Intro to Immunotherapy Flashcards

1
Q

Cancer Immunity

A

Cancer can express cancer-specific proteins called neoantigens

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2
Q

Neoantigens can be targeted by:

A

T cells

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3
Q

What are Neoantigens?

A

cancer-specific proteins

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4
Q

Cancer immunotherapy examples:

A
  1. ) Checkpoint inhibitors
  2. ) Adoptive cell transfer
  3. ) Therapeutic vaccines
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5
Q

What are the ways that cancer “evades” ?

A
  1. ) Escape immune detection

2. ) Suppress anti-tumor responses

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6
Q

Escape immune detection

A

by adopting certain features like loss of cell surface antigens.

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7
Q

suppress anti-tumor responses

A

by activating immune regulatory pathways that inhibit T-cell activity.

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8
Q

what’s a checkpoint inhibitor?

A

Targeted antibodies that reactivate anti-cancer immune responses by releasing the brakes on the immune system.

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9
Q

what is a CAR (T cell)?

A

Chimeric antigen receptor

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10
Q

What do they do?

A

They are T-cells that are re-engineered to express receptors that specifically recognize cancer cells.

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11
Q

What are TIL’s?

A

Tumor-infiltrating lymphocytes

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12
Q

What do they do?

A

cultured to produce large quantities of activated T cells that will re-infiltrate the tumor, recognize the cancer cells and destroy them.

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13
Q

What does our immune system do? if working properly?

A

instructs the body to elicit immune responses to fight pathogens and promote health and well-being.

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14
Q

Cancer cells can evade (escape) elimination by:

A
  • escaping immune surveillance mechanisms

- suppressing anti-cancer responses

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15
Q

Cancer immunotherapy eliminates cancer indirectly by promoting what?

A

anti-cancer immune responses (stimulates T cell activation and detection of cancer antigens)

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16
Q

What are the 3 types of immunotherapies that stimulate T cell reactivity against cancer?

A

1) checkpoint inhibitors
2) adoptive T cell transfers
3) cancer vaccines

17
Q

What’s the goal with fighting cancer in the body?

A

For the T-cell to recognize the antigen

18
Q

What is PD-L1 and PD-1?

A

Proteins that recognize and bind to each other.

19
Q

What does the PD-L1 inhibitor do?

A

it makes the T-cell able to recognize the antigen and kill the tumor cell (cancer).

20
Q

How is the presence of PD-L1 determined on the tumor?

A

Immunohistochemistry. (IHC) looking for proteins on the tumor.

21
Q

Facts about the inhibitors

A
  • checkpoint inhibitor drugs, line of immunotherapy

- multiple inhibitors have FDA approval for a variety of applications

22
Q

What is the most studied and best known PD-1 inhibitor?

A

pembrolizumab (Keytruda)

23
Q

What are PD-L1 clones?

A

nearly identical antibodies that come from different cell lines. Different but function the same way.

24
Q

What is the hottest immunotherapy marker right now?

A

TMB*

25
Q

3 biggest immunotherapy markers

A
  • MSI
  • TMB
  • PD-L1
26
Q

Describe what is meant by PD-L1 clone?

A

almost identical antibodies but slightly different than each other. Because of this, you have to run different immunotherapies.

27
Q

The clinician needs to know which clone they are wanting to oder. True or false?

A

True

28
Q

Tempus has a default clone that we offer? True or false

A

True

29
Q

Which immunotherapy metric other than PD-L1 is analyzed at Tempus using IHC?

A

mismatched repair deficiency

30
Q

Why is tumor mutational burden (TMB) an indicator for immunotherapy?

A

they make it easier for the immune system to recognize a cancer cell

31
Q

Why is MSI an indicator for immunotherapy ?

A

they make it easier for the immune system to recognize a cancer cell.

32
Q

More neoantigens produced by tumor=higher chance cancer cells will be recognized and killed by immune cells? true or false?

A

True

33
Q

Tumor mutational burden

A

a proxy for neoantigen production

34
Q

Measuring microsatelllite instability

A

We are trying to see how many error-prone areas are in a cell.

35
Q

Different microsatellite instability

A
  1. ) MSI-H
  2. ) MSS
  3. ) MSE
36
Q

Microsatellite Instability- High (MSI-H)

A

a number of microsatellites in tumor cells is significantly different than the number of repeats in the DNA of a normal cell.

37
Q

Microsatellite Stable (MSS)

A

number of microsatellites in tumor cells is not significantly different than the number of repeats in the DNA of a normal cell.

38
Q

Microsatellite Equivocal (MSE)

A

tumor cannot be classified as either MSI-H or MSS based on test values.