way

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15
Q

role of ILCs in TME

A

depends, any type can have pro- or anti-tumour activity depending on env’t/stimulation

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16
Q

cancer associated fibroblasts formation

A

acidic TME promotes transformation of fibroblasts to CAFs

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17
Q

% of cells in TME that are fibroblasts

A

20-40%

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18
Q

do CAFs express OSM receptor?

A

yes

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19
Q

what is an engager

A

a molecule that can help antibodies bind antigens, usually tumour antigens

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20
Q

which kind of engager has an equilibrium reaction with its target antibody and antigen?

A

covalent engagers

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21
Q

ternary complex

A

three molecule complex, usually a bifunctional/engager molecule, a target antigen/Fc receptor, and an antibody

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22
Q

common tumour antigens Rullo mentioned

A

uPAR, PSMA

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23
Q

why does effectiveness of bifunctionals decrease when dose gets too high?

A

when there are too many molecules, some will bind target A and others will bind target B, meaning you will not get both A and B bound to the bifunctional at the same time as often as at lower concentrations

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24
Q

CD64

A

FcyR1, found on macrophages

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25
avidity
number of immune-target interactions
26
role of avidity in regulating immune response
many interactions (like interactions of an effector cell with a cancer cell) require a certain number of target molecules to bind (like tumour antigens on a cell surface) in order to respond to that target cell. this helps avoid autoimmunity
27
how can you increase avidity while keeping the same dose of bifunctional?
increasing the number of target-binding termini so that one bifunctional can bind multiple targets
28
correlation between T cell infiltrate and cancer prognosis
positive, more T cells = better prognosis
29
which costimulatory signal upregulates checkpoint receptors on T cells?
MHC-TCR engagement
30
which costimulatory signal causes T cell target cells to upregulate checkpoint ligands?
cytokines
31
how can you treat people who don't have many anti-tumour cells?
adoptive cell transfer. either engineer their own cells and give them back or get a donor
32
why are T cells ideal for cellular medicines?
easily cultured, can be sourced from healthy donors, many phenotypes and functions
33
how can you find tumour-specific T cells from a donor?
with an HIV vector covered in tumour antigens
34
why is it hard to manipulate the alpha/beta TCR chain to induce tumour-specific T cells in people?
everyone's MHC is different, so you would have to consider that in each unique case
35
what is the only essential CD3 component required for T cell activation?
zeta
36
which CD3 chains contain ITAMs, and which one has 3 instead of 1?
gamma, delta, epsilon, and zeta. zeta has 3.
37
ITAM
immunotyrosine-based activation motif
38
what does a CAR consist of?
a custom ligand binding domain and CD3-zeta
39
what is a drawback of CAR therapy?
it is like strict T cell activation, it doesn't account for inhibition
40
what is a T cell antigen coupler
the custom ligand from CAR therapy put on a CD3 binding domain, which is attached to a CD4 co-receptor domain, which is bound to Lck which is required for ITAM phosphorylation
41
how to use a tumour model to test for T cell activity and toxicity
implant tumour, wait a month and infuse T cells, monitor tumour growth/weight loss/cytokines
42
how does mouse body weight change when on CAR vs TAC therapy?
Weight drops considerably over first two weeks on CAR before recovering, TAC mice stay basically identical to controls or even slightly heavier if anything
43
how well do CAR therapies manage tumour growth in mice vs TAC?
CAR kind of maintains tumour size, while TAC actually destroys it
44
why might NK cell immunotherapy be safer than CAR T?
NK cells can differentiate healthy from malignant cells, T cells cannot
45
how much better is adoptive NK cell therapy in combination with normal cancer treatment compared to just the normal treatment
survival goes from 55% to over 90%
46
how does long term NK cell ex vivo culturing in Ascites/Pleural E. change NK cell phenotype
makes CD56+++ population
47
are human tumour associated NKs (taNKs) effective at preventing tumour growth in vivo?
no
48
are human peripheral blood NKs (pbNKs) effective at preventing tumour growth in vivo?
they're decent, better than human taNKs
49
how are pbNKs cultured in ascTME at preventing tumour growth?
really bad. TME form the ascites makes them mostly nonfunctional
50
how does TME change NK cell function? Is there a marker? Is it metabolic?
metabolic changes, taNK cells have reduced glycolysis and TCA cycle
51
what metabolic pathways are affected in NK cells by TME?
DNA replication, mismatch repair, nucleotide metabolism, cell cycle pathways
52
Nrf2
protein involved in antioxidation pathways
53
how can you target NK cell metabolism with a drug to increase NK cell function in TME?
Use a drug called RTA-408 that blocks Keap1, which allows more Nrf2 antioxidant function. Increases glycolysis and TCA cycle
54
how effective is RTA-408 in combination with pbNK cells in preventing tumour growth in vivo
quite effective, more than either on their own
55
how can pbNK cells from ovarian cancer patients be made effective against tumours in vivo?
culturing them in ascites with IL-21
56
how is the metabolism of exNK cells (cultured in ascites with IL-21) different from that of normal pbNK cells?
metabolism prefers glycolysis and lactate over TCA, just like cancer cells. So it can use all that excess lactate in the TME to its advantage
57
how does Warburg-NK cell function change in the TME compared to normal NK cells?
function actually increases more than 2x, whereas normal NK cells lose their function within 12 hours
58
what kind of cancers were found to go away after some viral infections that lead to the idea of oncolytic viral immunotherapy?
lymphomas
59
4 main strategies to achieve safe tumour targeting of OVs
attenuation, transcriptional targeting with tumour-specific promoters, cellular targeting with viral binding receptors specifically for tumours, differential effect on normal vs tumour cells
60
do OVs kill all tumour cells directly or recruit immune cells to finish the job?
recruit immunity
61
how do OVs recruit immune system?
make the tumour inflammatory rather than sterile, T cells come to deal with virus and that can lead to response against tumour
62
what does it mean to turn cold tumours hot?
recruit T and NK cells when there were none before
63
how are OVs manipulated (besides for safety) to improve vaccination effects of recruiting anti-tumour immunity
giving them cytokine/chemokine genes/anti-checkpoint inhibitor antibodies
64
how can you change OVs so that the response to them is also a response to tumours?
by putting tumour antigens in their genome so they will express them and elicit an immune response
65
is OVV more potent than OV on its own?
yes of course
66
OVV vs OV
OVV is a vaccine form, includes other things to induce anti-tumour T cell response
67
ARMs
antibody-recruiting small molecules
68
are ARMs covalent or non-covalent?
non-covalent
69
what is a common molecule ARMs use as the antibody binding domain?
DNP (dinitrophenyl)
70
what mediators do CD8 T cells release to kill tumours
IFNy, TNFa, Granzyme, Perforin
71
what cell surface receptor do NK cells use for ADCC?
CD16
72
does the NK cell source matter when generating Warburg NK cells?
no, can be taNK, pbNK, etc. just need to expose them to IL-21 then train in asc
73
which SyAM is best at mediating ADCP of cancer cells and why
SyAM-P3 because it has 2 Fc- and PSMA-binding regions each

4II3 (3 decks)

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