day 2 oncology

Question 1

MOA of epipodophyllotoxins

Answer 1

Act by inhibiting DNA topoisomerase II

prevents proper unwinding of DNA resulting in blockade of DNA synthesis and cell division

Question 2

uses of epipodophyllotoxins

Answer 2

• Etoposide: lung cancer, germ cell cancer, gastric cancer

teniposide- pediatric leukemia***

Question 3

2 types of epipodophyllotoxins

Answer 3

Etoposide

teniposide

Question 4

3 adverse effects of epipodophyllotoxins

Answer 4

Myelosuppression
• Alopecia
• Hypotension

Question 5

What are antitumor antibiotics?

Answer 5

Derived from microorganisms (bacteria)

compounds are produced and used by bacteria to compete with other microorganisms for resources

Question 6

What are some examples of antitumor antibiotics?

Answer 6

Anthracyclines/Anthracenedione
Mitomycin
Doxorubicin
Bleomycin
Daunorubicin
Epirubicin
Idarubicin

Question 7

MOA of anthracyclines

Answer 7

– Inhibit topoisomerase 2
generate free radicals
bind to DNA and intercalate DNA strands

Question 8

DNA intercalation is what?

Answer 8

Drug binds to areas on both strands preventing DNA from being replicated

Question 9

Free radical formation

Answer 9

Free radicals are very damaging to tissues by binding to metabolic products and disrupting cellular function

Question 10

uses of anthracyclines

Answer 10

• Doxorubicin: breast CA, myeloma, leukemia, lymphoma
daunorubicin and idrarubicin- leukemia
epirubicin- breast, gastroesophageal CA
mitoxantrone- leukemia, lymphoma, prostate CA, multiple sclerosis

Question 11

adverse effects of anthracyclines

Answer 11

• Myelosuppression
• Alopecia
• N/V
• Mucositis
• Vesicant if extravasated 
cardiotoxicity
mitoxantrone- turns urine blue/ green
doxo/ dauno/ ida/ epirubicin turn urine reddish/ orange

Question 12

acute cardiotoxicity from anthracyclines

Answer 12

• Within 24-72 hours of admin
arrythmias, pericarditis, myocarditis
usually subclinical

Question 13

chronic cardiotoxicity from anthracyclines

Answer 13

• Dose dependent
delayed by years
results in cardiomyopathy and heart failure

Question 14

Cardiotoxicity of anthracycline

Answer 14

– 1 -2% risk for doxorubicin doses 500

Question 15

Use of dexrazoxane

Answer 15

Reduces free radical formation in cardiac tissue

may reduce therapeutic effect of doxorubicin

Question 16

Bleomycin MOA

Answer 16

Binds DNA and forms free radicals that destroy DNA and prevent DNA replication

Question 17

Bleomycin uses?

Answer 17

lymphoma, germ cell tumor, head and neck cancer, SCC

Question 18

What is a major concern with the use of bleomycin?

Answer 18

Pulmonary toxicity

symptoms include, cough, pnemonitis dyspnea

Question 19

Pleural effusion is what?

Answer 19

• Pleural is fluid build up around the lung
prevents normal expansion upon inhalation
risk factors = age >70
supplemental oxygen
cumulative doses >400
underlying pulmonary disease

Question 20

Tyrosine kinase inhibitors MOA

Answer 20

Inhibiting tyrosine kinases can target and block specific regulatory pathways and promote cancer cell death through apoptosis

Question 21

What are the differences between the TKI’s?

Answer 21

– Target different TK that vary in level activity in different cancers
differ in binding affinity to their targets making some more potent inhibitors than other
some bind with less restricition

Question 22

Resistance to TKI’s

Answer 22

Mutations in the amino acid sequence of tyrosine kinases could prevent the TKI from binding to the target site and make the drug inactive

Question 23

Adverse effects of TKIs

Answer 23

– Rash
– Myelosuppression 
– Fatigue
– Fluid
diarrhea
CHF

Question 24

Drug interactions of TKI’s

Answer 24

• Many metabolized by CYP450 enzyme system
enzyme inhibitors decrease metabolism and increase risk for side effects
enzyme inducers increase metabolism and decrease risk for side effects
reduced bioavailability with concomitant use of stomach acid reducers like PPI and H2 antagonists

Question 25

possible MOA of immunomodulators?

Answer 25

– May alter tumor necrosis factor may increase activity of NK cells and interferons may promote apoptosis

Question 26

immunomodulators MC used for what?

Answer 26

Mc used for multiple myeloma | in combo with dexamethazone

Question 27

3 examples of immunomodulators

Answer 27

Thalidomide Lenalidomide Pomalidomide

Question 28

adverse effects of immunomodulators

Answer 28

``` peripheral neuropathy thromboembolism fatigue rash dizziness myelosuppression ```

Question 29

proteasomes inhibitors MOA

Answer 29

inhibit complexes of proteins that would otherwise breakdown unneeded or damaged proteins

Question 30

proteasomes inhibitors used to treat what?

Answer 30

used in treatment for multiple myeloma

Question 31

adverse effects of proteasome inhibitors

Answer 31

``` peripheral neuropathy neuralgia rash N/V/D heart failure pulm toxicity ```

Question 32

monoclonal antibodies MOA

Answer 32

target specific proteions in cancer cells that block their standard function (various sites on the surface of the cell)

Question 33

how mAb kill tumor cells

Answer 33

could block receptors required for activating cell functions could bind to free protein ligands looking to bind to receptors could bind to receptors and cause apoptosis could bind to receptors and cause antibody dependent cellular cytotoxicity

Question 34

uses of mAb

Answer 34

rituximab- lymphoma trastuzmab- HER2 breast cancer panitumumab- colorectal cancer cetuximab- colorectal, lung, head and neck CA bevacizumab- colorectal, breast, lung, renal cell cancer

Question 35

adverse effects of mAb

Answer 35

infusion related reactions heart failure hypomagnesemia delayed wound healing

Question 36

aspariginase MOA

Answer 36

breaks down asparagine to aspartate which will deprive the tumors of a vital amino acid leading to stress and apoptosis

Question 37

forms of aspariginase

Answer 37

Ecoli PEG erwinia

Question 38

use of aspariginase

Answer 38

part of combination chemo to treat ALL

Question 39

adverse effects of aspariginase

Answer 39

hypersensitivity pancreatitis neurologic toxicity clotting bleeding d/o