Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SBL week 2 > Cancer Pharmacology > Flashcards

Cancer Pharmacology Flashcards

1
Q

Activation of oncogenes overrides what part of cell cycle?

Inactivation of tumor suppressor genes overrides?

A

1) G1 arrest

2) G2 arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What anticancer drugs have cell cycle effects on the S-phase?

A

1) Methotrexate
2) 5-fluorouracil
3) 6-mercaptopurine
4) Topotecan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What anticancer drugs have cell cycle effects on the S-G2 phase?

A

Etoposide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What anticancer drugs have cell cycle effects on the G2-M phase?

A

Bleomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What anticancer drugs have cell cycle effects on the M phase?

A

1) Paclitaxel
2) Vinblastine
3) Vincristine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of chemotherapy is done in order to reduce the size of the primary tumor before surgical resection?

A

Neoadjuvant chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What type of chemotherapy is done after surgical resection in order to prevent relapse?

A

Adjuvant chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is growth fraction?

A

Ratio of proliferating cells to G0 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

As a general rule, antineoplastic agents are more effective on cells with what type of growth fraction?

A

High growth fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why can solid tumors be more difficult to treat with chemotherapeutic agents?

A

Because their growth fraction decreases over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antineoplastic therapy follows what order of kinetics?

What does this mean?

A

1) First-order kinetics

2) Given dose of drug destroys constant fraction of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why do we use high-dose intermittent chemotherapy?

A

Allows recovery of normal, healthy tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Primary/inherent resistance to anti-cancer drugs in the natural products category can be due to high baseline expression of what?

A

p-Glycoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do bone marrow, GI tract, hair follicles, oral mucosa and sperm forming cells all have in common in terms of cancer therapy?

A

They are are the major sites of toxicity due to being rapidly proliferating tissues (tissues with high growth fractions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What pharmacologic agents help decrease adverse effects such as neutropenia, thrombocytopenia, and anemia?

What is used to decrease emetogenic effects?

What is used to delay skeletal complications?

A

1) Hematopoietic agents
2) Serotonin receptor antagonist (ondansetron)
3) Bisphosphonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What nitrogen mustard is the most widely used alkylating agent and one of the most emetogenic agents?

A

Cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the MOA for alkylating agents?

A

Form covalent linkages with DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Because Cyclophosphamide is a pro-drug, what must activate it?

A

CYP2B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an adverse effect of cyclophosphamide?

What metabolite of CP causes it?

What can be given to inactivate the metabolite and is used for prophylaxis?

A

1) Hemorrhagic cystitis
2) Acrolein
3) Mesna

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are adverse effects of Cisplatin?

A

1) Renal tubular damage

2) Ototoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the adverse effects of Busulfan?

A

Pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antimetabolites block or subvert pathways that are involved in, or lead to?

A

Cell replication (nucleotide and nucleic acid synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the MOA for methotrexate?

A

It inhibits dihydrofolate reductase and leads to reduction in dTMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Methotrexate is an analog to what compound?

A

Folic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Administration of what drug is used in conjunction with high-dose methotrexate therapy to rescue normal cells? (also antidote for accidental drug overdose)

A

Leucovorin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Fluorouracil (5-FU) is a structural analog to what compound?

A

Pyrimidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the MOA of fluorouracil?

A

Active compound FdUMP covalently binds thymidylate synthetase and blocks de novo synthesis of thymidylate

28
Q

Mercaptopurine (6-MP) is activated into monophosphate nucleotide 6-thioinosinic acid by what enzyme?

A

HGPRT

29
Q

Allopurinol, a xanthine oxidase inhibitor, is often used as supportive care in the treatment of acute leukemias to prevent?

A

Hyperuricemia due to tumor cell lysis

30
Q

Simultaneous administration PO 6-MP with what other drug results in increased levels of 6-MP and increased toxicity?

A

Allopurinol

31
Q

What is the MOA for the vinca alkaloids, vinblastine and vincristine?

A

Bind to β-tubulin and inhibit microtubule assembly (depolarization)

32
Q

What are common adverse effects of vinblastine and vincristine?

A

Alopecia and bone marrow depression

33
Q

Which vinca alkaloids causes myelosuppression to a greater extent?

A

Vinblastine

34
Q

Which vinca alkaloids causes cumulative neurological toxicities to a greater extent?

A

Vincristine

35
Q

What is the MOA for taxanes such as paclitaxel?

A

Bind to β-tubulin and stabilize microtubule formation

36
Q

What are common adverse effects of paclitaxel?

A

1) Hypersensitivity reactions in hands and toes

2) Change in taste

37
Q

Paclitaxel and taxanes have been the traditional treatment for?

A

Breast cancer

38
Q

What is the MOA for topotecan?

A

Inhibit topoisomerase I which causes DNA damage and leads to cell death

39
Q

What is the MOA for etoposide and doxorubicin?

A

Inhibit topoisomerase II

40
Q

All of the anticancer antibiotics currently in use are products of various strains of what soil microbe?

A

Streptomyces

41
Q

What are adverse effects of doxorubicin?

A

Produce free radicals that cause cardiotoxicity which can lead to dysrhythmias and heart failure

42
Q

What is the MOA of Bleomycin?

A

Induces single- and double-stranded DNA breaks

43
Q

What are adverse effects of Bleomycin?

A

Can cause significant pulmonary toxicity and usually presents as pneumonitis with cough, dyspnea, dry inspiratory crackles

44
Q

Asparaginase is used in targeted therapy for?

A

Acute lymphoblastic leukemia (ALL)

45
Q

What is the MOA for asparaginase?

A

Hydrolyzes circulating L-asparagine into aspartic acid and ammonia, effectively inhibiting protein synthesis

46
Q

Asparaginase is cell cycle specific to what phase?

A

G1

47
Q

When mutated, overexpressed, or structurally altered, tyrosine kinases can become potent?

A

Oncoproteins

48
Q

What drug is used to treat Chronic myelogenous leukemia?

What is its MOA?

A

1) Imatinib

2) Inhibits ABL tyrosine kinase

49
Q

What is a recombinant fusion protein made up of portions of the extracellular domains of human VEGF receptors (VEGFR) 1 and 2 fused to the Fc portion of the human IgG1 molecule?

A

Ziv-aflibercept

50
Q

What is the MOA of Ziv-aflibercept?

A

Inhibition of VEGFR signaling by binding VEGF ligands

51
Q

What inhibits cellular growth, alters the state of cellular differentiation, interferes with oncogene expression, alters cell surface antigen expression, increases phagocytic activity of macrophages, and augments cytotoxicity of lymphocytes for target cells?

A

Interferon-α2a and -α2b

52
Q

What increases cytotoxic killing by T cells and NK cells?

A

IL-2

53
Q

What is the major toxicity of IL-2?

A

Capillary leak syndrome

54
Q

What is the treatment for Non-Hodgkins lymphoma?

A

Rituximab

55
Q

What is the MOA of rituximab?

A

Rituximab binds to the CD20 antigen which leads to selective killing of B-cells

56
Q

Dacarbazine and cisplatin are the most active cytotoxic agents used to treat?

A

Malignant melanoma

57
Q

Drugs that end in -nib act where specifically?

Drugs that end in -mabs act where specifically?

A

1) Intracellular

2) Extracellular

58
Q

Mucositis is an adverse effect of what drug?

A

Methotrexate

59
Q

Pulmonary fibrosis is an adverse effect of what drugs?

A

Bleomycin and busulfan

60
Q

Peripheral neuropathy is an adverse effect of what drug?

A

Vincristine

61
Q

Ototoxicity is an adverse effect of what drug?

A

Cisplatin

62
Q

Cardiotoxicity is an adverse effect of what drug?

A

Doxorubicin

63
Q

Nephrotoxicity is an adverse effect of what drugs?

A

Cisplatin and cyclophosphamide

64
Q

Hemorrhagic cystitis is an adverse effect of what drugs?

A

Cyclophosphamide and ifosfamide

65
Q

What is used to treat APML?

A

Tretinoin

66
Q

What are common adverse effects of tretinoin?

A

Vitamin A toxicity and retinoic acid syndrome

67
Q

Erlotinib and gefitinib both inhibit the activity of?

A

EGFR

SBL week 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions