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Cancer Biology > Final Exam > Flashcards

Final Exam Flashcards

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1
Q

what are 2 pieces of evidence in support of the theory of immunosurveillance

A
  • mice without immune system = more cancer
  • humans immunosuppressed = more cancer
  • TILS = positive prognosis markers
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2
Q

describe the three Es of immunosurveillence

A

1) elimination- cancer cells arise but eliminated by immune system, immunosurveillence
2) equilibrium
3) escape - clinically detectable tumor

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3
Q

describe one way in which a self antigen can become altered or foreign looking in a tumor

A

during a viral infection, a virus infects a self cell and self proteins/peptides altered or messed up because of mutation, translocation, oncogene activation, overexpression

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4
Q

how can an immune response to an acute infection be potentially useful in preventing the emergence of a tumor

A

acute infections result in immune responses to altered self peptides and immune responses are protective against some tumor antigens
-odds ratio/childhood infections

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5
Q

describe what happens during an acute infection

A
  • self cell stressed and gets messed up
  • altered self antigens during infection
  • memory T cells remain in body
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6
Q

what are the two general approaches for immunotherapy treatments?

A

stimulate existing response and passive immunotherapy

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7
Q

limitations to immunotherapy

A

price, big protein or cell into tumor, old person or person with cancer for a long time has not well immune system

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8
Q

innate immune system

A
  • fast, immediate
  • less specific
  • cells (macrophages, NK, dendritic)
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9
Q

adaptive immune system

A
  • slower to start (3-5 days)
  • very specific
  • cells (T/B)
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10
Q

steps for a virus/bacteria infection

A

1) innate immune system recognizes infection
2) dendritic cells take samples of the viral/bacterial proteins
3) dendritic cell processes proteins into peptides and present peptides on its cell surface with MHC
4) dendritic cell “looks for” T cell that can recognize the foreign peptide
5) T cell that recognizes the peptide will proliferate and differentiate into killer T cell
6) T cell returns to infection and kills infected cells with peptide presented on MHC

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11
Q

cancer steps related to infection

A

1) maybe? the innate immune system recognizes tumor presence
2) dendritic cells (DC) take samples of tumor proteins (antigens)
3) DC processes proteins into peptides and present peptides on its cell surface with MHC
4) DC looks for T cells that can recognize tumor peptide
5) T cell that recognizes the peptide will proliferate and differentiate into killer T cell
6) T cell returns to tumor and kills cells with tumor peptide

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12
Q

How do T cells kill a tumor cell?

A
  • release of cytotoxic granules from T cell into tumor cell (initiate extrinsic apoptosis)
  • express Fas protein on T cells to induce extrinsic apoptosis
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13
Q

how does T cell recognize a different peptide/MHC?

A

each T cell that your body makes has a unique T cell receptor

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14
Q

different peptides T cell can recognize

A

foreign invader peptides, tumor peptides, healthy self peptides

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15
Q

why are healthy self peptides bad for a tumor to have

A

T cells that recognize healthy self peptides get destroyed

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16
Q

define immunosurveillance

A

immune system constantly patrols the body and eliminates tumor cells as they arise

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17
Q

evidence for immunosurveillance (related to just mouse)

A

strongly immunogenic tumor is rejected/destroyed/killed in WT mouse and strongly immunogenic tumors don’t develop in WT mouse

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18
Q

define immunogenic

A

if a tumor is immunogenic, it has foreign looking proteins that the immune system recognizes

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19
Q

what must tumors do to avoid immunosurveillance

A

make proteins that look foreign

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20
Q

antigen is what

A

peptide on MHC protein

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21
Q

a cancer cell is a self cell with

A

self proteins

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22
Q

how can a self antigen become altered or foreign

A
  • mutation
  • cancer germline genes
  • oncogenic virus
  • gene overexpresssion
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23
Q

mutation

A

change in an aa gets presented, looks foreign to T cell

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24
Q

cancer germline genes

A

we have genes that aren’t expressed as adults- that T cells don’t get trained against so can be tumor antigens

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25
Q

oncogenic virus

A

can insert a foreign gene

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26
Q

gene overexpression

A

protein isn’t mutated, several fold increase in expression, rare self reactive T cell is more likely to bump into its peptide

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27
Q

3 Es

A

1) elimination
2) equilibrium
3) escape

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28
Q

elimination

A

cancer cells arise but are slim by immune system, immunosurveillance

29
Q

escape

A

clinically detectably tumor

30
Q

how have cancer cells evolved strategies to avoid immune selective pressure?

A

1) antigen loss variance
2) stop making MHC protein
3) tumors can produce immunosuppressive cytokines
4) tumor associated macrophages inhibit T cells
5) tumor cells often outcompete T cells for nutrients
6) tumor cells can overepxress proteins on their surface that inhibit immune cells (PD-L1 and CTLA-4)

31
Q

antigen loss variance

A

cancer cells have tumor antigens that T cells can recognize but if a cancer cell stops making the protein that the T cell is recognizing then the cancer cell can survive

32
Q

stop making the MHC protein downside

A

NK cells can recognize and kill self cells without MHC

33
Q

stop making the MHC protein

A

T cells can’t “see” peptide samples

34
Q

example of stop making the MHC protein

A

if mutated Ras is a tumor antigen

35
Q

how are acute infections involved in immunosurveillance

A

acute infects are correlated with protection against some types of cancer

36
Q

acute infections result in immune responses to BLNK and immune responses are protective against some tumor antigens

A

altered self peptides

37
Q

what can happen during a viral infection?

A

virus infects a self cell and self proteins/peptides can be altered or messed up (post translational modifications)

38
Q

an immune response to altered self during an infection will…

A

persist as memory and then if the same altered self peptides pop up on a tumor, memory immune cells can eliminate the tumor cells

39
Q

approaches to immunotherapy

A

stimulate the immune response and passive immunization

40
Q

stimulate the immune response

A

assumes an existing immune response that needs to be boosted

41
Q

passive immunization

A
  • bypass the immune response to tumor antigens
  • don’t need an immune response to tumor antigens
  • drug uses the immune system
42
Q

therapies that utilize some aspect of the immune system include

A

antibodies, bone marrow transplants, CAR T cells

43
Q

standard therapies for cancer

A

chemo, radiation,(kill rapid replicating cells) surgery (not metastasis)

44
Q

immunotherapy advantages

A

more specific, fewer side effects, better at killing, can deal with metastasis

45
Q

what are the different types of immunotherapies

A
  • checkpoint blockage
  • tumor antigen virus
  • adoptive T cell therapy
  • provenge/sipuleucel T
46
Q

checkpoint blockade therapies

A

proteins on dendritic cells and tumor cells that limit T cell function ($$)

47
Q

goal of checkpoint blockade therapies

A

boost limited T cell responses

48
Q

how checkpoint blockade works

A
  • make antibodies specific to checkpoint proteins
  • inject the antibody and block checkpoint protein
  • T cell boosted and bypass checkpoint inhibition
49
Q

examples of checkpoint blockade

A

CTLA4: blocks checkpoint during T cell and dendritic cell interactions
PD-L1: antibody blocks interaction between T cell and tumor cell

50
Q

checkpoint and radiation

A

good

51
Q

checkpoint and chemo

A

bad, suppress immune

52
Q

tumor antigen vaccines

A

requires that cancer cells have protein that look foreign ($$), no clinical effective

53
Q

adoptive T cell therapy

A

-labor intensive and patient specific
-after injection, T cells can kill tumor cells remaining in body
-expand T cells
$$$$$

54
Q

goal of adoptive T cell therapy

A

T cells kill tumor cells before tumor cells have a chance to mutate

55
Q

provenge/sipulecuel T other name

A

adoptive dendritic cell therapy/dendritic cell vaccine

56
Q

provenge/sipulecuel T

A

-isolate blood, isolate monocytes (immune dendritic cells)
-dendrion company (mature the dendritic cells with GM-CSF, expose to PAP)
-reinject dendritic cells
-dendritic cell must find T cells that it can activate
$$$$$

57
Q

therapies that utilize some aspect of immune system

A

antibodies, bone marrow transplants, CAR T

58
Q

antibodies actual name

A

antibody dependent cellular cytotoxicity (ADCC)

59
Q

ADCC

A
  • design antibodies to bind to a tumor protein
  • tumor gets coated
  • NK cells kill antibody coated tumor cells
60
Q

examples of antibody immunotherapy

A

Herceptin/trastuzumab and Rituximab

61
Q

Herceptin/trastuzumab

A
  • antibody binds HER2/new growth factor

- HER2/new expressed by breast epithelial cells/overexpressed on some breast cancers

62
Q

mab

A

monoclonal antibody

63
Q

Rituximab

A
  • leukemia/lymphoma

- binds to CD20, expressed by B cells and over expressed on some leukemia/lymphoma

64
Q

conjugated antibodies examples

A
  • rituximab + radioisotope–> delivers radiation to cancer cells
  • herceptin + chemo–> deliver chemo to cancer cells
65
Q

benefits of conjugated antibodies

A

use lower doses of rad/chemo and localized drug delivery, less side effects

66
Q

bone marrow transplant

A
  • irradiate host/patient to kill their bone marrow cells, and cancer cells
  • transfer done bone marrow (repop immune system)
67
Q

CAR T cells

A

chimeric antigen receptor T cells, doesn’t require MHC or altered self but $$$$$$

68
Q

CAR T cells advantage

A

could be any tumor protein, not just altered self or MHC and when CAR binds its target on tumor cell, signals to T cell to release cytotoxic granules

69
Q

how does CAR T cell therapy work?

A
  • isolate the cancer patient’s blood, isolate T cells
  • transfer the chimeric antigen receptor gene
  • expand T cells in a lab
  • transfer T cells to patient
  • severe symptoms from CAR T cells killing tumor cells

Cancer Biology (4 decks)

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