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Molecular Basis Of Disease/ Microbiology And Immunology > Anti-tumour Immunity And Immunotherapy For Cancer > Flashcards

Anti-tumour Immunity And Immunotherapy For Cancer Flashcards

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1
Q

Which tumours does immunodeficiency lead to?

A

Kaposi sarcoma and lymphoma

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2
Q

What does tumour immunosurveillance describe?

A

A process where the immune system continually recognises cancerous and pre-cancerous cells leading to their elimination

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3
Q

What are the three phases of immunoediting?

A

Elimination
Equilibrium
Escape

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4
Q

What cells are involved in the elimination phase of immunoediting?

A

NK, NKTs, macrophages and dendritic cells

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5
Q

What chemicals lead to tumour death?

A

INFgamma and chemokines

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6
Q

What happens in the elimination phase of immunoediting?

A

Tumour specific dendritic cells activate adaptive immunity to drain lymph nodes
Tumour specific CD4+ and CD8+ T cells join to clear the tumour

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7
Q

When does the equilibrium phase happen?

A

If the elimination phase is incomplete

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8
Q

What happens in the equilibrium phase of immunoediting?

A

Tumour cells lie dormant and may modulate tumour antigen expression and stress signals

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9
Q

What is tumourigenesis?

A

Normal cells undergoing change develops tumour antigens

Danger signals such as extracellular matrix products can be detected by the immune system

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10
Q

How does the BCG vaccine help with bladder cancer?

A

Involves DC activation
Direct NK activation
Bystander T cell activation

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11
Q

What are type 1 interferons produced by?

A

Virally infected cell

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12
Q

What do type 1 interferons do?

A

Upregulates MHC class1, tumour antigens and adhesion molecules
Activates T cells, B cells and dendritic cells

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13
Q

What is type 1 interferon used in the treatment of?

A

Metastatic melanoma

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14
Q

What is a T cell growth factor?

A

Interleukin-1

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15
Q

What is interleukin-1 used for?

A

Renal cell carcinoma and melanoma

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16
Q

What are LAK cells?

A

PBMC treated with IL-2 and re-infused into patients

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17
Q

What does GM-CSF do?

A

Stimulates APCs

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18
Q

What can GM-CSF be used to treat?

A

Melanoma

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19
Q

What ways can antibodies affect tumour growth?

A

Direct tumour cell killing
Immune-mediated tumour cell killing
Vascular and stromal cell ablation

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20
Q

How does antibody direct tumour cell killing work?

A

Antibodies block receptors and enzymes so they’re conjugated to toxins

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21
Q

How does immuno mediated direct tumour cell killing work?

A

Antibodies binding to cell surface of tumour cell exposes fc portion of the fc receptors on macrophages which then destroy the cell

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22
Q

What is vascular and stromal cell ablation?

A

Removal/destruction of vascular and stromal cells to prevent growth of tumour

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23
Q

What blocks ERBB2 signalling?

A

Herceptin

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24
Q

What does avastin target?

A

VEGF and blocks signalling

25
Q

What is avastin used against?

A

Colon cancer
NSCLC
Gliblastoma
Kidney cancer

26
Q

What is rituximab used for?

A

Anti-CD20 used for CD20 positive B cell non-Hodgkin lymphoma and chronic lymphocytic lymphoma

27
Q

What is alemtuzumab?

A

AntiCD52

28
Q

What is alemtuzumab used for?

A

B-CLL

29
Q

How does ipilimumab work?

A

Blocks the inhibition of CTLA-4 signalling

30
Q

What is ipilimumab used in?

A

Metastatic melanoma

31
Q

What are the ways in which immunotherapy drugs can be delivered?

A

90-yttrium labelled ibritumomab tiuxetan
Brentuximab vedotin
Ontak

32
Q

How does 90-yttrium labelled ibritumomab tiuxetan work?

A

Antibody to CD20 delivering radiotherapy to follicular B cell non-Hodgkin lymphoma

33
Q

How does brentuximab vedotin work?

A

Antibody to CD30 delivering MMAE

34
Q

How does Ontak work?

A

IL-2 delivering diphtheria toxin in T cell lymphoma

35
Q

How does checkpoint inhibition work?

A

Antibody against PD-1

36
Q

What are the cell based therapies for cancer?

A

LAK, NK-T, gamma delta T cells

Dendritic cells

37
Q

What does LAK stand for?

A

Lymphokine activated killers

38
Q

How does LAK cell therapy work?

A

PMBCs taken from patients and cultured with IL-2 in vitro

Causes formation of NK cells which then have higher than normal anti-tumour activity

39
Q

What do NK cells recognise?

A

Lack of MHC-1

40
Q

What are NK-T cells used for?

A

In vitro expanded NKT based vaccines

41
Q

What is the main cell type of NK cells?

A

LAK populations

42
Q

What are the gamma delta T cells structurally similar to?

A

Alpha beta cells

43
Q

What may the gamma delta T cells not need?

A

Normal antigen presentation mechanisms

Recognise peptides and therefore no need for protein processing

44
Q

What do gamma delta T cells recognise/respond to?

A

Respond to MICA and MICB expressed on stressed cells and recognise small organic molecules secreted by bacteria

45
Q

How do you derive dendritic cells for cell based cancer therapy?

A 
Isolate monocytes from a patient
Derive them into immature dendritic cells using GM-CSF  and IL-4
Load DCs with a tumour antigen
Mature DCs into APCDCs
Put back into patient
46
Q

What is the prognosis if lymphocytes are seen in a tumour?

A

Good

47
Q

What is the prognosis if there is a high CD8+/Treg ratio?

A

Higher

48
Q

What has pre-existing antigen specificity of TILs been correlated with?

A

Outcome in immunotherapy on melanoma

49
Q

What is the method for adoptive cell therapies with TILs?

A

Tumour biopsy
In vitro polyclonal stimulation
Lymphodeletion of patient
Stimulated T cells reintroduces into the patient

50
Q

What are the results of adoptive cellular therapy with TILs?

A

Cytotoxicity against tumour cells culture

Homing of transferred T cells to tumour in vivo

51
Q

When do you get the best results for adoptive cellular therapy with TILs?

A

Patients are pre-treated with peripheral lymphodeletion regimen of total body irradiation

52
Q

What are the disadvantages of adoptive cellular therapy with TILs?

A

Need enough tumour to generate sufficient CTLs
TILs may be refractory to stimulation
Time consuming and labour intensive (requires infrastructure)
Culture time may be too long or influence the quality of T cells
High failure rate of culture

53
Q

What does CAR stand for?

A

Chimeric antigen receptors

54
Q

What is CAR composed of?

A

Antibody recognition domains

Cytoplasmic tail with multiple signalling domains that activate T cells

55
Q

What are the advantages of CAR?

A

Specificity and high affinity

56
Q

What is the point of theraputic vaccination?

A

To induce a long lasting response against tumour
Stimulate the adaptive arm of the immune response
Use professional APC such as dendritic cells

57
Q

What happens in high affinity TCR transduction?

A

TCRs reactive to TAAs are characterised and cloned
Alpha and beta chains of TCR are engineered into retro viral vector
Patients CD8+ T cells from peripheral blood are removed and transducers with TCR virus
Adoptive transfer back into patients

58
Q

What are the issues with high affinity TCR transduction?

A

Initial results -> 2/15 patients with clinical response
T cells remain in peripheral blood for up to one year
Epitopes need to be characterised and matched to HLA
Must be present in the tumour
Becomes a patient specific therapy

Molecular Basis Of Disease/ Microbiology And Immunology (57 decks)

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