Brainscape's Knowledge GenomeTM

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


See full index

PATH3309 > Module Four: Cancer Immunology > Flashcards

Module Four: Cancer Immunology Flashcards

1
Q

What is the fundamental prediction hypothesis?

A

Immunodeficient individuals should display a dramatic incidence in tumour incidence

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

Who published the paper which demonstrated no difference in cancer incidence between nude mice and normal mice?

A

Osias Stutman

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

Transgenic animal studies reveal that tumour elimination requires

A

Interferon-gamma, perforin, TRAIL, Type 1 INF (INF alpha/beta)

And the following effector cells:
Innate immunity: NK cells, NKT cells, gamma/delta T cells
Adaptive Immunity: CD8 T cells (cytotoxic T Cells)

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

What are the three E’s of immunoediting?

A

Stage 1: elimination (immunosurveillance)
Stage 2: equilibrium
Stage 3: escape

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

What is transformation?

A

The process of a cell becoming carcinogenic/malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does MIC activate?

A

NKG2D on NK cells

Release perforin

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

What causes the activation and maturation of dendritic cells?

A

The presence of tumour cells and tumour antigens initiates the release of danger cytokines such as INF alpha and heat shock proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CD8 T cells present antigen to what?

A

Class One MHC

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

What is the anecdotal evidence for immune reactivity to tumours in humans?

A
  • autopsy studies reveal that incidence of tumours may be much greater than incidence of cancer
  • spontaneous regression of established tumours have been reported
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the more direct evidence for immune reactivity to human tumours

A
  1. Immunosuppressed transplant recipients have increased incidence of non-viral cancers
  2. Cancer patients can develop spontanous adaptive and innate responses to their tumours
  3. The presence of tumour inflitrating lymphocytes is often a positive prognostic indicator of survival
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Evidence of equilibrium

A

Cancers that come back in transplant patients

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

How to sustain equilibrium?

A
  1. Cellular dormancy
  2. Angiogenic dormancy
  3. Immune dormancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the tumour escape mechanisms?

A

Low immunogenicity
Antigen modulation
Immune suppression by tumour cells or regulatory T cells
Induction of lymphocyte apoptosis

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

How do tumour cells induce apoptosis in T lymphocytes?

A

FAS activation

Cancer cells express FAS ligand and bind to FAS receptor on T lymphocytes leading to apoptosis

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

What is immunotherapy? And who are the key players?

A

Treatment of disease by inducing, enhancing or suppressing the immune system.

Dendritic cells, B cells and T cells

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

How do we induce an adaptive immune response?

A

Antigen
Effector cells (CD4 and CD8)
Antigen presenting cell
Immune target (pathogen/ tumour)

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

How do APCs present antigen?

A 
Class one (endogenous I.e. Inside out)
Class Two (exogenous I.e. Outside in)
Dendritic cells
18
Q

What are the three signals for T cell activation?

A

Signal One: MHC:: TCR interaction
Signal Two: co-stimulation: CD80/86::CD28 interaction
Signal Three: competitive inhibition or co-stimulatory signals: CTLA-4 out competes CD28 for binding to CD80/86

19
Q

Types of cancer immunotherapy?

A

Adoptive cell transfer
Vaccination
Monoclonal antibodies
Immune modulators

20
Q

Examples of adoptive cell therapy

A

Lymphokine activated killer therapy

Tumour infiltrating lymphocytes therapy

21
Q

Genetic modifications of TILs

A

Increase TCR avidity to target
Chimeric Ag receptors
Transgenic approach (humanised mouse) - useful against colon cancer and melanoma

22
Q

Pros of TIL

A

ACT can eradicate tumours
GE modification to increase avidity/ specificity and helped identify best ACT cell populations
Potential for personalised medicine
May compliment other treatment modalities

23
Q

Cons of TIL therapy

A

Limited to patients that tolerate pretreatment conditioning
Most successful in melanoma - not applicable to all cancers
Not FDA approved
Expensive and laborious - requires specialised training and facilities

24
Q

Examples of anti cancer vaccines

A 
Whole tumour cell vaccines
 Peptide vaccines
 Pathogen vector vaccines
 GM tumour cell vaccines 
DNA vaccines 
Fusion vaccines (tumour cells/ antigen + APC)
Prime boost vaccines
25
Q

What was the first FDA approved therapeutic vaccine to treat cancer?

A

Spiuleucel T (Provence) For chemo refractory metastatic prostate cancer

26
Q

What is a 223 AA protein that is expressed on activated lymphocytes?

A

CTLA-4

27
Q

What are the function properties of CTLA-4?

A

In vitro X-linking with CTLA-4 inhibits T cell proliferation
Blockade of CTLA4 with soluble intact Fab fragment promotes T cell proliferation
soluble anti-CTLA-4 fab fragments enhance T cell responses to Peptide AG
CTLA-4 KO mice exhibit severe T Cell proliferative disorders

28
Q

What are the two FDA approved humanised anti-CLTA-4 monoclonal antibodies ?

A

Ipilimumab (IgG1)

Tremelimumab (IgG2)

29
Q

Role of PD -1

A

Maintains peripheral tolerance and prevents autoimmunity

30
Q

Issues with immunotherapy

A

Not all cancers respond as well as melanoma
Side effects: colitis, skin and endocrine side effects
Cost

31
Q

What is a cold tumour?

A

Have very little inflammatory cells
Enriched in immunosuppressive cytokines
High numbers of Treg cells and MDSC

32
Q

What are hot tumour cells

A

Enriched in Thelper 1 Chemokines

High number of effector immune cells high number of functional APCs

33
Q

What do tumour specific CD8 T cells need to recognise on the surface of tumour cells before they will mount an attack?

A

Antigens

34
Q

Why isn’t recombinant interferon used much in cancer patients today?

A

It makes them too sick

And quality of life is diminished

35
Q

How do you identify tumour specific antigens (neo-antigens)?

A

Next generation sequencing

36
Q

How many nucleotides in the full human genome?

A

6 billion

37
Q

What is the name of the component that codes for proteins

A

Exome

38
Q

How many nucleotides code for protein?

A

1-2%

39
Q

How many nucleotides code for an amino acid?

A

3

40
Q

Which tumours are the most highly mutated and which have the lowest mutational burdens?

A

Lung cancer/ melanoma - most highly carcinogens

Vs

Childhood

41
Q

What is the ATTAC cancer trial?

A

Antigen-targeted therapy against cancer

42
Q

Steps of ATTAC cancer program

A

Cancer patient => tumour sampling and bio banking => gene sequencing => neo antigen prediction => advance T cell monitoring => next generation immunotherapy => systems biology => animal models => novel clinical trials

PATH3309 (5 decks)

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