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Medical Pharmacology Exam 2 > Anti-neoplastic Agents > Flashcards

Anti-neoplastic Agents Flashcards

1
Q

Regarding the cell cycle, activation of oncogenes overrides with checkpoint? What about inactivation of tumor suppressors; what checkpoint in overidden? Where are majority of cells (and tumor cells)?

A
  • G1 arrest
  • G2 Arrest
  • G0 (just higher proportion of tumor cells growing faster than others)
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2
Q

The p53 tumor suppressor is associated with which checkpoint?

A

G2

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3
Q

The proportion of tumor cells that are not in G0 are referred to as _. This is the proportion [responsive/unresponsive] to chemotherapeutics.

A

Tumor cell growth fraction

Responsive

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4
Q

The presumed ultimate cause of lethality following cancer are _. These are [responsive/unresponsive] to chemotherapeutics. Why are they hard to detect?

A

Micrometastases
Responsive
Below the level of detection

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5
Q

The two examples of bischlorethamines (alkylating agents) provided are _. Which is the orally bioavailable and less reactive version that requires activation in target tissues or in the liver?

A

Mechlorethamine and Cyclophosphamide

Cyclophosphamide

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6
Q

What is the mechanism of action of the bischlorethamines?

A

Cause the formation of cross-linked guanine residues in DNA, leading to cell death (necrosis?)

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7
Q

As a class of alkylating agents, a major characteristic of nitrosoureas compared to others is _. This makes them particularly suitable for tumors located in _.

A

They cross the BBB

CNS tumors

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8
Q

Procarbazine is an alkylating agent that metabolized to _. As with other alkylating agents, its mechanism if action is _

A

Free radical intermediates (reactive)

Cross linking DNA to cause damage

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9
Q

Nitrosoureas and procarbazine are profoundly cross reactive with other antineoplastic agents. True or false?

A

False. Both groups non-cross reactive

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10
Q

A major risk with the use of procarbazine is _

A

It is leukemogenic, especially worse than the other alkylating agents

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11
Q

Methotrexate is an antitumor antimetabolite. It is an analog to _. Its works by targeting _ enzyme, preventing the synthesis of DNA, RNA and proteins

A 
Folic acid 
Dihydrofolate reductase (converts dihydrofolate to tetrahydrofolate)
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12
Q

Methotrexate accumulates in cells as a _ derivative. It is specific to _ phase of the cell cycle.

A

Polyglutamate derivative

S (synthesis) phase

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13
Q

To rescue a cell from the toxic effects of methotrexate, _ can be given at the same time

A

Folinic acid (Leukovorin)

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14
Q

What are 4 mechanisms by which methotrexate resistance can occur in cells?

A

Increased DHFR expression
DHFR mutation
Reduced methotrexate uptake
Increase methotrexate efflux

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15
Q

The 2 purine antagonists provided as examples are _. They work by inhibiting _.

A

6 mercaptopurine , 6 thioguanine

denovo purine synthesis

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16
Q

Purine antagonists function during what phase of the cell cycle?

A

S (synthesis) phase

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17
Q

What is the enzyme required for the activation of 6 mercaptopurine and 6 thioguanine? What is the effect of a mutation or downregulation of this enzyme?

A

hypoxanthine-guanine phosphoribosyl
transferase (HGPRT)
Cell resistance to the drugs

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18
Q

How is xanthine oxidase related to the administration of 6 mercaptopurine? What is a very common source of xanthine oxidase?

A

Xanthine oxidase inactivates 6 mercaptopurine

Cow’s milk

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19
Q

What is a common drug coadminstered with 6 mercaptopurine to inhibit the enzyme xanthine oxidase? How does this affect the needed dose of 6-mercaptopurine?

A

Allopurinol

Need to reduce the dose of 6 mercaptopurine

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20
Q

5FU (flurouracil) is a pyrimidine antagonist that is metabolized into _, which inhibits the enzyme _. Inhibition of said enzyme results in _

A 
fluorodeoxyuridine monophosphate (FdUMP)
Thymidylate synthetase
Thymineless death (no thymine made)
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21
Q

A pyrimidine antagonist, 5FU is active in what phase of the cell cycle?

A

S (synthesis) phase

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22
Q

What is capecitabine? What are 2 types of cancers that it is used for?

A

A prodrug of 5FU

Colon cancer, refractory breast cancer

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23
Q

What is the major enzyme that metabolizes capecitabine to 5FU? This enzyme might preferentially activate this drug in tumor tissues

A

Thymidine phosphorylase

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24
Q

What is the metabolite of cytarabine (araC) that is an inhibitor of DNA synthesis? What class of drug does cytarabine belong to? How does it exert its functions?

A

araCTP
Pyrimidine antagonists
it incorporates and terminates the DNA strand

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25
Q

What is the enzyme requred for the activation of cytarabine? Loss of this enzyme is a common cause of tumor resistance

A

Deoxycytidine kinase

26
Q

Among antitumor antibiotics, what are the 2 examples provided of anthracyclines? What is their mechanism of action? What tissue is damaged irreversibly with high doses?

A

Daunorubicin, doxorubicin
DNA intercalation
Irreversible cardiac toxicity

27
Q

Bleomycin is an antitumor antibiotic. What is its main mechanism of action? At high doses, what type of tissue damage occurs? What is a major consideration when using this drug?

A

DNA scission
pulmonary fibrosis
anaphylactic shock

28
Q

What property of bleomycin makes it desirable for use in combination of other antineoplastics? What is a potential caution with its use?

A

No significant myelosuppression.

Natural product - anaphylaxis risk

29
Q

What are the 2 examples of vinca alkaloids provided? How do they function? What phase of the cell cycle are they specific to?

A

Vinblastine and vincristine
Prevent tubulin polymerization
Function in M phase

30
Q

What are 2 major differences between vincristine and vinblastine?

A

Vinblastine - dose limiting bone marrow suppression

Vincristine - significant neurotoxicity (muscle weakness)

31
Q

What gene mutation is able to affect the effectiveness of the vinca alkaloids?

A

Tubulin

32
Q

What is the mechanism of action of paclitaxel? What types of cancer is it indicated for?

A

Blocks tubulin dissasembly

Ovarian and advanced breast cancer

33
Q

Topotecan and irinotecan are examples of _. They bind _ enzyme, preventing religation of [single/double] strand DNA breaks

A

Camptothecins (topoisomerase inhibitors)
Topoisomerase 1
Single

34
Q

Topotecan and irinotecan work during _ phase of the cell cycle. Side effects include _.

A

S phase

Myelosuppression and diarrhea

35
Q

Etoposide, daunorubicin and doxorubicin work by blocking the activity of _. This prevents _

A

Topoisomerase II

Religation of double stranded DNA breaks

36
Q

What are the two example of platinum containing agents provided? What phase of the cell cycle do they function in? What are 2 notable toxicities noted with these drugs?

A

Cisplatin and carboplatin
phase non-specific
Nephrotoxicity, acoustic nerve dysfunction

37
Q

What are 3 examples of hormone dependent cancers? (1 male, 2 female)

A

Prostate
Breast
Endometrial

38
Q

How is tamoxifen related to estrogen? What is the drug class? What is its efficacy from tissue to tissue? What types of cancer is it used for? (2)

A

It is a partial agonist at the estrogen receptor
Selective Estrogen Response Modulator (SERM)
Varies from tissue to tissue
Breast and Uterine Tissues

39
Q

What is a widely acknowledged side effect of tamoxifen?

A

Hot flashes

40
Q

What criteria (estrogen receptor-wise) has to be met for tamoxifen for work?

A

The tumor has to be estrogen receptor positive

41
Q

What is a benefit of tamoxifen in post-menopausal women? What are 2 risks associated with tamoxifen therapy?

A

Reduced bone fractures

Increased thrombosis/embolism, increased endometrial cancer

42
Q

Raloxifen is another SERM. How does it compare to tamoxifen with regards to reducing breast cancer occurence? With risk of endometrial cancer and thrombotic events?

A

Raloxifen reduces breast cancer like tamoxifen

Reduced risk of endometrial cancer and thrombotic events

43
Q

THe drugs letrozole, anastrozole and exemestane block the enzyme _. This prevents the conversion of _ to _. This is particularly effective for reducing estrogen production in _ population

A

Aromatase
Angrogens to estrogens
Postmenopausal women

44
Q

Why are letrozole, anastrozole and exemestane not used in premenopausal women?

A

Ineffective because of compensatory gonadotropin and ovarian estrogen production

45
Q

How to letrozole, anastrozole and exemestane compare to tamoxifen for the treatment of estrogen receptor positive tumors?

A

They are more effective

46
Q

What is an advantage of aromatase inhibitors (letrozole, anastrozole and exemestane ) over SERMs, risk-wise? What is a disadvantage?

A

No enhanced risk of thrombosis or uterine cancer

Loss of bone density

47
Q

What is leuprolide? What is the effect of pulsatile delivery? What is the effect of continuous high dose delivery?

A

Synthetic analog of GnRH (gonadotropin releasing hormone)
Pulsatile - increased androgens / estrogens in men/ women
High dose - decreased androgens / estrogens in men/ premenopausal women

48
Q

What is flutamide? What drug does it have to be coadministered with? Why? What is it used to treat?

A

Flutamide is an androgen receptor antagonist
It is coadministered with leuprolide
Alone, not very effective because of high mutation rate of the androgen receptor
Prostate cancer

49
Q

The major mechanism by which prednisone work is by causing _ in leukemia. While it isn’t able to cure leukemia, it is used as _ for other cancers

A

Apoptosis in leukemia cells

Paliative agent

50
Q

What is oncogene addiction?

A

Tumor survival / proliferation becomes dependent upon activated oncogenes

51
Q

There are 2 examples of EGF receptor kinase inhibitors provided. What are they? How are their mechanisms different?

A

Erlotinib and cetuximab
Erlotinib inhibits the kinase
cetuximab binds and blocks the receptor

52
Q

There are 2 HER2 protein tyrosine kinase inhibitors provided as examples. What are they? How are their mechanisms different?

A

Lapatinib and trastuzimab
lapatinib inhibits EGFR kinase and HER2 kinase
trastuzimab in humanized HER2 receptor antibody

53
Q

Trastuzimab is used to treat refractory metastatic breast cancer. What is a criteria that must be met for it to be effective?

A

The tumor has to be HER2 positive

54
Q

What is the drug used to block the activity of the bcr/abl fusion protein? What is the common name of the rearranged chromosome that produces this protein? What is the disease for which this drug is indicated?

A

Imatinib
Philadelphia chromosome
Chronic myelogenous leukemia

55
Q

What is the toxin associated with brentuximab? What receptor is targeted / mediates the internalization of brentuximab?

A

Vedotin

CD30

56
Q

What is the target of brentuxumab vedotin? What is the mechanism by which this drug works? What are the 2 diseases for which this drug is indicated?

A

CD30
It is an igG congugated to a mitotic spindle toxin, it is internalized and it is cleaved to release toxin
Hodgkins and non-Hodgkins lymphoma

57
Q

What is the log kill hypothesis for chemo?

A

With each chemo treatment, 1 log unit of cells killed. Recovery during the interval, but the next chemo treatment will kill another log of cells. Overall downward trend in cell numbers

58
Q

True or false, chemo is mostly used after surgery?

A

False, can also be used as neoadjuvant therapy (pre-surgery)

59
Q

What is the enzyme target if the antitumor antibiotics daunorubicin and doxorubicin?

A

The block DNA topoisomerase II, causing DNA scission

60
Q

Compare the mechanisms of the vinka alkaloids and paclitaxel.

A

Vinca alkaloids - prevent polymerization of tubulin

Paclitaxel - Prevents depolymerrization of tubulin

61
Q

What is multidrug resistance? What is the example of the nonspecific drug efflux pump that can mediate this effect?

A

A “survitor” with resistance to one agent can be resistant to several unrelated cytotoxic agents
MDR1

62
Q

What are the 3 tenets of multidrug therapy?

A

Use drugs without cross resistance
Minimize side effect
Use highest tolerable dose of each drug

Medical Pharmacology Exam 2 (16 decks)

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