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Y2 Immunology > Tumour immunology and immunotherapy of cancer > Flashcards

Tumour immunology and immunotherapy of cancer Flashcards

1
Q

Give a diagnostic test for paraneopalstic cerebellar degeneration

A

Detection of anti-CDR2 antibody in the serum

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2
Q

Describe the use of anti-CDR2

A

Brown colour shows Ig binding

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3
Q

Describe how a cancer can lead to auto-immune diseases

A

Certain tumours can express antigens that are absent from (or not detectable in) corresponding normal tissues. The immune system can detect such abnormally expressed antigens and launch an attack against the tumour.

In certain cases, this may result in auto-immune destruction of normal somatic tissues

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4
Q

What is the evidence for immune control of tumours in humans

A

Many adults have microscopic colonies of cancer cells

Patients treated for melanoma are used as donors for organs but their recipient develop tumours

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5
Q

What is the relationship between immunosuppression and malignancy

A

Deliberate immunosuppression (e.g. in transplantation) increases risk of malignancy

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6
Q

What is the relationship between malignancy mortality and gender

A

Men have twice as great chance of dying from malignant cancer as do women (women typically mount stronger immune responses)

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7
Q

Which receptors are found on T and B cells

A

alpha-beta T cell receptor
(MHC restricted)

B cell receptors (antibodies)

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8
Q

Describe the cancer-immunity cycle

A
  1. Release of cancer cell antigens (cancer cell death)
  2. Cancer antigen presentation on dendritic cells/APCs
  3. Priming and activation, APCs and T cells
  4. Trafficking of T cells to tumours
  5. Infiltration of T cells into tumours (CTLs, endothelial cells)
  6. Recognition of cancer cells by T cells (CTLs, cancer cells)
  7. Killing of cancer cells
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9
Q

What events may imitate cancer

A

Irradiation
Chemical mutagens
Spontaneous errors during NDA replication
Tumour virus-induced changes in genome

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10
Q

Describe the initiation of tumour growth

A

Aberrant regulation of apoptosis and cell cycle results in tumour growth
Tumour growth (eventually) results in inflammatory signals
Recruitment of innate immunity and subsequent recruitment of adaptive, antigen-specific immunity

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11
Q

Which cells are unbolted in innate immunity to tumours

A

Dendritic cell
Macrophage
Natural killer cell

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12
Q

What are the requirements for activation of an adaptive anti-tumour immune response

A

Local inflammation in the tumour (“danger signal”)

Expression and recognition of tumour antigens

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13
Q

What are the problems that can arise in immune surveillance of cancer

A

It takes the tumour a while to cause local inflammation

Antigenic differences between normal and tumour cells can be very subtle (e.g. small number of point mutations)

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14
Q

Describe the recognition of tumour cells by T cells

A

T cells can ‘see’ inside cells, and canrecognise tumour-specific antigens

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15
Q

Give examples of tumour-specific viral antigens

A 
Epstein Barr Virus (EBV)
Human Papillomavirus (HPV)
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16
Q

Give and example of tumour-specific mutated cellular antigens

A

TGF-beta receptor III

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17
Q

What cancer is caused by post-transport immunosuppression

A

EBV-positive lymphoma

18
Q

What cancer is caused by post-transport HIV

A

HHV8-positive Kaposi sarcoma

19
Q

Give examples of cancers found in immunocompetent individuals

A

HTLV1-associated leukaemia/lymphoma
HepB virus- and HepC virus-associated hepatocellular carcinoma
Human papilloma virus-positive genital tumours

20
Q

Which cancer is HPV associated with

A

Cervical cancer

21
Q

Which antigens are expressed on tumour cells in HPV

A

E6 and E7 oncoproteins

Maintain and induce cervical cancer

22
Q

Describe the HPV vaccination

A

Target antigens (no DNA)
Surface proteins, incorporated into Virus-Like Particles (VLPs)
Intracellular Onco proteins (E6,E7) are targets
GARDASIL

23
Q

What happens in the patients who do not produce an immune response to the HPV16 infection

A

Immune failure
Cervical neoplasia
No immunity
Non-functional immunity

24
Q

What are tumour-associate antigens

A

Tumour-associated antigens (TAA) are normal cellular proteins which are aberrantly expressed (timing, location or quantity).
Because they are normal self proteins, or an immune response to occur tolerance may need to be overcome.

25
Q

Give an example of an ectopically expressed auto-antigen

A

Cancer-testes antigens (developmental antigens): Silent in normal adult tissues except male germ cells (some expressed in placenta).

26
Q

Give an example of cancer-testes antigen

A

MAGE familexpressed in other tumoursy: Melanoma associated antigens. Identified in melanoma also

27
Q

Give examples of tumour-associated antigens

A

Human epidermal growth factor receptor 2 (HER2): overexpressed in some breast carcinomas

Mucin 1 (MUC-1): membrane-associated glycoprotein, overexpressed in very many cancers

Carcinoembryonic antigen (CEA): normally only expressed in foetus/embryo, but overexpressed in a wide range of carcinomas

Prostate-specific antigen (PSA)
Prostate-specific membrane antigen (PSMA)
Prostatic acid phosphatase (PAP)

28
Q

What is tolerance induced by

A

negative selection in the thymus: central tolerance

29
Q

Describe the tolerance of melanocytes/melanomas

A

differentiation antigens
e.g. tyrosinase (melanin production): poor self-tolerance
Local auto-immune depigmentation in melanoma patients

30
Q

What are the two major problems of targeting tumour-associated auto-antigens for T-cell mediated immunotherapy of cancer

A

Auto-immune responses against normal tissues

Immunological tolerance

  • Normal tolerance to auto-antigens
  • Tumour-induced tolerance
31
Q

What are the approaches used for tumour immunotherapy

A 
Antibody-based therapy
Therapeutic vaccination
Immune checkpoint blockade
Adoptive transfer of immune cells
Combination of those above
32
Q

Give examples of “naked” monoclonal antibody-based therapy

A

Trastuzumab (Herceptin®) anti HER2, anti CD20, anti CD52, anti EGFR

33
Q

Give examples of “conjugated” monoclonal antibody-based therapy

A

radioactive particle e.g. Ibritumomab tioxetan (Zevalin®), anti CD20 linked to yttrium-90

drug e.g. Trastuzumab emtansine (Kadcyla®), anti HER2 linked to cytotoxic drug

34
Q

Describe “bi-specific” antibodies and give an example

A

Genetically engineered to combine 2 specificities, e.g. anti CD3 and anti CD19 (Blinatumomab, approved for use in patients with B cell tumours)

35
Q

Which vaccine is FDA approved to treat cancer

A

Provenge® (sipuleucel-T) for advanced prostate cancer

36
Q

What does Provenge do

A

Patient’s own WBC are treated with a fusion protein between prostatic acid phosphatase (PAP) and the cytokine GM-CSF

Stimulates DC maturation and enhances PAP-specific T cell responses

37
Q

Describe the immune checkpoint blockade

A

Rather than directly stimulate responses, this approach seeks to reduce/remove negative regulatory controls of existing T cell responses
Targets CTLA-4 and PD-1 pathways

38
Q

What does CTLA-4 and PD-1 bind to

A

CTLA-4 binds to CD80/86 (costimulatory molecules on APC)

PD-1 binds to PD-L1/L2 (complex expression patterns, may be upregulated on tumours)

39
Q

Give examples of immune checkpoint blockade drugs

A

Ipilimumab (anti CTLA-4), Nivolumab (anti PD-1), antagonistic antibodies

40
Q

What are CARs cells

A

Chimaeric Antigen Receptors
Allows modification of T cell specificity
Activation of CARs as it binds to tissue, it recognises the antibody fragment and causes activation of T cells

Y2 Immunology (5 decks)

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