Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology PY2 > Lecture 32: Cancer > Flashcards

Lecture 32: Cancer Flashcards

1
Q

t/f cancer is known as the “emperor of all maladies”

A

t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cancers derive from alterations in “self” cells that enable _____

A

autonomous proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

immune mechanisms contribute to both tumour ____ and _____

A

growth and control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what type of therapies try to support immune-mediated tumour growth?

A

tmmunotherapies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the 2 steps of tumour growth and metastasis?

A
  1. cell acquires DNA mutation(s) that cause excessive growth
  2. Tumour growth outpaces neighbouring cells
  3. tumor cells invade tissues and may impact function (considered malignant)
  4. tumour cells leave the primary site and seed in distal locations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

tumour accumulate _____ mutations that enable autonomous growth

A

genetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the 3 types of genes that underlie cancer?

A
  1. Proto-oncogenes
  2. Tumour suppressor genes
  3. cell death regulators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are proto-oncogenes?

A

proteins that induce cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

if proto-oncogenes are present, the cancer is associated with ____ of function

A

gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the role of tumour suppressor genes

A

restrict cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

if tumour-suppressor genes are present, the cancer is associated with ____ of function

A

loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the function of cancer death regulators?

A

gain or loss of function impacts cancer growth (cells should be induced to die if they have irreparable DNA damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

t/f some cancers have viral origins

A

t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the general mechanism of viral origin cancers?

A

generally associated with insertion and disruption of DNA leading to pro-proliferative features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

t/f some viral cancers can be prevented by vaccination

A

t (ex; HPV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

development of cancer represents an accumulation of unrepaired _____, often occurred over time

A

DNA mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

people with increased cancer risk may have an inborn error in one/more _____

A

oncogenes/tumour suppressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

_____ and _____ mechanisms eliminate most potentially cancerous cells before they cause problems

A

immunologic and non-immunologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the 3 methods of immunoediting?

A
  1. elimination
  2. equillibrium
  3. esca[e
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is elimination by immunoediting?

A

cells that have been damaged exhibit characteristics of “stress” that enable detection and control by immune cells (immunosurveillance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

explain the equilibrium method of immunoediting

A

tumour cells have co-evolved with immune function; they co-exist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

explain the escape method of immunoediting

A

tumour establishes conditions that enable growth despite the immune pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

tumour cells are “self” so why cant lymphocytes detect them well?

A

most self-reactive lymphocytes are negatively selected in the thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are two type of antigens that help lymphocytes recognize cancer cells?

A
  1. tumour-associated antigens

2. tumour-specific antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are tumour-associated antigens?

A

self proteins that are either not selected against, or inappropriately expressed (wrong tissue, wrong time, over expressed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are tumor-specific antigens?

A

non-“self” proteins/peptides that arise from oncogenic virus infection or mutations that create new epitopes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

lymphocytes may recognize tumour-associated/specific antigens and mount what type of immune response?

A

adaptive anti-tumour response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

tumours with normal to high expression of MHC 2 interact with ___ cellls

A

T cells

29
Q

tumours may downregulate ____ to evade recognition by T cells

A

MHC 1

30
Q

if a tumour downregulates MHC1, that is a signal for what cells to come attack it?

A

NK cells

31
Q

what are 5 ways tumours avoid recognition & cause further growth?

A
  1. establish pro-tumour (immunosuppressive) microenvironment
  2. Express co-inhibitory of immune checkpoints that slow/stop antii-tumor immune responses
  3. downregulate MHC1
  4. chronic inflammation which can cause tissue remodeling, blood vessel formation, metastasis and invasion
  5. resistance to apoptosis
32
Q

what is an example of a co-inhibitory or immune checkpoint that slows/stops antitumour immune responses?

A

CTLA-4 and PD-L1

33
Q

what are 2 MOA of medications that can be used in the treatment of cancer?

A
  1. MABs (Anti TAA/TSA)

2. Anti-checkpoint

34
Q

what is the general MOA of MABs for treatment of cancer?

A

Anti-TAA/TSA and induce complement, ADCC

35
Q

give 2 examples of MABs used in the treatment of cancer

A
  1. Rituximab

2. Trastuzumab

36
Q

what is the general MOA of anti-checkpoint medications?

A

interfere with regulatory fx

37
Q

give 4 examples of anti-checkpoint MABS medications used in the treatment of cancer

A

ipilimumab, bretuximab vedotin, pembrolizumab, atezolizumab

38
Q

advanced melanoma treated with ____ and ____ is associated with significantly extended survival

A

anti-PD-L1 and anti-CTLA4

39
Q

what are is the goal of BiTES, BiKEs and TriKEs?

A

redirect killing by engaging an antigen (or two) and an activating molecule (such as CD16)

40
Q

in BiTES, BiKEs and TriKEs, what do: Bi/Tr; K; and E stand for?

A
  1. Bi/Tri: Bi or Tri specific
  2. K: killer, refers to NK; T cells
  3. E: enganger
41
Q

_____ cells are autologous T cells engineered to express an antigen-specific receptor that binds to an antigen (MHC independent)

A

chimeric receptor (CAR)-T cells

42
Q

chimeric antigen receptor (CAR) T cells are connected to intracellular signalling domain (usually ______) and 2nd and 3rd genration give co-stimulatory signals through ______ and/or _____

A

CD3z; CD28 and/or 4-1BB

43
Q

chimeric antigen receptor (CAR) T cells take advantage of ______

A

normal T cell activation pathways and downstream signalling

44
Q

chimeric antigen receptor (CAR) T cells may “overstimulate” and lead to ____

A

cytokine release syndrome

45
Q

what is special about using chimeric antigen receptor (CAR) T cells for cancer?

A

they need to be engineered for each patient (personalized medicine) to avoid rejection reactions

46
Q

what are the 5 steps in using CAR T-cells in cancer treatment?

A
  1. isolation of cells from hst
  2. equip cells w/ new TCR
  3. activation of cells
  4. expansion of cells
  5. re-infusion (go back into patient)
47
Q

luxury “CAR” models attempt to relieve some challenges of ____

A

CAR-T cell therapies

48
Q

CAR__ cells are associated w/ fewer side effects than CAR-T cells and do not need to be autologous

A

NK

49
Q

the truck CAR model

A

use antitumor cytokines to make an anti-tumour microenvironment

50
Q

the universal CAR model

A

no allogenic markers, universally accepted

51
Q

what is the self-driving CAR model?

A

carrying a tumour homing chemokine receptor

52
Q

what is armoured CAR model?

A

dysfunctioning immune checkpoint receptors; T cell resists immunosuppression and activates local immune cells

53
Q

self-destruct CAR

A

externally-delivered signal stops the activity of the T cell

54
Q

conditional CAR model

A

externally-delivered signal starts activity of the T cell

55
Q

viruses are normally inhibited by ____ and/or ____ of infected cells

A

type 1 IFN and/or apoptosis

56
Q

oncolytic viruses take advantage of the tumours loss of _____ and or _____ to grow

A

IFN-1 signalling and or apoptosis

57
Q

what is the function of lysis on oncolytic viruses?

A

lysis allows virus to spread throughout the tumor AND recruits immune cells

58
Q

what are the requirement for MAB treatment?

A
  1. identification of TAA/TSA

2. availability of cells w/i tumour if ADCC is mode of action

59
Q

what are the requirements of BITES, BIKES, and TRIKES for cancer treatment?

A

identification of TAA/TSA

availability of cells w/i tumor/effective cells

60
Q

what are the requirements for cancer treatment with checkpoint blockade?

A
  1. lymphocytes with anti-tumour activity (T and NK cells)

2. Lymphocyte infiltration to tumours

61
Q

what are the requirements for treatment with CAR-T cells?

A

outgrowth of antigen loss variants (i.e. escape of mutants)

62
Q

what are the requirements for treatment with CAR-NK cells?

A

outgrowth of antigen loss variants (i.e. escape mutants)

63
Q

what are the requirements for treatment with oncolytic viruses?

A

if concurrently vaccinating, need to ID antigens

Virus must find and replicate in the tumor (and not elsewhere)

64
Q

what is a potential pifall of MAB treatment?

A

outgrowth of antigen loss variants

risk of autoimmunity/off target effects

65
Q

what are potential pitfalls of BITES, BIKES, TRIKES treatment?

A

may be immunogenic, not yet approved for clinical use

66
Q

what are potential pitfalls of checkpoint blockade as cancer treatment?

A
  1. risk of autoimmunity
  2. outgrowth of antigen loss of variants
  3. loss of T cell fx if MHC 1 is down regulated
67
Q

what are potential pitfalls of CAR-T cells?

A
  1. expensive
  2. potentially time consuming as cells need to be autologous
  3. severe sde effects (cytokine release syndrome)
68
Q

what are potential pitfalls of CAR-NK cell treatments?

A

can be allogeneic

may be more affordable and available than CAR-T cells, but still pricy etc.

69
Q

what are potential pitfalls of using oncolytic viruses for cancer treatment?

A
  1. virus infection needs to be carefully controlled

2. tumour can still inhibit virus infection (spread might be incomplete)

Immunology PY2 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions