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OCN ONS Bundle > Cancer Treatment Modalities: Biotherapy (Immunotherapy and Targeted Therapy) > Flashcards

Cancer Treatment Modalities: Biotherapy (Immunotherapy and Targeted Therapy) Flashcards

1
Q

Biotherapy =

A

Any form of treatment that uses the body’s natural abilities, or made from living organisms/lab to fight invading organisms, disease processes, or effects of treatment

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2
Q

Difference between biotherapy and chemotherapy =

A

Focus on body’s biologic role in tumor development or its response to a tumor or treatment (indirectly acts on immune system) vs. cytotoxic chemo affects all cells not just tumor cells

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3
Q

Targeted therapy =

A

Treatment that uses drugs or other substances to identify and attack specific cancer cells with less harm to normal cells

  • some block action of certain enzymes, proteins, molecules involved in growth and spread of cancer cells
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4
Q

Immunotherapy =

A

Uses substances to stimulate or suppress immune system to help body fight cancer, infection, diseases

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5
Q

Growth signal inhibitors, Angiogenesis inhibitors, Apoptosis inducing drugs are all examples of?

A

Targeted therapy

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6
Q

Types of biotherapy (2)

A

Immunotherapy

Targeted therapy

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7
Q

Immunotherapy works by? (3)

A

1) Boost immune system
2) Enable immune system to
3) Recognize and fight tumor
Stop or slow cancer growth

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8
Q

Classes of immunotherapy (5)

A

1) Monoclonal antibodies
2) Vaccines
3) Cytokines
4) Adoptive cell therapy
5) Checkpoint inhibitors

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9
Q

Cytokines =

A

Hormone-like proteins with low molecular weight that are secreted by various cell types, which regulate intensity and duration of immune response and mediate cell to cell communication

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10
Q

Classes of Cytokines (3)

A

1) CSFs, HGFs, GCSFs
2) Interferons (IFN alpha 2a, beta 1a, beta 1b, gamma 1b)
3) Interleukins (ILs)

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11
Q

Mechanism of action of Interferons (INFs) =

A

Slows growth of cancer cells and encouraging normal cell behavior (naturally occurring substances in body)

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12
Q

Potential SE of Interferons (IFNs)

A
  • Flu like sx
  • Fatigue, Anorexia
  • Neuropsychiatric sx
  • Electrolyte disturbance
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13
Q

Example of an interleukin

A

IL-2

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14
Q

Mechanism of action of interleukins =

A

T cell growth factor

Stimulates growth of natural killer NK cells and cytotoxic T cells to enhance antibody response by binding to receptors on surface of T cells

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15
Q

Potential SE of Interleukins

A
  • Capillary leak syndrome
  • Hypotension
  • Infusion reactions, rigors, chills, muscle pain, fever, SOB, skin rash/flushing
  • Cardiac arrhythmia
  • Diarrhea
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16
Q

Cancer Vaccines =

A

Treat existing* cancers or prevent development of cancer by boosting immune system

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17
Q

Cancer prevention (prophylactic) vaccines (2)

A

Hepatitis B vaccine -> prevents liver cancer

Human papillomavirus (HPVP -> prevents cervical cancer

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18
Q

Cancer treatment (therapeutic) vaccines (2)

A

Sipuleucel T -> hormone refractory prostate CA

Talimogene laherparepvec -> metastatic melanoma

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19
Q

Monoclonal antibodies =

A

Antibodies made in lab that target tumor specific antigens which are proteins that some tumors have

Can make many copies of that antibody hence monoclonal (mAbs)

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20
Q

What does it mean that mAbs are passive?

A

Do not result in any immunologic memory

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21
Q

3 most common monoclonal antibodies

A

Rituximab
Trastuzumab
Bevacizumab

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22
Q

How do mAbs work? (3)

A

1) Flag cancer cells for destruction
2) Block growth signals and receptors
3) Deliver other anticancer agents to site of tumor (when they are bound to other drugs or radiation particles, cancer cell engulfs and digests the mAb, attached chemo/radiation induces cellular death

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23
Q

Where are mAbs derived from before they get to the lab? Whose antibodies?

A

Human antibodies, animal antibodies, or a combination of the two

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24
Q

Types of mAbs derived from antibodies of

1) mouse
2) mouse and human
3) predominantly human
4) human only

A

1) Murine
2) Chimeric
3) Humanized
4) Human

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25
Q

Which antigens do these naked MOABS (those that can work alone) target?

1) Alemtuzumab (campath)
2) Trastuzumab (Herceptin)
3) Rituximab
4) Tositumomab
5) Obinutuzimab
6) Imatinib mesylate

A

1) CD52, CD20
2) HER2
3) CD20
4) CD20
5) CD20
6) Philadelphia chromosome

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26
Q

Mechanism of action of MOABS

A

Attaches to antigens expressed by specific cancer cells, acting as a marker for body’s immune system to destroy the cells

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27
Q

Antiangiogenic (anti-vascular endothelial growth factor) VEGF naked MOab agents =

A

Moabs that target the vascular endothelial growth factors that affects and may cause excessive tumor blood vessel growth (angiogenesis)

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28
Q

Examples of Antiangiogenic MOABS

A 
Bevacizumab (Avastin)
Pazopanib 
Sunitinib 
Sorafenib 
Axitinib 
Vandetanib
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29
Q

MoAb that treats CLL

A

Alemtuzumab (Campath) binds to CD52 antigen

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30
Q

MoAb that treats breast and stomach cancers that have antigen HER2

A

Trastuzumab (Herceptin)

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31
Q

Conjugated mAbs (2) =

tagged, labeled, loaded antibodies

A

mAbs combined with chemotherapy or radioactive particles

Radiolabeled antibodies
Chemolabeled antibodies

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32
Q

Ibritumomab tiuxetan (Zevalin) =

A

Radiolabeled mAb,

Targets CD20 antigen found on B lymphocytes
Tx for refractory or relapsed B Cell NHL

made of rituximab and radioactive substance (Yttrium-90)

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33
Q

Brentuximab Vedotin (Adcetris) =

A

Chemolabeled mAb

Targets CD30 antigen found on lymphocytes
Tx for refractory Hodgkin Lymphoma

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34
Q

Ado-Tastuzumab emtansine (Kadcyla, TDM-1) =

A

Chemolabeled mAb

Targets HER2 protein for Metastatic Breast CA

Attached to chemo drug DM1

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35
Q

Bispecific monoclonal antibodies =

A

Made up of 2 different mAbs -> can attach to 2 different proteins at the same time

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36
Q

Blinatumomab (Blincyto)

A

Bispecific mAb

Targets CD19 protein found on some leukemia and lymphoma cells and CD3 found on T cells

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37
Q

Cetuximab (Erbitux) =

A

Chimeric mouse and human antibody

Targets cell protein EGFR (epithelial growth factor receptor)

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38
Q

Adoptive T-Cell Transfer =

A

CAR-T cell

Collecting T cells which play a primary role in how immune system fights cancer from a patient and engineering them to recognize specific antigens on the surface of cancer cells -> then infusing them back into patient

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39
Q

Two major side effects of CAR-T cell therapy

A

Cytokine release syndrome

Neuro toxicities

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40
Q

Immune checkpoints =

A

Traffic lights that prevent over-activation of immune response (attack on healthy cells)

Key component of a healthy immune system

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41
Q

Examples of checkpoints on the surface of immune cells (3)

A

1) Programmed cell death protein (PD-1)
2) Programmed death ligand (PD-L1)
3) Cytotoxic T lymphocyte-associated protein 4 (CTLA-4)

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42
Q

Checkpoint inhibitors are a subset of?

A

mAbs

43
Q

How do checkpoint inhibitors work on cancer?

A

release breaks on the immune system making it more likely to respond to tumor cells -> enhances T cell activity against tumor cells

44
Q

Dose reductions are not possible with what immunotherapy?

A

Checkpoint inhibitors

45
Q

irAEs =

A

Immune related adverse events

46
Q

Most frequently cite iRAEs in clinical trials involving what 3 drugs?

A

Ipilimumab
Nivolumab
Pembrolizumab

47
Q

Adverse effects of Ipilimumab

A

Fatigue
Diarrhea, colitis, enterocolitis
Hepatitis

48
Q

Adverse effects of Nivolumab

A 
Fatigue/musculoskeletal pain 
Pruritis 
Pneumonitis**
Colitis 
Hepatitis* 
Endocrinopathies, hypophysitis (inflammation of pituitary gland), diabetes mellitus
49
Q

Adverse effects of Pembrolizumab

A

Fatigue
Endocrinopathies, hypophysitis, diabetes mellitus
Pneumonitis
Hepatitis*

50
Q

Because of the most common iRAEs what lab test should patients get?

A

Liver function tests

51
Q

Risk for iRAEs may directly correlate with high level expression of what checkpoint inhibitor on tumor cells?

A

PD-L1

52
Q

irAEs typically present when after initiating therapy?

A

6-12 weeks

53
Q

irAES cited most frequently in dermatologic and gastrointestinal areas why?

A

Immune cells are most active in those areas

54
Q

Targeted therapy =

A

Uses information about persons genes and proteins to target only a single or multiple abnormal protein on cancer cells without damaging normal cells

55
Q

Targeted therapies work by (3)

A

1) Blocking angiogenesis
2) Blocking signals inside or outside the cell
3) Delivering toxic substances to the cell

56
Q

Why is targeted therapy not always effective even though its suppose to work on your specific cancer?

A

Having the target does not mean the tumor will respond to the drug

57
Q

Difference between targeted therapy and chemotherapy?

A

Chemotherapy is cytotoxic whereas targeted therapy is cytostatic (blocks tumor cell proliferation)

58
Q

Types of Targeted therapy

A 
Signal Transduction Inhibitors 
Tumor Specific Antigens
Apoptosis Inducers 
Angiogenesis Inhibitors 
Small Molecule Agents 
Targeted Therapy
59
Q

Signal Transduction Inhibitors =

A

Targeted therapy that blocks signal transduction that regulates cell growth, function, and apoptosis

60
Q

Cell signals that come from outside the cell =

A

growth factors and growth factor receptors

61
Q

Cell signals that come from inside the cell =

A

tyrosine kinase receptors

62
Q

Process of cell signaling

Signal is transmitted by _____ to the cell’s control ____ (____) through a series of biochemical _____. Control center ____ these signals and produces an appropriate _____. Activation of ____ ___ triggers biochemical ____ of cell signaling events. In cancer these signals are _____ “on” and malignant cells are stimulated to _____ continuously without being prompted by outside signals.

A 
proteins
center (nucleus) 
reactions, reads
response
tyrosine kinases 
cascade
stuck
divide
63
Q

Examples of signal transduction inhibitors used in treatment of cancer (5)

A 
EGFR inhibitors
HER2 inhibitors 
BCR-ABL (tyrosine kinase) inhibitors
ALK (multikinase) inhibitors
BRAF inhibitors
64
Q

Examples of drugs that block the following signal transduction inhibitors

1) EGFR inhibitors
2) HER2 inhibitors
3) BCR-ABL (tyrosine kinase) inhibitors
4) ALK (multikinase) inhibitors
5) BRAF (multikinase) inhibitors

A

1) Cetuximab, Erlotinib
2) Trastuzumab, Pertuzumab
3) Imatinib, Dasatinib
4) Crizotinib, Certinib
5) Vemurafenib, Dabrafenib

65
Q

Tumor specific antigen =

A

A protein or other molecule that is unique to cancer cells or is much more abundant in them

66
Q

Tumor specific antigens are usually found in what part of the cell?

A

Plasma (outer) membrane

67
Q

For a tumor antigen to be best suited for targeted therapy it should be

1) _____ to tumor cells
2) Located on the _____ of tumor cells
3) Present in ____ numbers
4) Involved in tumor cell _____

A

1) Specific
2) Surface
3) large
4) survival

68
Q

Tumor specific antigens are very important in treating what types of cancers?

A

Leukemia, Lymphomas

69
Q

CD20 =

A

Found on normal and malignant pre-B lymphocytes and mature B lymphocytes

Tx for certain types of B cell lymphomas and leukemia

70
Q

What drug targets and destroys B cells that have CD20?

A

Rituximab

71
Q

CD33 =

A

Found on myeloid (myeloid specific) cells but also some lymphoid

Tx for AML

72
Q

CD52 =

A

A protein present on surface of mature lymphocytes but not on stem cells from which these lymphocytes were derived; also found on monocytes and dendritic cells associated with some types of lymphoma

Tx for some types of lymphoma

73
Q

Drug that targets CD52, marking the CD52 lymphocytes for destruction =

A

Alemtuzumab

74
Q

The CD Antigens (3)

A

CD20
CD52
CD33

75
Q

Apoptosis Inducers =

A

Cause cancer cells to undergo apoptosis

76
Q

Proteasome inhibitor =

A

An apoptosis inducer that stops proteasome from breaking down proteins that cause cell death -> cell death

77
Q

What is a proteasome?

A

A complex of enzymes inside a cell that helps destroy proteins no longer needed by the cell

78
Q

Bortezomib and Carfilzomib are examples of?

A

Apoptosis inducers

79
Q

Angiogenesis Inhibitors =

A

Block tumor angiogenesis where tumors create their own blood supply needed for growth and metastasize

80
Q

Two ways to inhibit tumor angiogenesis

1) Inhibit the action of what protein or receptor?
2) Target ____ on the surface of ____ cells or other proteins in downstream signaling pathways that stimulate a new blood ____ growth

A

1) Vascular endothelial growth factor (VEGF)

2) receptors, endothelial, vessel

81
Q

Popular Angiogenesis Inhibitors (3)

A

Bevacizumab

Sorafenib and Sunitinib

82
Q

Bevacizumab =

A

An Angiogenesis inhibitor that specifically recognizes and binds to VEGF

Tx for Metastatic Colorectal Ca
Bad for wound healing

83
Q

Sorafenib and Sunitinib =

A

Angiogenesis inhibitors that bind to receptors on surface of endothelial cells or to other proteins in downstream signaling pathways, blocking their activities

84
Q

Small molecule targeted therapies =

A

Developed for targets that are located inside* the cell (intracellular) because these agents are able to enter cells more easily -> disrupts function of cells, causing cell death

85
Q

Examples of Small Molecule Agents (5)

A

1) Tyrosine Kinase Inhibitors (TKIs)
2) Tyrosine Kinase inhibiting MOABS
3) Kinase inhibitors
4) P13K inhibitors
5) Hedgehog pathway inhibitors

86
Q

TKIs and Tyrosine Kinase Inhibiting MOABS

1) Which antigen is targeted?
2) Examples (7)
3) Mechanism of action:

A

1) Epidermal Growth Factor Receptor (EGFR)
2) END IN TINIB* for TKI
Cetuximab, Gefitinib, Erlotinib, Lapatinib, Panitumumab, Vandetanib, Zivaflibercept
3) TKIs bind to tyrosine kinase in EGFR -> inactivating or limiting its activity

87
Q

How do monoclonal antibodies with TKI capabilities work?

A

They bind to extracellular component of EGFR to prevent actual substrates from binding to receptors, inhibiting EGFR activation

88
Q

TKI drug route =

So those administering should be aware of

1) A____ to therapy
2) Interactions with:

A

Oral agents

1) Adherence
2) food/drug and drug/drug that influences when to take and what food/drink to avoid

89
Q

Examples of TKIs

A

End in Tinib*

Erlotinib 
Sunitinib 
Ponatinib 
Imatinib 
Dasatinib 
Ibrutinib
90
Q

TKIs and the cancers they treat

1) Erlotinib
2) Sunitinib
3) Ponatinib
4) Imatinib
5) Dasatinib
6) Ibrutinib

A

1) Advanced NSLCA and pancreatic CA
2) Advanced RCC, GIST (gastrointestingal stromal tumors)
3) CML
4) Philadelphia chromosome + CML
5) Philadelphia chromosome + CML
6) Mantle cell lymphoma, Waldenstroms macroglobulinemia, CML

91
Q

Kinase Inhibitors

1) What is it?
2) Target what pathway?
3) Drug names end in?
4) Nursing considerations:

A

1) Type of Small Molecule Agent Targeted Therapy
2) RAF/RAS/MET pathway
3) nib
4) Oral agent -> be aware of drug/food interactions, when to take, foods to avoid

92
Q

Examples of Kinase Inhibitors

A

Sorafenib
Dabrafenib
Trametinib
Vemurafenib

93
Q

P13K Inhibitors

1) What is it?
2) Targets what pathway?
3) Drug names end in?
4) Nursing considerations:

A

1) Small molecule agent targeted therapy
2) P13K pathway
3) Lisib
4) Oral agent -> food/drug interactions, when to take, foods to avoid

94
Q

Idelalisib =

Treats what? (2)

A

P13K inhibitor

1) Follicular B cell non-Hodgkin Lymphoma
2) Relapsed CLL

95
Q

What is the Hedgehog pathway?

Aberrant signaling of this pathway leads to?

A

Plays a role in brain and spinal cord development and controls cell division and differentiation in adult stem cells

Different forms of cancer
Therefore, targeting this pathway may prevent/treat cancers

96
Q

Hedgehog pathway inhibitors

1) What is it?
2) Drug names end in?
3) Nursing considerations:

A

1) Small molecule agent targeted therapy
2) Gib
3) oral agent -> food/drug interactions, when to take, what foods to avoid

97
Q

Sonidegib and Vismodegib =

What conditions do they treat?

A

Hedgehog pathway inhibitors

Locally advanced basal cell carcinoma
Metastatic or recurrent local advanced basal cell carcinoma

98
Q

Targeted therapy main side effects (5)

A 
Infusion reaction/hypersensitivity 
Skin reactions 
Cardiovascular effects 
Bleeding and clotting abnormalities 
Impaired wound healing

Other SE
N/V, diarrhea/constipation, mucositis, cough, dyspnea, fatigue, HA, edema, organ toxicity, colitis, risk for infection

99
Q

Hormone therapy =

A

Treatment that adds, blocks, removes hormones from body to help slow or stop growth of cancer cells

100
Q

What are hormones? Where are they produced?

A

The body’s chemical messengers

Endocrine glands (thyroid, pancreas, ovaries, testes)

101
Q

What type of cancers do hormone therapies usually treat?

A

Breast and Prostate

usually used with chemo/RT

102
Q

Hormone therapy mechanisms of action (3)

A

1) Block hormone receptors
2) Blocks the body’s production of the hormone
3) Eliminates or changes shape of hormone receptors on cell surface

103
Q

Examples of Hormone therapy drugs (4)

A

1) Antiestrogens (tamoxifen, fulvestrant)
2) Aromatase inhibitors (Anastrozole, exemestane)
3) Antiadrogens (Biculatamide, Flutamide)
4) Luteinizing hormone releasing hormone (LHRH) agonist (Goserelin, leuprolide)

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