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MFM > Cancer Therapy/Treatment > Flashcards

Cancer Therapy/Treatment Flashcards

1
Q

5 types of cancer treatments or therapies

A
  1. surgical therapy
  2. chemotherapy
  3. targeted therapy
  4. radiation therapy
  5. cancer immunotherapy
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2
Q

5 types of surgical therapy

A
  1. diagnostic
  2. staging
  3. curative
  4. debulking
  5. palliative surgery
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3
Q

what is diagnostic surgery for cancer?

A

a biopsy done to make a definitive diagnosis, either incisional or excisional

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4
Q

what is incisional biopsy

A

removal of a piece of suspicious area for examination

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5
Q

what is excisional biopsy

A

removal of entire suspicious area, like unusual lump or mole

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6
Q

why is surgical staging used

A

to determine stage of tumor, and if/where it has spread, removes lymph nodes near cancer, used to decide what treatment is best and predicting prognosis

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7
Q

what is the most common cancer surgery?

A

curative surgery

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8
Q

what does curative surgery entail?

A

complete removal of tumor as well as some of normal tissue margins, may be combined with chemotherapy or radiation therapy

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9
Q

what does debulking surgery entail

A

as much of tumor removed as possible, but not ENTIRETY, used when the complete removal is not possible or might cause excessive damage, then chemo or radiation is used to eliminate the rest of the cancer cells

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10
Q

what does palliative surgery entail

A

relieves side effects that are caused by a tumor, to improve quality of life for patients with advanced cancer or widespread disease

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11
Q

examples of palliative surgery

A
  1. pain relief/restoration of physical function if tumor is pressing on nerve/spinal cord, blocking or creating pressure
  2. to stop bleeding via suture ligation
  3. to prevent broken bones
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12
Q

what is Mohs Surgery

A

skin cancer is removed one layer at a time as to preserve as much normal tissue as possible, each layer microscopically examined to determined if all cancer cells have been excised

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13
Q

what do chemotherapeutic drugs target in general?

A

cells with a high rate of division throughout their cell cycle

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14
Q

what is the downside of the general nature of chemo drugs?

A

do not specifically recognize neoplastic drugs, so normal cells may be affected

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15
Q

what tissues have high turnover rates and therefore may be affected by chemo drugs?

A

GI tract, hair follicles, germ cells

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16
Q

what chemo drugs are mitotic inhibitors?

A

vinca alkaloids and taxanes

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17
Q

what is the MOA of vinca alkaloid mitotic inhibitors?

A

microtubule destabilizers, promote loss of microtubules by inhibiting their growth, they bind to free tubulin dimers and prevent them from being incorporated into microtubule polymers (stop + growth, and disrupt microtubule “movement”)

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18
Q

what are vinca alkaloid and taxane mitotic inhibitors used to treat?

A

some forms of breast cancer, lung cancer, myeloma, lymphoma, leukemias

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19
Q

what are vinca alkaloid drugs?

A

vincristine, vinblastine

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20
Q

what are taxane drugs?

A

paclitaxel, docetaxel

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21
Q

MOA of taxanes?

A

microtubule stabilizers, bind to cap on + end of microtubule and prevent GTP to GDP conversion, inhibits shrinkage of microtubule

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22
Q

what are taxane drugs derived from?

A

plants of taxus genus

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23
Q

what are vinca alkaloid drugs derived from?

A

periwinkle plant, and now synthetically made

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24
Q

what are the anti-metabolites?

A

methotrexate, fluorouracil (5-FU)

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25
Q

general MOA of anti-metabolites

A

cause cell to die a thymineless death due to absence of dTTPs and the inability to replicate DNA, the adenine does not have a thymidine to pair with

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26
Q

what are the anti-metabolites used to treat?

A

leukemias, breast, ovarian, GI cancers

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27
Q

what is methotrexate

A

an analogue of folic acid that competitively inhibits DHRF (dihydrofolate reductase)

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28
Q

what does DHRF (dihydrofolate reductase) do?

A

converts dihydrofolate to tetrahydroflolate, which is the methyl donor to dUMP to make dTMP (essential for synthesis of thymidine)

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29
Q

what is fluorouracil (5-FU)

A

a pyrimidine analogue that inhibits thymidylate synthase and therefore the synthesis of thymidine

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30
Q

what is thymidylate synthase

A

enzyme that methylates dUMP to form dTMP and assists in the synthesis of thymidine

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31
Q

risk of DNA damaging agent chemo drugs?

A

they cause DNA damage to normal cells of which can induce other cancer, aka increased risk of leukemia

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32
Q

general MOA of DNA damaging agents

A

induce DNA damage mediated by topoisomerase inhibition or DNA intercalation, causing significant and overwhelming amount of DNA damage, causing the cells to die

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33
Q

what is the relation of DNA damaging agents specific to cancer?

A

in normal cells, there are DNA damage checkpoints that cause cells to arrest, but in some cancers the checkpoints don’t work and allow cell to continue in the cycle despite significant damage

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34
Q

examples of DNA damaging agents

A

doxorubicin, dactinomycin (actinomycin D), streptozocin, bisulfan

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35
Q

usual type of drug that are used as DNA damaging agents

A

antibiotics and some alkylating agents

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36
Q

specific MOA of dactinomycin

A

intercalates into minor groove of DNA double helix and inhibits transcription, can inhibit DNA replication at high doses which causes DNA to break down

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37
Q

what is targeted cancer therapy?

A

drugs that block the growth and spread of cancer by interfering with SPECIFIC molecules that are involved with growth, progression, or spread of cancer

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38
Q

benefit of using targeted cancer therapy versus general chemotherapeutics

A

target specific proteins KNOWN to be mutated in specific cancers, so there are FEWER side effects compared with general chemo

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39
Q

types of chemotherapeutic drugs

A

mitotic inhibitors, antimetabolites, DNA damaging agents

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40
Q

2 main groups of targeted therapeutics

A
  1. small molecule inhibitors

2. therapeutic monoclonal antibodies

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41
Q

what are small molecule inhibitors

A

small compounds that bind to and prevent activity of their target, may have off-target effects

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42
Q

what are therapeutic monoclonal antibodies?

A

antibodies that have been modified to effectively bind and inhibit the activity of cancer promoting molecules, that are VERY specific for their target

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43
Q

difference between chemotherapeutic and targeted therapeutics?

A

targeted are cytostatic, not cytotoxic, and block tumor cell proliferation rather than inducing death of tumor cells

44
Q

what drugs are small molecule EGRF inhibitors?

A
  1. afatinib
  2. gefitinib
  3. erlotinib
45
Q

what does the “tinib” suffix indicate?

A

they are tyrosine kinase inhibitors that inhibit growth factor receptor pathways (either receptor itself or downstream kinases)

46
Q

what are small molecule EGFR inhibitors used to treat?

A

non small cell lung cancers

47
Q

what targeted therapeutic inhibits RAS?

A

small molecule inhibitor of RAS is lonafarnib

48
Q

what is lonafarnib, MOA

A

small molecule inhibitor of RAS by inhibiting farnesyltransferase so that RAS is not anchored in the plasma membrane so it cannot locate to site where activity is needed

49
Q

what drugs are small molecule Raf inhibitors

A

dabrafenib, vemurafenib

50
Q

what are small molecule Raf inhibitors used to treat

A

sporadic unresectable or metastatic melanoma with B-RAF V600E or V600K mutations

51
Q

what are the small molecule MEK inhibitors

A

trametinib

52
Q

what is trametinib used to treat

A

unresectable or metastatic melanoma with B-RAF V600E or V600K mutations

53
Q

what drugs are small molecule Jak tyrosine kinase inhibitors?

A

ruxolitinib, tofacitinib

54
Q

what are Jak tyrosine kinase inhibitors used to treat?

A

myelofibrosis (bone marrow cancer)

55
Q

small molecule inhibitors of SMO?

A

sonidegib, vismodegib - “gib” or “soni-“

56
Q

what are small molecule inhibitors of SMO used to treat?

A

advanced basal cell carcinoma

57
Q

specific treatments for basal cell carcinoma

A

cyclopamine (naturally occurring SMO inhibitor), vismodegib (synthetic SMO inhibitor)

58
Q

how is cyclopamine produced?

A

corn lily plant

59
Q

what is the downside of SMO inhibitors used to treat basal cell carcinoma?

A

highly teratogenic, may cause cyclopia as fetal defect

60
Q

what is the small molecule inhibitor of CDK4/6?

A

palbociclib

61
Q

what is palbociclib used to treat?

A

metastatic breast cancer

62
Q

reminder of how CDK4/6 works , and why it is helpful when it is blocked

A

cyclin D-ckd4/6 inactivates Rb, causing transcription and cell proliferation, inactivating cdk4/6 leaves Rb active, thus blocking transcription and proliferation

63
Q

what is the most common oncogenic fusion protein (from fusion of chromosomes)

A

BCR-ABL

64
Q

what are the small molecule inhibitors of BCR-ABL

A

imatinib, dasatinib

65
Q

difference and similarities between imatinib and dasatinib?

A

both are tyrosine kinase inhibitors, but dasatinib has more specificity for BCR-ABL than imatinib

66
Q

MOA of small molecule inhibitor of BCR-ABL

A

tyrosine kinase inhibitors of BCR-ABL and treatment of Philadelphia chromosomes

67
Q

what are small molecule inhibitors of BCR-ABL used to treat?

A

Philadelphia chromosome positive leukemias like CML (chromic myelogenous leukemia)

68
Q

what drug is an antibody inhibitor of HER2?

A

trastuzumab (mab = monoclonal antibody)

69
Q

MOA of trastuzumab

A

block dimerization of HER2 receptor by binding to its monomers

70
Q

what does trastuzumab treat?

A

sporadic breast cancer (HER2 positive)

71
Q

what are antibody inhibitors of EGFR

A

cetuximab, panitumumab

72
Q

what an antibody inhibitors of EGFR used to treat?

A

squamous cell carcinoma of head and neck, metastatic CRC

73
Q

MOA of antibody inhibitor of EGFR

A

binds to receptor and blocks dimerization - stops RAS pathway

74
Q

unique quality of antibody inhibitors of VEGF

A

target signaling molecule/ligand instead of receptor

75
Q

what is ziv-aflibercept

A

NOT monoclonal ab, is a fusion of VEGF-binding domain of the VEGF receptor to the Fc portion of IgG

76
Q

what are antibody inhibitors of VEGF

A

bevacizumab, ziv-aflibercept

77
Q

MOA of antibody inhibitors of VEGF

A

bind to VEGF molecules OUTSIDE OF the cell, sequesters them to they cannot interact with VEGF receptors on cell surface

78
Q

what are ab inhibitors of VEGF used to treat?

A

metastatic forms of CRC, cervical, renal cell, NSCLC, glioblastoma

79
Q

what are the antibodies that induced cell death?

A

rituximab

80
Q

what is rituximab used to treat?

A

some types of B-cell non-Hodgkin Lymphoma

81
Q

MOA of rituximab

A

binds to CD20 on surface of B cells and mediates their destruction by natural killer cells (NK cells)

82
Q

what radioactive isotopes are used for systemic radiation therapy?

A

IV or oral radioactive isotopes of iodine, strontium, phosphorus

83
Q

what is systemic radiation therapy used to treat?

A

thyroid cancer, prostate, bone

84
Q

what is brachytherapy

A

form of internal radiation therapy where radioactive seeds/rods are placed near the tumor and give a high radiation dose to the tumor (localizes, rather than systemic)

85
Q

which radiation therapy methods make the patient’s body radioactive?

A

systemic radiation and internal radiation therapies

86
Q

which radiation therapy method DOES NOT make the patient’s body radioactive?

A

machine radiation therapy

87
Q

what is brachytherapy used to treat?

A

some lung cancers, prostate cacners

88
Q

benefit of brachytherapy vs systemic therapy?

A

reduces radiation therapy in surrounding healthy tissues

89
Q

what is machine radiation therapy?

A

targeted, external radiation therapy delivered by machine outside the body, high energy rays directed into tumor

90
Q

methods of external radiation therapy

A

gamma knife, proton therapy

91
Q

what is gamma knife therapy?

A

several gamma rays focused on tumor at the same time, creating very intense dose (usually one dose) of radiation specifically on target, produces DNA damage that kills cancer cells

92
Q

when is gamma knife therapy used?

A

small to medium brain tumors

93
Q

what is cyber knife therapy?

A

lower doses of gamma rays focused on tumor, less intense requires multiple treatments

94
Q

what is proton therapy?

A

particle beam therapy where beam of protons is focused precisely on tumor to cause DNA damage in cancer cells, preserves surrounding tissues best (minimal extraneous damage)

95
Q

what is proton therapy best for?

A

cancers where surrounding tissues must be preserved, prostate cancer and pediatric brain tumors MEDULLABLASTOMA

96
Q

what is immunotherapy

A

uses the body’s own immunological defense to eliminate cancer, affects 2 steps in T cell recognition of cancer cells

97
Q

what steps does immunotherapy focus on in the T cell recognition of cancers?

A
  1. activation phase

2. effector phase

98
Q

what occurs during the activation phase of T cell recognition in a cell with cancer

A

CTLA-4 that is expressed on the T cell surface suppresses the immune system and B7 (CD80), an inhibitory molecule is expressed on antigen presenting cell (that presents tumor antigens), together inhibiting T cell from finding and binding to the cancer cells

99
Q

what occurs during effector phase of T cell recognition in a cell with cancer?

A

PD-L1 is expressed on surface of tumor cells, inhibiting PD-1 (expressed on T cell that signals programmed cell death, downregulates T cell) thus preventing T cell from killing tumor

100
Q

checkpoint inhibitor drugs

A

ipilipmumab, nivolumab

101
Q

MOA of ipilipmumab

A

monoclonal ab inhibits CTLA-4, therefore inhibits the inhibitory interaction between CTLA-4 and CD80 on the antigen presenting cell, allowing for the activation of the T cell and their recognition of cancer cells

102
Q

MOA of nivolumab

A

monoclonal ab inhibitor of PD-1, inhibits inhibitory interaction between PD-L1 molecule on cancer cells and PD-1 on T cells, allowing for T cell to kill cancer cell

103
Q

what class of drug is called “checkpoint inhibitors” of Tcells?

A

cancer immunotherapy, ipilipmumab, nivolumab, pembrolizumab

104
Q

what is pembrolizumab?

A

PD-1 inhibitor, treated Jimmy Carter’s melanoma that metastasized to his brain

105
Q

MOA of PD-1 inhibitors?

A

monoclonal ab inhibitor of PD-1 inhibits the inhibitory action between PD-L1 on the cancer cell (which binds to PD-1 on T cell and tells it to downregulate) and PD-1 on the T cell

106
Q

what combination is best effective for treating metastatic melanoma and NSCLC?

A

checkpoint inhibitor immunotherapy combination of ipilimumab and nivolumab

MFM (39 decks)

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