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Block 7 Week 1 > Cancer Chemotherapy-Duan > Flashcards

Cancer Chemotherapy-Duan Flashcards

1
Q

What was the first anticancer drug?

A

mustine (for hodgkins lymphoma)

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2
Q

Cancer is caused by (blank) with a shift in the control mechanisms for cell proliferation and differentiation

A

altered host cells

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3
Q

What all does a cancer cell do?

A

shorter (accelerated) cell cycle
excessive proliferation
higher activity of nucleic acid and protein synthesis
altered cell-cell communication
invasive (disrupt normal healthy tissues)
migration to distant sites (metastasis)

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4
Q

T or F

cancer cells use the same nutrients and metabolic process as normal host cells.

A

T

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5
Q

What exactly is chemotherapy?

A

drugs that can destroy cancer cells (hopefully not normal cells)

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6
Q

An understanding of the (blank) is essential for the proper use of the current generation of anticancer agents and the search for new drugs.

A

cell-cycle kinetics

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7
Q

WHat is the order of the cell cycle?

A

G0-> G1-> S-> G2-> M-> G1

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8
Q

What do you need to give to G0 to make it turn into G1?

A

growth factor, G-protein CR

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9
Q

What does mitomycin c do?

A

cross links DNA via alkylations to inhibit DNA and protein synthesis

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10
Q

What cell cycle specific drugs block DNA synthesis?

A 
cytosine arabinoside
hydroxyurea
6-MP
MTX
5-FU
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11
Q

What cell cycle specific drug blocks DNA and protein synthesis?

A

etoposide

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12
Q

(blank) inhibits topoisomerase II and causes DNA degredation

A

Etoposide

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13
Q

What blocks mitotic spindle formation?

A

vincristine, vinblastine, and taxanes

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14
Q

What are the 2 main categories of alkylating agents?

A

nitrogen mustards

nitrosoureas

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15
Q

What are the three kinds of nitrogen mustards?

A

mechlorethamine
cyclophosphamide
ifosfamide

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16
Q

What are the three kinds of nitrosoureas?

A

carmustine
lomustine
streptozotocin

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17
Q

(blank)interact with DNA non-specificaly and are active even for the resting cells in GO

A

alkylating agents

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18
Q

How do alkylating agents affect cells in GO?

A

damage the cell now and kill it during the next cell division

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19
Q

Are alkylating agents cell cycle/phase specific?

A

no

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20
Q

What is the MOA of alkylating agents?

A

impair cell function by forming covalent bonds with amino, carboxyl, sulfhydryl and phosphate groups in important molecules

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21
Q

The electron rich nitrogen at the (blank) in DNA is particularly susceptible to alkyation from an alkylating agent.

A

N7 position of guanine

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22
Q

What was the first chemotherapy agent used in humans?

A

nitrogen mustards

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23
Q

What is a nitrogen mustard?

A

prototype alkylating agent

main toxicity comes from DNA cross linkage

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24
Q

What is the MOA of nitrogen mustards?

A

chloroethyl side chains forms strong electrophile that causes akylation of nitrogen 7 of guanine residues in DNA

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25
Q

WHy does alkylation of the 7 nitrogen of guanine residues in DNA cause cross linking and thus DNA synthesis messing up?

A

guanine replaces a thymine resulting in opening of the imidazole ring->mono alkylation results-> if second alkylation then cross-inking of chains results

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26
Q

What 2 drugs causes crosslinking between strands of DNA?

A

chlorambucil and melphalan

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27
Q

What drug causes cross linking within the same strand

A

cis-platinum

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28
Q

What are the adverse reactions of nitrogen mustards?

A

teratogenic
immunosuppresive
carcinogenic

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29
Q

What are the clinical uses of nitrogen mustards

A

lymphomas

leukemias

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30
Q

What is mechlorethamine?

A

a nitrogen based analogue of mustard gas (which is sulfur-based) and was derived from chemical warfare research.

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31
Q

What is the the primary drug in the combination chemotherapy regimen used to treat hodgkins disease?

A

mechlorethamine

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32
Q

What are the four drugs used in the combination chemotherapy regiment used to treat hodgkins disease?

A

Mechlorethamine
Oncovin (vincristine)
Procarbazine
Prednisone

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33
Q

Mechlorethamine is more toxic to (blank) cells. What are some negative effects of this drug?

A

proliferating
bone marrow depression (limiting use)
Infertility
GI toxicity

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34
Q

What class of drug is cyclophosphamide?

A

individual nitrogen mustards

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35
Q

How does cyclophosphamide work?

A

it is a broad spectrum drug that can be taken orally or via IV

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36
Q

What is the MOA of cyclophosphamide?

A

1) “prodrug” converted to phosphoramide mustard and acrolein by P450.
2) ‘DNA cross-link (N7 of guanine)

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37
Q

What are the major clinical uses of cyclophosphamide (cytoxan, neosar)?

A 
non-neoplastic diseases (nephrotic syndrome)
non-hodgkin's lymphomas (Chop regimen)
Acute lymphoid leukemia
Breast cancer 
Carcinoid
Neuroblastoma
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38
Q

What are the adverse effects of cyclophosphamide?

A

bone marrow depression
alopecia
disturbed GI
hemorrhagic cystisis

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39
Q

What is ifosfamide?

A

an analog of cyclophosphamide

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40
Q

How do you activate ifosfamide?

A

in liver by ring hydroxylation

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41
Q

(blank) to treat germ cell testicular cancer, pediatric and adult sarcomas (soft tissue and osteogenic), and several other cancers including cervical cancer, lung cancer, bone cancer, ovarian cancer, and breast cancer

A

multidrug regimen w/ ifosfamide (ifex)

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42
Q

What are the adverse effects of ifosfamide?

A 
bone marrow depression
alopecia
disturbed GI
hemorrhagic cystisis
HUGE platelet suppression 
SEVERE urotherial damage
INTERNAL bleeding (w/out mesna)
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43
Q

Why should you use ifosfamide (ifex) with mesna?

A

to reduce urinary toxicity

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44
Q

What is the mode of action of nitrosoureas?

A

spontaneous degredation to from 2 chlorethyl carbonium ion

-> crosslink DNA strands, break DNA strands, and carbamoylate protein

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45
Q

What are the adverse effects of nitrosoureas?

A 
highly carcinogenic and mutagenic
profound, cumulative myelosupresion
renal failure (long-term use)
alopecia
hepatotoxicity
pulmonary toxicity (busulfan)
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46
Q

What are 3 individual nitrosoureas?

A

carmustine
lomustine/semustine
streptozotocin

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47
Q

How do you give carmustine?

A

via IV and it is highly lipophilic

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48
Q

How do you give lomustine/semustine?

A

orally

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49
Q

What are the clinical uses of carmustine and lomustine/semustine?

A

Brain tumor treatment (including glioma, gliobastoma multiforme, medulloblastoma, astrocytoma)
GI neoplasma
Hodgkins disease

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50
Q

What are carmustine and lomustine/semustine awesome for treating brain tumors?

A

because they are highly lipophilic and can cross the blood-brain barrier

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51
Q

What is this:

water-soluble, not orally effective; methylate DNA and RNA and is particularly toxic to pancreatic islet cells

A

streptozotocin

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52
Q

What are the clinical uses of streptozotocin?

A

insulinoma (pancreatic islet cell carcinoma and carcinoid, excessive insulin secretion), metastatic cancer of the pancreatic islet cells

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53
Q

What is an important alkyl sulfonates?

A

busulfan

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54
Q

What does busulfan do?

A

selectively myelosupressive and inhibits granulocytopoiesis

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55
Q

What are the clinical uses of busulfan?

A

chronic myelogenous leukemia (CML) and other myeloproliferative disorders

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56
Q

What are the adverse effects of busulfan (alkyl sulfonates)?

A

myelosuppresion

“busulfan lung”: a rare but fatal pulmonary fibrosis

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57
Q

What are these:

structurally similiar to important endogenous molecules in the synthesis of DNA and RNA

A

Antimetabolites

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58
Q

What are the three general groups of antimetabolites?

A

purine analogs, pyrimidine analogs, and folate antagonists

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59
Q

What do antimetabolites do?

A

act as enzyme inhibitor

create false products to inhibit nucleic acid synthesis

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60
Q

What am I talking about:

the effect is to slow down the synthesis of nucleic acis (s-phase specific)

A

antimetabolites

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61
Q

What do purine antagonists do?

A 
inhibit purine ring biosynthesis 
NT interconversion (6-MP)
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62
Q

What do pyrimidine antagonists do?

A

Inhibits pyimidine synthesis (pala azaribine)

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63
Q

What do folate anatgonists do?

A

inhibit dehydrofolate reduction and blocks purine and TMP synthesis (MTX)

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64
Q

What does 5-fluorouracil (5-Fu)?

A

inhibits dTMP synthesis

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65
Q

What does Cytarabine do?

A

inhibits DNA synthesis

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66
Q

What is 6-mercaptopurine (6-MP)?

A

purine antagonist

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67
Q

What is this:

a land marker in anticancer and immunosuppresive therapy

A

purine antagnist (6-MP)f

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68
Q

What is the MOA of 6-MP and what phase is it specific for?

A

S-phase
structural analog of adenine that is activated by enzymatic (HGPRT) which inhibits the first step in de novo synthesis of purine: impeding DNA replication and RNA transcription

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69
Q

What is the clinical use of 6-MP?

A

maintenance therapy for acute lymphoid leukemia (ALL) in chidren

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70
Q

What are the adverse effects of purine antagonist (6-MP)?

A

Bone marrow suppression
Immunosuppression
GI disturbance
Liver toxicity

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71
Q

How can you get resistance to purine antagonist 6-MP?

A 
decreased activation (lack of HGPRTase)
increased breakdown of 6-TIMP by alkaline phosphatase
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72
Q

What is the mechanism of purine antagonist 6-thioguanine and what phase is it specific for?

A

S-phase specific
enzymatic (HGPRT) conversion toa nucleotide which in tubr becomes incorporated into DNA as dTGTP. AND it is an enzyme inhibitor

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73
Q

What is the clinical use of 6-thioguanine?

A

leukemias

particularly valuable in treating acute granulocytic leukemia when given with cytarabine

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74
Q

What are the adverse effects of pure antagonist 6-thioguanine?

A

bone marrow suppression, mild nausea

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75
Q

How can you get resistance to purine antagonist 6-thioguanine?

A

decreased conversion of the drug

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76
Q

What is the MOA of pyrimidine antagonist 5-fluorouracil (5FU) and what phase does it affect?

A

s-phase
pyrimidine is bioactivated to 5fdump which complexes with folic acid. This complex inhibits thymidylate synthesis (TS inhibition), causing decreased dTMP and termination of DNA synthesis.

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77
Q

What does 5-fluorouracil require to exert its cytotoxic activity?

A

enzymatic conversion to nucleotide (ribosylation and phosphorylation)

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78
Q

What are the clinical uses of pyrimidine antagonist 5-fluorouracil?

A 
basal cell carcinoma
solid tumors of digestive system 
lymphomas
leukemias
KERATOSES OF THE SKIN
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79
Q

What are the adverse reactions of pyrimidine antagonist (5-fluorouracil)?

A

bone marrow depression (leucopenia, thrombocytopenia)
Alopecia
Disturbance of GI system
Hand and foot syndrome (palmar-plantar erythrodysesthesia)

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80
Q

How do you give the pyrimidine antagonists (cytidine analogs such as cytarabine, cytosine arabinosie, araC)?

A

via continuous IV infusion

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81
Q

What is the mechanism of the pyrimidine antagonist cytidine analogs and what phase is it specific for?

A

S phase

nucleotide formed in the target cell terminates DNA chain elongation

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82
Q

What is the clinical use of pyrimidine antagonists (Cytidine analogs)?

A

first-line choice for acute myelogenous leukemia and lymphomas

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83
Q

What are the adverse effects of pyrimidine antagonists (cytidine analogs)?

A

bone marrow depression, severe bone marrow hypoplasia

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84
Q

What kind of drug is methotraxate?

A

a folate antagonist

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85
Q

What is the mode of action of methotrexate and what phase does it affect?

A

S-phase specific
structural analog of folic acid
reversibly inhibits dihydrofolate reductase, resulting in decreased dTMP; directly inhibits the folate-dependent enzymes of de novo purine and thymidylate synthesis

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86
Q

What do you use folate antagonist methotrexate for?

A 
acute lymphoblastic leukemia (ALL)
choriocarcinoma
osteocarcinoma
rheumatoid arthritis (severe)
psoriasis
multidrug regiments for other cancers
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87
Q

How do you get resistance to methotrexate?

A

decreased uptake

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88
Q

What are the adverse reactions to methotrexate?

A 
neurotoxicity (intrathecal use)
nephrotoxicity
interstitial pnemonitis
hepatoxicity
BAD
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89
Q

What do you use in combination with MTX to rescue normal cells?
How does it work?

A

leucovorin

it is a reduced folate analog that normal cells can absorb in presence of MTX (usually given 24 hours after MTX)

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90
Q

What does doxorubicin and mitoxantrone do?

A

damage DNA and repair

Inhibits RNA synthesis

91
Q

What does bleomycin and etoposide do?

A

inhibits topoisomerase II

92
Q

What does Mitomycin C do?

A

cross links DNA

93
Q

What are the cancer antibiotics?

A

doxorubicin (adriamycin), Daunorubicin, Epirubicin, Idarubicin

94
Q

(blank) acts by binding to DNA where it can inhibit the progression of the enzyme topoisomerase II, which unwinds DNA for transcription.

A

Doxorubicin

95
Q

(blank) inhibition, which prevents DNA strand break from being resealed by the enzyme thereby stopping the process of replication.

A

topoisomerase II complex

96
Q

What is the MOA of cancer antibiotics doxorubicin?

A

Topoisimerase II inhibition
Reduce O2 w/ semiquinones produces free radials
inercalating DNA
Plasma mebrane disruption

97
Q

(blank) is in the same category as doxorubicin and is also used as the starting material for semi-synthetic manufacturing of doxorubicin, epirubicin and idarubicin.

A

Daunorubicin

98
Q

What is the clinical use of Daunorubicin?

A
  • most common for treating leukemia (acute myeloid leukemia, acute lymphocytic leukemia)
  • hodgkins disease
  • soft tissue sarcoma
  • breast cancer
  • lung cancer
  • Kahlers disease
99
Q

(blank) is one of the most effective drug in treating breast, ovary, endometrium, bladder, thyroid and lung cancers.

A

Daunorubicin

100
Q

Daunorubicin and (blank) are used for AML

A

Idarubicin

101
Q

(blank) is used for breast cancer.

A

Epirubicin

102
Q

What are the side effects of Doxorubicin?

A

BAD (bone marrow suppression, alopecia, Disturbed GI tract)
heart arrythmias
AND
if you hit a toxic cumulative dose of 450 mg/m2 you get irreversible cardiomyopathy

103
Q

Doxorubicin cardiotoxicity is characterized by a dose-dependent decline in (blank). this causes an interaction between doxorubicin and iron which damages myocytes, causing myofibrillar loss and cytoplasmic vacuolization.

A

mitochondrial oxidative phosphorylation.

104
Q

T or F
some adults who were treated with doxorubicin when they were children have developed dilated cardiomyopathy up to 15 years later.

A

T

105
Q

How can you alleviate the cardiomyopathy associated with doxorubicin?

A

dexrazoxane

106
Q

What is this:

A glycosylated linear nonribosomal peptide antibiotic produced by the bacterium Streptomyces verticillus

A

Bleomycines

107
Q

Bleomycin refers to a family of structurally related compounds. When used as an anticancer agent, the chemotherapeutical forms are primarily bleomycin (blank) and (blank)

A

A2 and B2.

108
Q

What is the MOA of bleomycins?

A

free-radical induced DNA strand break

109
Q

How exactly does bleomycin cause free-radical induced DNA strand breakage?

A

bleomycin chelates metal ions (primariy iron) producing a pseudo enzyme that reacts with oxygen to produce superoxide and hydroxide ree radicals that break single and double-strand DNA chains.

110
Q

What phase of the cell replication cycle does bleomycin affect?

A

G2

111
Q

In addition to forming the metal oxygen superoxide species, what else does bleomycin do?

A

mediate lipid peroxidation and INHIBITS incorporation of THYMIDINE into DNA strands

112
Q

What do you combine bleomycin with to treat advanced testicular cancer, lymphomas, squamos carcinomas (epithelial tumors) of cervix, head and neck, lungs?

A

viblastine and cisplatin

113
Q

(blank) alternating with MOPP in a defined cyclical schedule is the treatment of choice for advanced (stage III and IV) of Hodgkin’s disease and can be curative (50-80%).

A

ABVD

114
Q

What does ABVD stand for?

A

Adriamycin, bleomycin, vinblastine, dacarbazine

115
Q

What are the adverse effects of bleomycin?

A

Lung toxicity (worst complication)
Erythema/skin toxicities
Raynades phenomemnon

116
Q

(blank) is a disease characterized by spasm of the arteries in the extremities, especially the fingers ( Raynaud’s phenomenon ). It is typically brought on by constant cold or vibration, and leads to pallor, pain, numbness, and in severe cases, gangrene

A

Raynaud’s phenomenon

117
Q

What is the MOA of mitomycin c?

A

activated to alkylating agent, causes crosslinking in DNA-> cleavage of DNA w/ free radicals.

118
Q

What phase of the cell cycle is mitomycin specific for?

A

G1!!!!

119
Q

What is the clinical use of mitomycin C?

A

adenocarcinomas of the breast, colon, stomach and lung (not as effective as other antibiotics)

120
Q

What are the adverse effects of mitomycin C?

A

severe delayed cumulative bone marrow suppression, nausea, renal toxicity, carcinogenicity

121
Q

What does vinca alkaloids do?

A

inhibits microtubules

122
Q

What does etoposide do?

A

inhibits topoisomerase II

123
Q

What is the mode of action of etoposide?

A

arrests cell cyce at S-G2 interface through inhibition of topoisoerase II by binding to the DNA topoisomerase complex and prevent the enzyme from resealing the double strand DNA breaks initially created by the enzyme.

124
Q

What phases of the cell cycle does etoposide work at?

A

S and G2

125
Q

What are the cinical uses of etoposide?

A

testicular cancer, lung cancer, lymphomas, acute nonlymphocytic leukemia, breast cancer

126
Q

What are the major side effects of etoposide?

A 
Bone marrow suppression
Allergy/anahylaxis
Loss of hair
Disturbed GI tract
(BALD)
127
Q

What are 2 common vinca alkaloids?

A

vincristine and vinblastine

128
Q

What is this the MOA of :
Bind to tubulin dimers, the protein that forms microtubules (e.g. in the mitotic spindle), and inhibit their polymerization. This impedes mitotic spindle formation and blocks cell division, DNA synthesis, and intracellular transport. Cell cycle stops in the metaphase of mitosis (M-phase specific).

A

vinca alkaloids

129
Q

what phase are vinca alkaloids specific for?

A

M phase

130
Q

So what is the MOA for vinca alkaloids?

A

impedes mitotic spindle formation and blocks cell division, synthesis and transport and works at the M phase

131
Q

What is the clinical use of Vincristine?

A 
Children's tumors
Wilm's tumor
Ewing's sarcoma
ALL  (acute leukemias and lymphomas)
Neuroblastoma
132
Q

What are the clinical uses of vinBlastine?

A

Boy’s tumores (testicular cancer)

lymphomas (hodgkins and non hodgkins)

133
Q

What does cisplatin and procarbazine do?

A

cross links DNA

134
Q

What does L-asparaginase do?

A

inhibits protein synthesis

135
Q

(blank) contains precious metal platinum complexes with chlorine and amine groups. Chlorine atoms dissociate and the platinum-amine complex binds to DNA in a manner similiar to the bifunctional alkylating agents.

A

Cisplatin

136
Q

(blank) contains platinum complexes to a more complex organic moiety. Liberation of a platinum-amine complex which binds to DNA is also cytotoxical though this occurs more slowly than with cisplatin.

A

Carboplatin

137
Q

What is the clinical use of cisplatin?

A

broad spectrium agnet, good for cancers of epithelial origin. Very effective against testicular and ovarian cancers and is usually combined w/ vinblastine and bleomycin

138
Q

What is the clinical use of carboplatin?

A

treats sensitive tumors in individuals who cant tolerate cisplatin because of impaired renal functions

139
Q

What is the adverse reactions of carboplatin?

A

bone marrow suppression

140
Q

What are the adverse reactions to cisplatin?

A

nephrotoxicity!!! ototoxicty, Gi distress, bone marrow suppression (not severe)

141
Q

What is the mode of action of procarbazine?

A

autooxidation of drug yields toxic free radicals that degrade DNA. causes transmethylation of guanine residues in DNA - > chromosomal breakage

142
Q

What is the clinical use of procarbazine?

A

used in MOPP regiment to treat hogdkins diease. Also used in non-hodgkins lymphomas and to treat oat-cell carcinoma

143
Q

What are the special side effects of procarbazine?

A

Monoamine oxidase (MOA) inhibition
Disulfiram-like reaction to alcohol
Neurological (drowsiness, sedation, etc)

144
Q

What is this:
an enzyme that degrades asparagine and also glutamine which are essential to some leukemic cells. (normal cells can synthesize these on their own but cancer cells cannot) the sensitive luekemic cells will thus get their DNA synthesis halted and die.

A

L-asparaginase

145
Q

What is the clinical use of L-asparaginase?

A

acute lymphoblastic leukemia

146
Q

What are the adverse effects of L-asparginase?

A

hypersensitivity, nausea, liver and pancreatic toxicity

147
Q

How do you get resistance to L-asparaginase?

A

induction of de novo asparagine synthetase

148
Q

What is the MOA of hormonal therapy?

A

tumors arising from hormone target tissues often retain responsiveness to growth promoting effects of hormones. These tumors may be inhibited by altering the hormone supply.

149
Q

What are the four ways to modify hormones to destroy tumor cells?

A

1) ablation of hormone secreting organ
2) use hormones to suppress other hormones
3) hormone antagonists
4) high doses of supporting hormone inhibits tumor growth

150
Q

What glucocortocoid is used to treat cancer and how does it work?

A

prednisone-cuz its toxic to lymphocytes and can be used to treat acute and chronic lymphocytic leukemia, lymphomas and multiple myeloma

151
Q

What is MOPP made up of?

A

mechlorethamine + Oncovin (vincristine) + Procarbazine + Prednisone

152
Q

In breast cancer, hormonal therapy works be st when tumor cells have high concentrations of (blank)

A

estrogen receptors

153
Q

What is tamoxifen?

A

competitive antagonist of estrogen receptor
orally effective
concentrated in estrogen target tissues such as ovaries, vaginal epithelium, and breast;
remission is estrogen receptor-dependent

154
Q

What are the adverse responses to breast cancer?

A

hot flashes, hypercalcemia

155
Q

What is the MOA of imatinib (gleevac)?

A

tumor-specific tyrosine kinase inhibitor on Bcr-ABl oncoprotein found on philadelphia chromosome

156
Q

Why is it a good thing to mess up tyrosine kinase on Bcr-Abl

A

because substrate phosphorylation catalyzed by tyrosine kinase is involved in the pathogenesis of chronic myelogenous leukemia (CML)

157
Q

what is the clinical use of imatinib (gleevec)?

A

used in Philadelphia Chromosome-positive CML: second line drug for chronic phase CML inadequately controlled with interferon a; first line drug for chronic phase, accelerated phase or blast crisis.

AND other tumors over-expressing c-kit kinase or platelet-derived growth factor kinase Malignant gastrointestinal stromal tumors (GISTs)

158
Q

What are the major side effects of imatinib?

A

Diarrhea and other GI upsets
Edema in the ankle and perioribital area due to water retention
Myalgia (painful muscles)

159
Q

WHy does imatinib have drug interactions?

A

it is a substrate and rather powerful inhibitor of several p450 cytochromes

160
Q

How do you get resistance to imatinib?

A

mutation in bcr-abl kinase gene

161
Q

How does Iressa work?

A

orally active tyrosine kinase inhibitor selective for the epidermal growth factors (EGF) receptor tyrosine kinase

162
Q

T or F

EGF receptor and EGF signaling are over activated in sensitive tumors.

A

T

163
Q

What is iressa being used for?

A

clinical trial in the treatment of various solid tumors, including head and neck cancer, breast cancer and non-small cell lung cancer.

164
Q

What are the adverse effects of iressa?

A

diarrhea, skin rashes

165
Q

What is this:

any intervention to ENHANCE the body’s NATURAL ability TO DEFEND ITSELF against malignant tumors

A

immunotherapy

166
Q

What are so immunotherapy drugs?

A 
interferons
interleukins
colony-stimulating factors
monoclonal antibodies
vaccines: (cancer specific antigens, dendritic cell vaccines etc)
gene therapy
nonspecific immunomodulators
167
Q

WHat is this:
monoclonal antibody humanized against HER-2 antigen that is overexpressed on tumor cell surface in ~25% of breast cancer patients.

A

Herceptin

168
Q

(blank) overexpression marks an aggressive estrogen receptor-negative form of breast cancer.

A

HER-2/neu/erbB2

169
Q

How do you give herceptin?

A

IV infusion in combo with paclitaxel for metastatic breast cancer

170
Q

What are the adverse effects of herceptin?

A 
infusion-reated hypotension
flushing
bronchoconstriction
skin rashes
cardiotoxicity
171
Q

How does Rituximab work?

A

a chimeric monoclonal antibody against the protein CD20 on the surface of B lymphocytes and destroy B cells.

172
Q

What does the chimeric antibody of rituximab due exactly to B cells?

A

it sticks to it and forces proteins to slide over there and makes a cap for NK cells to better attach to which allows NK cells to more successfully kill the B cells

173
Q

What do you use rituximab?

A

To treat diseases characterized with

  a) excessive numbers of B cells (lymphomas, leukemias)
   b) overactive B cells (transplant rejection)
   c) dysfunctional B cells (autoimmune disorders)
174
Q

What are the adverse effects of Rituximab?

A

a) Severe infusion reaction
b) Tumor lysis syndrome (acute renal failure)
c) Infections (Hepatitis B reactivation, Progressive multifocal leukoencephalopathy)

175
Q

What are the 6 classes of anticancer drugs?

A
  1. Alkylating
  2. Antimetabolites
  3. Antibiotics
  4. Hormones
  5. Nature products
  6. Miscellaneous
176
Q

What are three alkylating agents?

A

Nitrogen mustards
Nitrosoureas
Alkyl sulfonate

177
Q

What are the nitrogen mustards?

A

Mechlorethamine, cyclophosphamide

178
Q

What are the nitrosoureas?

A

carmustine, streptozotocin

179
Q

Whare the alkyl sulfonates?

A

busulfan

180
Q

What are the three antimetabolites?

A

folate antagonist
pure antagonist
pyrimidine antagonist

181
Q

What is the folate antagonist?

A

methotrexate

182
Q

What is the purine antagonist?

A

6-mercaptopurine

183
Q

What is the pyrimidine anatgonist?

A

5-fluorouracil

184
Q

What are the three kinds of anticancer antibiotics?

A

Doxorubicin
Bleomycin
mitomycin

185
Q

What is the doxorubicin?

A

adriamycin

186
Q

What is the bleomycin?

A

Blenoxane

187
Q

What are the three anticancer hormones?

A

leuprolife
tamoxifen
glucocorticoids

188
Q

What are the nature products that are anticancer?

A

Vinca Alkaloids

Etoposide

189
Q

What are the miscellanous anticancer drugs?

A

platinum compounds (cisplatin and carboplatin)
Procarbazine
l-asparaginase
imatinib

190
Q

What are these:
Nitrogen mustards (Mechlorethamine, cyclophosphamide)
Nitrosoureas (Carmustine, Streptozotocin)

A

Alkylating agents

191
Q

What are these:
Doxorubicin, Mitoxantrone, Dactinomycin, Bleomycin,
Mitomycin C* (G1?)

A

Antibiotics

192
Q

What can 1/2 of early cancer be cured by?

A

radiotherapy

193
Q

How many cancer patients go through surgery?

A

1/3rd

194
Q

What are the types of chemotherapy?

A

Cytotoxic chemotherapy
endocrine therapy
biological therapy
gene therapy

195
Q

What percent of cancer patients will undergo chemotherapy to remove micrometastasis? Chemotherapy is able to cure only about (blank) of all cancer patients.

A

50

10-15%

196
Q

What is this:

the disappearance of any evidence of tumor for several years with a high actuarial probability of a normal life span.

A

Cure

197
Q

T or F

Many cancers are now curable

A

T!!!!! Many cancers are now curable (40-80% cure rate):

198
Q

What do you treat with a drug alone?

A

testicular cancer, lymphomas, leukemia

199
Q

What kind of approach do you take with breast, colon, and rectal cancers?

A

drug in combo with surgery and/or radiotherapy with routine adjuvant therapy following local treatment

200
Q

What kind of approach do you take to treat head and neck, esophageal, lung, cervical cancesr, soft tissue sarcomas, pediatric solid tumors?

A

multimodality with drug/surgery and or radiotherpay combo

201
Q

Recently developed principles which have helped guide the treatment of neoplastic disease. 1. A single (blank) cell can produce enough progeny to kill the host.

  1. Unless few malignant cells are present, host immune mechanisms (blank) play a significant role in therapy of neoplastic disease.
  2. a given therapy results in destruction of a (blank) percentage as opposed to a constant number of cells, therefore, cell kill follows first order kinetics.
A

Clonogenic
DO NOT
constant

202
Q

Infrequent scheduling of treatment courses prolongs survival but does not (blank)

A

cure

203
Q

Early surgica removal of the primary tumor decreases the (blank) and (blank) will remove persistant secondary tumors.

A

tumor burden

Chemotherapy

204
Q

MOre intestive and frequent treatments will have what kind of results?

A

greater kill rate than growth rate :)

205
Q

What is the limited effectivness of anticancer treatment?

A

after rounds of chemo, some cells become resistant and side effects wil start to prevail over benefits so treatment must be stopped and tumor growth begins :(

206
Q

The faster rate of (blank) makes tumor cell more prone to cytotoxic effect of anticancer drugs.

A

cell division

207
Q

T or F

Normal cells with faster pace of division (hair follicles, bone marrow) are very susceptible to anticancer drugs.

A

T, thats why we have some sucky adverse reactions from anticancer drugs : ( why people lose hair

208
Q

What are some acute adverse reactions from chemo?

A

Acute –Bone marrow toxicity (infection, hemorrhage, etc.)
G.I. mucosa toxicity (diarrhea)
Hair follicle toxicity (hair loss)
Germline cell toxicity (infertility)…

209
Q

What are some chronic adverse reactions from chemo?

A

Chronic – Cardiomyopathy, neurotoxicity, G.I. tract distress, nephrotoxicity, mutagenesis, carcinogenesis

210
Q

Schedule of admin of cancer therapeutics depends on,,,,?

A
  • the pharmacokinetics of the drugs being used,
  • the cycle phase specificity of the drugs,
  • the patient’s general state of health,
  • the type of cancer being treated (eg. lymphoma or localized solid tumor).
211
Q

How are cancer therapeutics typically given?

A

in a cycle (drug, then drug free period)

212
Q

What is this:
In tumor cells that do not respond to initial therapy using currently available anticancer drugs.
Related to the frequency of spontaneous mutation.

A

primary resistance

213
Q

What is this:
Appears or develops during drug therapy.
Result of amplification of target genes, multidrug resistance gene (MDR1)
Changes in cellular targets of the drugs (e.g., in their affinity for drugs) or changes in transport or activating enzymes

A

Acquired Resistance

214
Q

T or F

combinations are usually more effective than single drug therapy/

A

T

215
Q

What are three Multdrug resistance modulators (MDR) or chemosensitizers are?

A

Cyclosporin A, verapamil, tamoxifen

216
Q

T or F

drugs acting by different cytotoxic mechanisms may have synergistic therapeutic effects

A

T

217
Q

T or F
Appears or develops during drug therapy.
Result of amplification of target genes, multidrug resistance gene (MDR1)
Changes in cellular targets of the drugs (e.g., in their affinity for drugs) or changes in transport or activating enzymes

A

T

218
Q

Multidrug regiments follow chemotherapy schedules. why do we use a shedule?

A

to permit recovery from acute toxicities

sever 6-8 cycles of treatment should be given

219
Q

What do you use ABVD (Adriamycin + Bleomycin + Vinblastine + Dacarbazine) for?

A

Hodgkins lymphoma

220
Q

What do you use MOPP (mechlorethaine+ oncovin (vincristine) + procarbazine + prednisone)?

A

Hodgkins lymphoma

221
Q

What is the ideal way to treat Stage III or Stage IV of hodgkins disease and results in a cure rate of 50-80%?

A

MOPP alternating with ABVD in a defined cyclical schedule

222
Q 
A 53-year-old truck driver presents to his primary care physician for a routine examination. He reports that he has spent most of his summer driving across the country. Physical examination reveals a 7-mm lesion on the left dorsal aspect of his left arm (see picture). Further evaluation reveals pearly papules with visible telangiectatic vessels. The lesion is biopsied and found to contain palisading nuclei. What is the most appropriate treatment for this patient?  
A) 5-Fluorouracil (5-FU)
B) 6-Mercaptopurine (6-MP)
C) Bleomycin
D) Busulfan (Myleran) 
E) Cyclophosphamide
A

A. 5-Fluorouracil – inhibiting thymidylate synthase and decrease dTMP, inhibiting S-phase of DNA replication

223
Q

15-year-old girl moves to your neighborhood and makes an appointment to see you. She is being treated for acute lymphoblastic leukemia. She tells you that she has been doing well, but recently she has had frequent severe headaches, and her mother said she has stumbled a couple of times during the past week for no apparent reason. She is being treated with cytarabine. If leukemic meningitis is suspected, what should be done next?

A

Immediately arrange for an evaluation of the CSF. If the CSF reveals leukemic cells, you can consider administering methotrexate 12 mg intrathecally every day for 4 days. With such a regimen subsequent evaluation of CSF often indicate no leukemic cells present. The headaches and balance problems typically disappear. Six months later, most patients show no evidence of leukemia

Block 7 Week 1 (10 decks)

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