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Block 7 Week 1 > Duan: Cancer Chemotherapy II > Flashcards

Duan: Cancer Chemotherapy II Flashcards

1
Q

What is the mechanism of action of the vinca alkaloids (vincristine, vinblastine)

A

INHIBIT MICROTUBULES:
bind to tubulin –> inhibits mitotic spindle formation –> blocks cell division

**stops cell cycle in M phase (metaphase of mitosis)

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2
Q

What is the vinca alkaloid VinCristine used for clinically?

A 
children's tumors
wilm's tumor
ewing's sarcoma
ALL
neuroblastoma
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3
Q

What is the vinca alkaloid VinBlastine used for?

A

testicular cancer

lymphomas

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4
Q

contain precious metal platinum complexed with chlorine and amine groups. Chlorine atoms dissociate and the platinum-amine complex binds to DNA in a manner similar to the bifunctional alkylating agents

A

cisplatin

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5
Q

contain platinum complexed to a more complex organic moiety. Liberation of a platinum-amine complex which binds to DNA is also cytotoxicalthough this occurs more slowly than with Cisplatin.

A

carboplatin

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6
Q

What is cisplatin used for clinically?

A

broad spectrum; esp cancers of epithelial origin. Very effective against testicular/ovarian cancers and is usually combined with vinblastine/bleomycin

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7
Q

Main adverse effect of cisplatin?

A

nephrotoxicity/ototoxicity

**carboplatin less nephrotoxic, but causes bone marrow suppression

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8
Q

What is the MOA of procarbazine?

A

autooxidation of the drug yields toxic oxygen and hydroxyl free radicals that degrade DNA and cause chromosomal breakage

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9
Q

What is the clinical use of procarbazine?

A

MOPP regimen to treat Hodgkin’s disease

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10
Q

INHIBITS PROTEIN SYNTHESIS:

An enzyme that degrades asparagine and also glutamine, amino acids essential to some leukemic cells. It can be synthesized by normal cells. The sensitive leukemic cells lack asparagine synthetase. In the absence of exogenous asparagine and glutamine protein synthesis and subsequently DNA synthesis halts, and the cells die

A

L-asparaginase

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11
Q

What is L-asparaginase used for clinically?

A

ALL

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12
Q

Tumors that arise from hormone target tissues can respond and grow due to the effects of hormones. How can you inhibit these tumors and alter the hormone supply?

A
  1. ablate the hormone secreting organ
  2. use other hormones to suppress the production of the supporting hormone
  3. hormone antagonists
  4. high doses of supporting hormone can actually inhibit some tumor growth
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13
Q

High doses of this drug is toxic to lymphocytes and can be used in treating acute and chronic lymphocytic leukemia, lymphomas and multiple myelomas.

A

prednisone

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14
Q

When does hormonal therapy for breast cancer work best?

A

when tumor cells have high concentrations of estrogen receptors

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15
Q

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

A

tamoxifen

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16
Q

Adverse reactions to tamoxifen?

A

hot flashes

hypercalcemia

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17
Q

New drug therapy: tumor-specific tyrosine (bcr-abl) kinase inhibitor

A

imatinib

18
Q

When is imatinib used clinically?

A

used in Philadelphia Chromosome-positive CML

19
Q

What is the major side effect to look out for with imatinib?

A

drug interactions bc it inhibits several CytoP450s

20
Q

New drug therapy: orally active tyrosine kinase inhibitor selective for the epidermal growth factor (EGF) receptor tyrosine kinase

A

Iressa

21
Q

Any intervention to enhance the body’s natural ability to defend itself against malignant tumors.

A

immunotherapy

22
Q

What are some things used in immunotherapy?

A

monoclonal antibodies
vaccines
IFN
interleukins

23
Q

monoclonal antibody humanized against HER-2 antigen that is overexpressed on tumor cell surface in ~25% of breast cancer patients.
HER-2/neu/erbB2 overexpression marks an aggressive estrogen receptor-negative form of breast cancer!
IV infusion in combination with paclitaxel for metastatic breast cancer

A

herceptin

24
Q

achimericmonoclonal antibodyagainst the proteinCD20 on the surface of B lymphocytes and destroy B cells;
used to treat diseases characterized with lots of B cells, overactive B cells, dysfunctional B cells

A

rituximab

25
Q

What class of anticancer drugs do these belong to?

Nitrogen mustards (Mechlorethamine, cyclophosphamide)
Nitrosoureas (Carmustine, Streptozotocin)			
Alkyl Sulfonate (Busulfan)
A

alkylating agents

26
Q

What class of anticancer drugs do these belong to?

Folate antagonist (Methotrexate), 
Purine antagonist (6-Mercaptopurine)
Pyrimidine antagonist (5-Fluorouracil)
A

antimetabolites

27
Q

What class of anticancer drugs do these belong to?

Doxorubicin (Adriamycin)
Bleomycin (Blenoxane)
Mitomycin

A

anitbiotics

28
Q

What class of anticancer drugs do these belong to?

Leuprolide
Tamoxifen
Glucocorticoids

A

hormones

29
Q

What class of anticancer drugs do these belong to?

Vinca Alkaloids
Etoposide

A

Nature products

30
Q

What are 3 cancer therapeutic modalities?

A

surgery
chemotherapy
radiotherapy

31
Q

What does “cure” refer to in chemotherapy?

A

the disappearance of any evidence of tumor for several years; a high probability of normal life span

32
Q

Does cancer therapy kill a constant number of cells or a constant percentage?

A

constant percentage; first order kinetics

33
Q

What is the most effective way to reduce the number of cancer cells?

A

early surgical removal of the primary tumor;

intense and frequent treatment in which the kill rate > growth rate

34
Q

Why does chemo have limited effectiveness?

A

after rounds of chemo and remission, tumor cells may become resistant to treatment

35
Q

T/F: The faster rate of cell division makes tumor cell more prone to cytotoxic effect of anticancer drugs

A

True

36
Q

Why is it a problem that anticancer drugs kill rapidly dividing cells?

A

normal cells that turn over quickly, like hair follicles and bone marrow are susceptible to these drugs

37
Q

What are the two types of resistance to multidrug regimens?

A
  1. primary *in tumor cells that don’t even respond to initial therapy
  2. acquired resistance *appears of develops during drug therapy
38
Q

Is it more effective to treat cancer with a single drug or a combination of drugs?

A

combination

39
Q

Why are combinations of anticancer drugs preferred?

A

drugs w different cytotoxic mechanisms can have synergistic therapeutic effects; combinations reduce the probability that resistant clones will emerge

40
Q

What permits recovery from acute toxicities in multidrug regimens?

A

intermittent scheduling

41
Q

What are the 4 drugs used to treat Hodgkin’s lymphoma?

A

Adriamycin
Bleomycin
Vinblastine
Dacarbazine

alternate with

Mechlorethamine
Oncovin (vincristine)
Procarbazine
Prednisone

Block 7 Week 1 (9 decks)

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