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Phar 301 > Anticancer Drugs > Flashcards

Anticancer Drugs Flashcards

1
Q

What are the three most prevalent types of cancer for each sec (4 total)

A

Males:
Prostate
Lung
Colorectal

Females:
Breast
Lung
Colorectal

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2
Q

What are the two hallmarks of cancer at the cellular level (What is altered)

A
  • Regulation of cell proliferation

- Regulation of cell differentiation

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3
Q

What are 3 of the 7 warning signs of cancer?

A
  • Change in bowel/blader habits
  • A sore that does not heal
  • Unusual bleeding or discharge
  • Thickening or a lump in breast/elsewhere
  • Indigestion or difficulty swallowing
  • obvious change in a wart or mole
  • Nagging cough or hoarseness
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4
Q

How is cancer cell growth described? (What does the graph look like)

A

Exponential growth over time (as opposed to gompertzian/sigmoidal)

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5
Q

True/False? Clinical detection of tumors is possible earlier on

A

False, happens after sigmoidal curve levels off

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6
Q

Name 6 ways to treat cancer cells

A
  • Destroy neoplastic cells (with radiation/drugs/host immunodefenses)
  • Removal via surgery
  • Prevent metastases
  • Convert tumor cells to normal cells
  • Halt neoplastic cell division
  • Block angiogenesis
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7
Q

What are the 3 principles of “classical” cancer chemotherapy?

A
  1. Cure = death of every malignant cell
  2. Do not rely on host mechanisms to eliminate moderate amounts of cancer cells
  3. Cell-kill follows first order kinetics (constant proportion)
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8
Q

True/False? The relationship between drug concentration and survival of cells is linear.

A

True

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9
Q

How do basic anticancer drugs kill tumor cells? (4 ways)

A
  • Antimetabolits (Substitute/inhibit synthesis)
  • Intercalation, damage, or alteration of DNA structure
  • Inhibition of DNA transcription/translation
  • Block of protein function within cells or on cell surface
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10
Q

Name 3 types of anticancer drugs

A

Alkylating agents
Anti-metabolites
Anti-tumor antibiotics

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11
Q

Name 2 alkylating agents used as anticancer drugs

A

Cyclophosphamide

Cisplatin

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12
Q

Name 3 antimetabolites used as anticancer drugs

A

Methotrexate
5-Fluorouracil
Cytarabine

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13
Q

Name 3 of the 6 Anti-tumor antibiotics

A

Vincristine
Vinblastine
Taxol

Doxorubicin
Etoposide
Bleomycin

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14
Q

True/False? Non-cell cycle phase-specific drugs are more effective than cell cycle phase specific drugs?

A

True

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15
Q

What type of anticancer drug are nitrogen mustards?

A

Alkylating agents

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16
Q

What do alkylating agents do, and what is the effect of their action? (4 consequences)

A

They alkylate DNA at the N-7 position of Guanine, this leads to:

  • Miscoding
  • Depurination
  • Strand Breaks
  • Cross links
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17
Q

Which is more effective, Monofunctional alkylating agent or a bifunctional one?

A

Bifunctional (by a lot)

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18
Q

True/False? Cyclophosphamide is the drug that is formed from metabolic activation of a prodrug

A

False

Cyclophosphamide is the prodrug, the active drug is Phosphoramide mustard

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19
Q

How do platins such as cisplatin work to prevent tumor proliferation? 4 methods

A
  • Monoadducts
  • Interstrand crosslinks
  • DNA-protein crosslinks
  • Intrastrand crosslinks
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20
Q

What are consequences of platin use? 3 symptoms

A

Ototoxicity, nephrotoxicity, nausea/vomitting

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21
Q

What are three causes of resistance to alkylating agents?

A
  • increased inactivation (nucleophilic “trapping agents”
  • Increased DNA repair
  • Decreased activation
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22
Q

What are four main targets of alkylating agent toxicity?

A 
(rapidly proliferating cells)
- hematopoietic system
- GI tract
- Gonads
May be associated with secondary malignancies
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23
Q

What is methotrexate an analog of?

A

Folic acid

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24
Q

What is the main action of methotrexate?

A

Inhibition of dihydrofolate reductase

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25
Q

What does a lower IC50 mean?

A

The drug is more effective at inhibiting its target

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26
Q

What metabolic pathway does methotrexate interrupt, and what can rescue this pathway?

A 
Thymidylate synthase (starves cell of thymidine)
Rescued by leucovorin
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27
Q

How does methotrexate need to be modified before it can alter the FH2 -> FH4 pathway?

A

It has to be polyglutamated

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28
Q

What are 2 mechanisms of methotrexate resistance

A

Impaired transport into cells

Impaired polyglutamate formation

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29
Q

What is 5-Fluorouracil an analog of?

A

Pyrimidine

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30
Q

What is the main action of 5-Fluorouracil?

A

Inhibition of Thymidylate synthase

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31
Q

Why are Methotrexate and 5-fluorouracil given together?

A

To shut down folate synthesis

32
Q

What does Cytarabine do and how?

A

Inhibits DNA polymerase

Incorporated into DNA - terminates chain

33
Q

What are 4 symptoms of antimetabolite resistance?

A

Changes in target enzymes
Decreased activation
Increased inactivation
Decreased access to target site

34
Q

What are two classes of drugs that target microtubules?

A

Vinca alkaloids and taxanes

35
Q

Name two vinca alkaloids

A

Vincristine

Vinblastine

36
Q

Name a taxane

A

Paclitaxel

37
Q

What are the main toxic effects of each vinca alkyloid?

A

Vincristine - neurotoxicity

Vinblastine - myelosuppression

38
Q

What do vinca alkyloids do to microtubules?

A

block polymerization of MT, continues disassembly

39
Q

What does Paclitaxel do to microtubules

A

Stabilizes polymerization

40
Q

What is Abraxane?

A

Paclitaxel in albumin-coated nanoparticles

41
Q

How do topoisomerase inhibitors function?

A

They inhibit topoisomerase II
Intercalate DNA, blocking DNA and RNA synthesis
Alter cell membrane fluidity and ion transport, generate free radicals

42
Q

What cell cycle stage to topoisomerase inhibitors function at?

A

S-G2

43
Q

Name a topoisomerase inhibitor

A

Bleomycin

44
Q

Why do current drug regimes fail?

A

Drug toxicity

Drug resistance

45
Q

Name 6 mechanisms of drug resistance

A
  • DNA-Synthesis gene overexpression
  • Altered target molecules
  • Enzymatic deactivation
  • Altered membrane transport - drug efflux
  • Enhanced DNA repair
  • Resisting drug induced cell cycle arrest/apoptosis
46
Q

What are the 4 conditions for drugs during combination chemotherapy?

A

Each drug should be:

  • Effective on its own
  • Synergistic
  • Have non-cumulative toxicities
  • Given in maximum tolerated doses
47
Q

What are three hormonal manipulations to treat cancer?

A

Glucocorticoid action
Block estrogen action
Block androgen action

48
Q

Name a glucocorticoid receptor agonist

A

Prednisone

49
Q

What are the effects of prednisone?

A

Triggers apoptosis, antilymphocytic effects

50
Q

What is tamoxifen and what does it do?

A

Competitive partial agonist/antagonist at estrogen receptors

Suppresses IGF-1 and upregulates TGF-beta

51
Q

What does anastrozole do and what is a consequence of its action?

A

Blocks aromatase (test - estradiol), blocks synthesis of estrogen from androgens

52
Q

How does ER+ cancer cell growth differ in pre and post menopausal women?

A

Post-menopausal women do not have active aromatase in the body, less estrogen in circulation therefore less estrogen reaches cancer cells, growth stunted

53
Q

What does Flutamide do?

A

Blocks androgen action at the receptor level

blocks interactions between co-activators and other factors

54
Q

What enzyme does Finasteride block and what is a consequence of this?

A

5-alpha reductase (testosterone -> dihydrotestosterone)

DHT production stopped

55
Q

True/False? Gonadotropin-releasing hormone agonists/antagonists can induce hypogonadism as well as suppress gonadotropin release

A

True

56
Q

What is L-asparaginase? When is it used? Why?

A

An enzyme given as a drug, converts Asparagine into aspartic acid.
Used in Acute lymphoblastic leukemia:
Tumor cells lack asparagine synthetase; L-asparaginase depletes the L-asparagine in the cells, prohibiting protein synthesis

57
Q

Name a cancer specific enzyme and the drug that targets it

A

Fused BRC-ABl (cancer specific tyrosine kinase) formed by translocation of chormosomes
Imatinib will inhibit this enzyme, preventing rapid proliferation but LEAVING THE CELL ALIVE

58
Q

True/False? Antibodies against specific growth factor receptors only bind to the receptor

A

False, can bind the ligand as well

59
Q

What does Trastuzumab target?

A

Human epidermal groowth factor receptor, HER2

60
Q

Why are solid tumors harder to treat?

A

Secrete factors that trigger angiogenesis

61
Q

What is Bevacizumab and what does it target?

A

VEGF-A (angiogenesis marker)

62
Q

What does Pembrolizumab target?

A

PD-1 (program death receptor)

Normally PD-L1 binds PD-1 and prevents death of tumor cell

63
Q

How does Brentuximab vedotin work?

A

Antibody-drug conjugate:
Antibody loaded with cytotoxic payload
Payload is removed once endocytosed (most likely by tumor cell)

64
Q

How can retinoic acid be used as an anticancer drug and what is a potential side effect?

A

Promotes terminal differentiation of leukemic promyelocytes

Teratogenic

65
Q

What is PARP?

A

Poly ADP Ribose Polymerase, involved with detection of DNA damage. Normally binds ds breaks and catalyses repair

66
Q

What is Olaparib?

A

PARP inhibitor, alters DNA damage detection pathway
If BRCA1/2 is mutated (e.g. in breast cancer) No homologous repair can happen and the cell dies
If cell is healthy, homologous recombination occurs and cell lives

67
Q

What is immunomodulation? give an example

A

Anticancer vaccine. eg interferon alpha

68
Q

What does Interferon Alpha do?

A

decreases cell proliferation and inhances immune activities

69
Q

Name a cancer treatment vaccine

A

Sipuleucel-T (neat and expensive!)

70
Q

What are the 4 steps in chimeric antigen receptor T-cells?

A

1) T cell collection
2) T cell transfection
3) T cell adoptive transfer
4) patient monitoring
eg Axicabtagene ciloleucel

71
Q

What are oncomirs and what do they do?

A

Proliferate cancer growth

72
Q

Name 4 oncomir inhibitors

A

miRNA sponges
Anti-miR oligos (AMOs)
Small molecule inhibots
miRNA masks/target protectors

73
Q

Name 2 anti-oncomirs

A

miRNA mimic

gene therapy

74
Q

What do miRNAs and anticancer drugs both promote?

A

Apoptosis

75
Q

What are the methods of treatment for Breast cancer in the case of: ER Positive (2 methods) and ER Negative (4 methods)?

A 
ER+:
- Aromatase inhibitors (after menopause)
- Anti-estrogens: tamoxifen 
ER-:
- Doxorubicin
- Docetaxel 
- Cyclophosphamide
- Trastuzumab (HER-2+)
76
Q

What are 3 drug treatments for prostate cancer?

A 
Hormonal therapy for metastases:
-Testosterone reduction: LHRH agonist plus androgen antagonist
Combination chemotherapy
- Docetaxel
- Prednisone
Hormone Refractory Prostate Cancer:
- Sipuleucel-T
77
Q

Three treatments for Gliobastoma?

A

Tumor resection
Radiotherapy
Temozolomide

IL13Ralpha2-targeted CAR-T cells(?)

Phar 301 (23 decks)

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