WEEK 5: CANCER IMMUNOLOGY AND IMMUNOTHERAPY Flashcards

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1
Q

what are the genes called that can mutate DNA causing cancer?

A

oncogenes

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2
Q

what are the 2 types of oncogenes?

A

v-onc (virus oncogenes)
c-onc (cellular oncogenes)

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3
Q

what is the function of a proto-oncogene?

A

its a gene involved in normal cell growth

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4
Q

when a proto-oncogene is disregulated, what does it become?

A

oncogene

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5
Q

what is the role of tumour suppressor genes?

A

inhibit cellular proliferation and regulate programmed cell death

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6
Q

how many mutations does a cell need to transform from a normal to a malignant cell?

A

1-10

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7
Q

how are tumours detected by T cells?

A
  • tumour-specific transplantation antigen (TSTA) (antigens only expressed by tumours)
  • mutated normal antigens
  • antigens expressed at wrong stage of cell growth
  • over expressed antigen
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8
Q

how do tumours prevent CTL recognition?

A

MHC or TAP recognition

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9
Q

can macrophages recognise tumours?

A

yes

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10
Q

how do macrophages destroy tumours?

A

when hyperactive ! , they produce TNF alpha which destroy blood vessels and causes tumour necrosis

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11
Q

how do NK cells target cancer cells?

A

target cells with low levels of MHC i and unusual surface proteins.

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12
Q

why can the antibody immune response be ineffective in destroying a tumour?

A

anti-tumour antibodies can block CTL response, consequently enhancing growth

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13
Q

what’s the difference between a v-onc and a c-onc?

A

v-oncs occur from viruses inserting DNA into our own sequences causing over growth in cells. C-oncs are genes in normal healthy cells that have mutated and then cause more growth than they should.

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14
Q

What is meant by immune surveillance?

A

Immunological surveillance is a monitoring process of the immune system to detect and destroy virally infected and neoplastically transformed cells in the body.

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15
Q

what is a monoclonal antibody?

A

man made antibodies - they all bind to the same epitope so are identical

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16
Q

name 3 monoclonal antibodies used in cancer therapy

A
  • antibody CD20 (CD20 found on cancerous B cells)
  • herceptin (binds to HER-2)
  • mylotarg (binds to CD33)
  • ipilimumab
17
Q

what is meant by passive therapy?

A

the transfusion of antibodies

18
Q

what antigens are targeted by the immune system on tumours?

A

tumour rejection antigens

18
Q

how does ipilimumab work?

A

it blocks negative signalling from CTLA-4 on T cells - stops the T cell being turned off

19
Q

why do tumour rejection antibodies appear on cells?

A

peptides of tumour cell proteins are presented to T cells by MHC molecules

20
Q

which 2 oncogenes are responsible for cervical cancer?

A

E6 and E7

21
Q

what are some of the ways in which vaccines work?

A
  • give the antigen as a protein in the vaccine
  • give the genetic material to the body as a virus
22
Q

what do adjuvants do?

A

make the tumour site more pro inflammatory which will activate macrophages which then activate T cells.

23
Q

what are the cons of cytokine therapy?

A

cytokines don’t stay in one area and may diffuse into other areas

24
Q

what are the pros and cons of using cytokine IL-2?

A

pro - activates T cells and NK cells
con - toxic, so local administration of cyotkine or gene

25
Q

what are the pros and cons of using cytokine interferons?

A

pro - increase MHC i expression on tumour cells which enhances T cell ability to target
pro - increase MHC ii expression on macrophages
pro - inhibit cell division of tumour cells
con - problems with keeping it in local area

26
Q

what are the pros and cons of using cytokine TNF alpha?

A

pro - directly kill and reduce proliferation in tumour cells but not normal cells
con - can affect all systems

27
Q

effective targets for immunotherapy?

A
  • sequestered antigens
  • antigens over expressed in cancer
  • viral antigens
28
Q

which immunotherapy aims to utilise T cells?

A

T cell trans therapies and dendritic cell vaccines which act to activate T cells

29
Q

effective vaccination requires…

A
  • pro inflammatory environment
  • t cell involvement
  • appropriate antigen
30
Q

what is T cell transfer therapy?

A

T cells are removed and go through clonal expansion followed by a transfer back into host which triggers death of the tumour

31
Q

how are T cells engineered?

A

Patient T cells with good anti-tumour responses isolated and their TCRs cloned and inserted into retroviruses or lentiviruses, which are then used to infect autologous T cells from the patient to be treated

32
Q

what are CAR-T cells?

A

a T cell with a genetically engineered binding site of an antibody.

33
Q

pro of CAR-T cells?

A

they can bind more antigens whilst ignoring MHC