Cancer Therapy/Treatment Flashcards
(106 cards)
1
Q
5 types of cancer treatments or therapies
A
- surgical therapy
- chemotherapy
- targeted therapy
- radiation therapy
- cancer immunotherapy
2
Q
5 types of surgical therapy
A
- diagnostic
- staging
- curative
- debulking
- palliative surgery
3
Q
what is diagnostic surgery for cancer?
A
a biopsy done to make a definitive diagnosis, either incisional or excisional
4
Q
what is incisional biopsy
A
removal of a piece of suspicious area for examination
5
Q
what is excisional biopsy
A
removal of entire suspicious area, like unusual lump or mole
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
7
Q
what is the most common cancer surgery?
A
curative surgery
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
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
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
11
Q
examples of palliative surgery
A
- pain relief/restoration of physical function if tumor is pressing on nerve/spinal cord, blocking or creating pressure
- to stop bleeding via suture ligation
- to prevent broken bones
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
13
Q
what do chemotherapeutic drugs target in general?
A
cells with a high rate of division throughout their cell cycle
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
15
Q
what tissues have high turnover rates and therefore may be affected by chemo drugs?
A
GI tract, hair follicles, germ cells
16
Q
what chemo drugs are mitotic inhibitors?
A
vinca alkaloids and taxanes
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”)
18
Q
what are vinca alkaloid and taxane mitotic inhibitors used to treat?
A
some forms of breast cancer, lung cancer, myeloma, lymphoma, leukemias
19
Q
what are vinca alkaloid drugs?
A
vincristine, vinblastine
20
Q
what are taxane drugs?
A
paclitaxel, docetaxel
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
22
Q
what are taxane drugs derived from?
A
plants of taxus genus
23
Q
what are vinca alkaloid drugs derived from?
A
periwinkle plant, and now synthetically made
24
Q
what are the anti-metabolites?
A
methotrexate, fluorouracil (5-FU)
25
general MOA of anti-metabolites
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
26
what are the anti-metabolites used to treat?
leukemias, breast, ovarian, GI cancers
27
what is methotrexate
an analogue of folic acid that competitively inhibits DHRF (dihydrofolate reductase)
28
what does DHRF (dihydrofolate reductase) do?
converts dihydrofolate to tetrahydroflolate, which is the methyl donor to dUMP to make dTMP (essential for synthesis of thymidine)
29
what is fluorouracil (5-FU)
a pyrimidine analogue that inhibits thymidylate synthase and therefore the synthesis of thymidine
30
what is thymidylate synthase
enzyme that methylates dUMP to form dTMP and assists in the synthesis of thymidine
31
risk of DNA damaging agent chemo drugs?
they cause DNA damage to normal cells of which can induce other cancer, aka increased risk of leukemia
32
general MOA of DNA damaging agents
induce DNA damage mediated by topoisomerase inhibition or DNA intercalation, causing significant and overwhelming amount of DNA damage, causing the cells to die
33
what is the relation of DNA damaging agents specific to cancer?
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
34
examples of DNA damaging agents
doxorubicin, dactinomycin (actinomycin D), streptozocin, bisulfan
35
usual type of drug that are used as DNA damaging agents
antibiotics and some alkylating agents
36
specific MOA of dactinomycin
intercalates into minor groove of DNA double helix and inhibits transcription, can inhibit DNA replication at high doses which causes DNA to break down
37
what is targeted cancer therapy?
drugs that block the growth and spread of cancer by interfering with SPECIFIC molecules that are involved with growth, progression, or spread of cancer
38
benefit of using targeted cancer therapy versus general chemotherapeutics
target specific proteins KNOWN to be mutated in specific cancers, so there are FEWER side effects compared with general chemo
39
types of chemotherapeutic drugs
mitotic inhibitors, antimetabolites, DNA damaging agents
40
2 main groups of targeted therapeutics
1. small molecule inhibitors
| 2. therapeutic monoclonal antibodies
41
what are small molecule inhibitors
small compounds that bind to and prevent activity of their target, may have off-target effects
42
what are therapeutic monoclonal antibodies?
antibodies that have been modified to effectively bind and inhibit the activity of cancer promoting molecules, that are VERY specific for their target
43
difference between chemotherapeutic and targeted therapeutics?
targeted are cytostatic, not cytotoxic, and block tumor cell proliferation rather than inducing death of tumor cells
44
what drugs are small molecule EGRF inhibitors?
1. afatinib
2. gefitinib
3. erlotinib
45
what does the "tinib" suffix indicate?
they are tyrosine kinase inhibitors that inhibit growth factor receptor pathways (either receptor itself or downstream kinases)
46
what are small molecule EGFR inhibitors used to treat?
non small cell lung cancers
47
what targeted therapeutic inhibits RAS?
small molecule inhibitor of RAS is lonafarnib
48
what is lonafarnib, MOA
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
what drugs are small molecule Raf inhibitors
dabrafenib, vemurafenib
50
what are small molecule Raf inhibitors used to treat
sporadic unresectable or metastatic melanoma with B-RAF V600E or V600K mutations
51
what are the small molecule MEK inhibitors
trametinib
52
what is trametinib used to treat
unresectable or metastatic melanoma with B-RAF V600E or V600K mutations
53
what drugs are small molecule Jak tyrosine kinase inhibitors?
ruxolitinib, tofacitinib
54
what are Jak tyrosine kinase inhibitors used to treat?
myelofibrosis (bone marrow cancer)
55
small molecule inhibitors of SMO?
sonidegib, vismodegib - "gib" or "soni-"
56
what are small molecule inhibitors of SMO used to treat?
advanced basal cell carcinoma
57
specific treatments for basal cell carcinoma
cyclopamine (naturally occurring SMO inhibitor), vismodegib (synthetic SMO inhibitor)
58
how is cyclopamine produced?
corn lily plant
59
what is the downside of SMO inhibitors used to treat basal cell carcinoma?
highly teratogenic, may cause cyclopia as fetal defect
60
what is the small molecule inhibitor of CDK4/6?
palbociclib
61
what is palbociclib used to treat?
metastatic breast cancer
62
reminder of how CDK4/6 works , and why it is helpful when it is blocked
cyclin D-ckd4/6 inactivates Rb, causing transcription and cell proliferation, inactivating cdk4/6 leaves Rb active, thus blocking transcription and proliferation
63
what is the most common oncogenic fusion protein (from fusion of chromosomes)
BCR-ABL
64
what are the small molecule inhibitors of BCR-ABL
imatinib, dasatinib
65
difference and similarities between imatinib and dasatinib?
both are tyrosine kinase inhibitors, but dasatinib has more specificity for BCR-ABL than imatinib
66
MOA of small molecule inhibitor of BCR-ABL
tyrosine kinase inhibitors of BCR-ABL and treatment of Philadelphia chromosomes
67
what are small molecule inhibitors of BCR-ABL used to treat?
Philadelphia chromosome positive leukemias like CML (chromic myelogenous leukemia)
68
what drug is an antibody inhibitor of HER2?
trastuzumab (mab = monoclonal antibody)
69
MOA of trastuzumab
block dimerization of HER2 receptor by binding to its monomers
70
what does trastuzumab treat?
sporadic breast cancer (HER2 positive)
71
what are antibody inhibitors of EGFR
cetuximab, panitumumab
72
what an antibody inhibitors of EGFR used to treat?
squamous cell carcinoma of head and neck, metastatic CRC
73
MOA of antibody inhibitor of EGFR
binds to receptor and blocks dimerization - stops RAS pathway
74
unique quality of antibody inhibitors of VEGF
target signaling molecule/ligand instead of receptor
75
what is ziv-aflibercept
NOT monoclonal ab, is a fusion of VEGF-binding domain of the VEGF receptor to the Fc portion of IgG
76
what are antibody inhibitors of VEGF
bevacizumab, ziv-aflibercept
77
MOA of antibody inhibitors of VEGF
bind to VEGF molecules OUTSIDE OF the cell, sequesters them to they cannot interact with VEGF receptors on cell surface
78
what are ab inhibitors of VEGF used to treat?
metastatic forms of CRC, cervical, renal cell, NSCLC, glioblastoma
79
what are the antibodies that induced cell death?
rituximab
80
what is rituximab used to treat?
some types of B-cell non-Hodgkin Lymphoma
81
MOA of rituximab
binds to CD20 on surface of B cells and mediates their destruction by natural killer cells (NK cells)
82
what radioactive isotopes are used for systemic radiation therapy?
IV or oral radioactive isotopes of iodine, strontium, phosphorus
83
what is systemic radiation therapy used to treat?
thyroid cancer, prostate, bone
84
what is brachytherapy
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
which radiation therapy methods make the patient's body radioactive?
systemic radiation and internal radiation therapies
86
which radiation therapy method DOES NOT make the patient's body radioactive?
machine radiation therapy
87
what is brachytherapy used to treat?
some lung cancers, prostate cacners
88
benefit of brachytherapy vs systemic therapy?
reduces radiation therapy in surrounding healthy tissues
89
what is machine radiation therapy?
targeted, external radiation therapy delivered by machine outside the body, high energy rays directed into tumor
90
methods of external radiation therapy
gamma knife, proton therapy
91
what is gamma knife therapy?
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
when is gamma knife therapy used?
small to medium brain tumors
93
what is cyber knife therapy?
lower doses of gamma rays focused on tumor, less intense requires multiple treatments
94
what is proton therapy?
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
what is proton therapy best for?
cancers where surrounding tissues must be preserved, prostate cancer and pediatric brain tumors MEDULLABLASTOMA
96
what is immunotherapy
uses the body's own immunological defense to eliminate cancer, affects 2 steps in T cell recognition of cancer cells
97
what steps does immunotherapy focus on in the T cell recognition of cancers?
1. activation phase
| 2. effector phase
98
what occurs during the activation phase of T cell recognition in a cell with cancer
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
what occurs during effector phase of T cell recognition in a cell with cancer?
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
checkpoint inhibitor drugs
ipilipmumab, nivolumab
101
MOA of ipilipmumab
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
MOA of nivolumab
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
what class of drug is called "checkpoint inhibitors" of Tcells?
cancer immunotherapy, ipilipmumab, nivolumab, pembrolizumab
104
what is pembrolizumab?
PD-1 inhibitor, treated Jimmy Carter's melanoma that metastasized to his brain
105
MOA of PD-1 inhibitors?
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
what combination is best effective for treating metastatic melanoma and NSCLC?
checkpoint inhibitor immunotherapy combination of ipilimumab and nivolumab
