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Pharmacology > Cancer and Carcinogens > Flashcards

Cancer and Carcinogens Flashcards

1
Q

What re the 3 stages of neoplastic development? How does it progress from each stage to the next?

A 
- Neoplastic cell
(growth/promotion)
- Differentiated neoplastic cell
(progression)
- Undifferentiated cancer
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2
Q

What are the 4 properties of chemical carcinogens?

A
  • Carcinogenesis is dose dependent
  • Long lag periods between exposure and appearance of tumors (> 20 years in humans)
  • Carcinogens are subject to activation and degradation
  • Active carcinogens are electrophiles
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3
Q

What is an active carcinogen called?

A

Pro-carcinogens

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4
Q

What were the findings of the Mega Mouse experiment?

A
  • Mice were given a carcinogen at very low levels
  • Kidney cancer developed linearly
  • Bladder cancer had no response
  • Some cancers respond linearly to carcinogen exposure
  • Some do not develop at all at low levels
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5
Q

How many different well established human chemical carcinogens have been discovered?

A

More than 20

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6
Q

What are 9 examples of human chemical carcingens?

A
  • Aflatoxins
  • Benzopyrene
  • Benzene
  • Conjugated estrogens
  • Cyclophosphamide
  • Mechlorethylamine
  • Phenacetin
  • TCDD
  • Vinyl chloride
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7
Q

What carcinogen develops in moldy food stuffs?

A

Aflatoxins

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8
Q

What carcinogen is a nitrogen mustard/ nerve gas?

A

Mechlorethylamine

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9
Q

What human chemical carcinogen is the most potent?

A

Aflatoxins

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10
Q

What human chemical carcinogen is a product of combustion?

A

Benzopyrene

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11
Q

What human chemical carcinogen is an immunosuppressant?

A

Benzene

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12
Q

What 2 human chemical carcinogens are alkylating agents?

A
  • Cyclophosphamide

- Mechlorethylamine

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13
Q

What human carcinogen results from DES exposure?

A

Cyclophosphamide

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14
Q

What human chemical carcinogen is a coal tar derivative?

A

Phenacetin

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15
Q

What human carcinogen is used to make PVC plastic?

A

Vinyl chloride

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16
Q

What human carcinogen is dioxin?

A

TCDD

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17
Q

How do direct acting carcinogens work?

A

Mechlorethylamide or another electrophile attach to reactive sites on DNA, altering genes

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18
Q

What activates carcinogens into procarcinogens?

A

Cytochrome P450

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19
Q

What are 3 types of epigenic carcinogens?

A
  • Immunosuppresors (Benzene)
  • Hormones (DES)
  • Solid-state carcinogens (Asbestos)
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20
Q

What are oncogenes?

A

Genes taht encode for transforming proteins that can cause cancer

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21
Q

What do oncogenes develop from?

A

Proto-oncogenes (genes in normal cells that encode for proteins involved in cellular regulation)

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22
Q

What are proteins involved in cell regulation?

A
  • G proteins
  • Tyrosine-specific kinases
  • Other protein kinases
  • Growth factors
  • Transcription regulators
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23
Q

What are anti-oncogenes?

A

Tumor suppressor genes

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24
Q

What stages of cell point do cells normally go through “checkpoints?

A
  • G1
  • G2
  • Metaphase
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25
Q

What are the oncogenes involved in breast cancer?

A
  • BRCA1

- BRCA2

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26
Q

What are 5 childhood tumors with high cure rates? What do they have in common?

A
  • Acute lymphocytic leukemia
  • Burkitt’s lymphoma
  • Ewing’s sarcoma - bone tumor
  • Retinoblastoma
  • Wilms’ tumor - kidney tumor

All fast growing

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27
Q

What are 5 adult tumors with high cure rates?

A
  • Hodgkin’s disease
  • Non-Hodgkin’s lymphomas
  • Trophovlastic choriocarcinoma
  • Testicular germ cell cancer
  • Ovarian germ cell cancer
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28
Q

How does chemotherapy work?

A
  • Inhibits cell proliferation

- Cancer cells are rapidly proliferating, and are especially sensitive

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29
Q

What non-cancer cells are affected by chemo?

A
  • Bone marrow
  • Hair
  • GI
  • Oral mucosa
  • Other rapidly dividing cells
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30
Q

What drug is used to increase WBCs in combination with chemo?

A
  • Filgrastim (Neupogen)
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31
Q

Why do patients often experience nausea during chemotherapy?

A
  • Chemical trigger zone is one of only areas without blood brain barrier, and is sensitive to the drug
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32
Q

What drug can be used to prevent the nausea associated with chemo?

A

Ondansetron (Zofran)

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33
Q

What causes resistance to chemotherapy?

A

Cancer cells divide fast, and adapt to the drugs. The most common mechanism is P-glycoprotein that pumps the toxins of the chemotherapy out of the tumor

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34
Q

How can multiple agents be used in chemotherapy?

A

Use drugs that different different parts of the cell cycle

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35
Q

What is the ABVD regimine therapy for Lymphoma-Hodgkin’s?

A
  • Doxorubicin
  • Bleomycin
  • Vinblastine
  • Dacarbazine
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36
Q

What type of drugs generally work in the DNA synthesis portion of the cell cycle?

A

Anti-metabolites

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37
Q

What is growth fraction?

A

Proportion of cells actively profliterating

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38
Q

What are the grow characteristics of tumors?

A
  • Grows rapidly initially

- Slows because it can’t support its own growth due to hypoxia, poor nutrient supply, immunological defenses

39
Q

What is the log kill hypothesis?

A

Chemotherapy reduces the tumors to a level at which the body’s immunological responses can take over and completely eliminate the cancer

40
Q

What is the MOA of alkylating agents?

A
  • Transfer alkyl groups to DNA, inhibiting cell division
41
Q

What portion of the cell cycle do alkylating agents affect?

A

Non-specific

42
Q

What are 3 adverse effects of alkylating agents?

A
  • Bone marrow suppression
  • Nausea
  • Vomiting
43
Q

Why must alkylating agents be administered via IV?

A

They have vesicant properties, meaning outside of the blood vessel, it can cause tissue damage and necrosis

44
Q

What are 2 examples of alkylating agents?

A
  • Mechlorethamine (mustargen)

- Ifosfamide (lfex)

45
Q

Why can Ifosfamide be taken orally even though it is an alkylating agent?

A

It is activated by the body

46
Q

What is the MOA of platinum coordination compounds?

A

Similar to alkylating agents

- Use meta complexes

47
Q

What are 2 examples of platinum coordination compounds? What do they target?

A
  • Cisplatin (testies, lymph tissue, ovaries)

- Carboplatin (paraplatin) (ovarian cancers)

48
Q

What is an adverse effect of platinum coordination compounds?

A

Kidney toxicity

49
Q

What is the MOA of antimetabolites?

A

Inhibit metabolic steps required for DNA synthesis

50
Q

What phase of the cell cycle do antimetabolites act on?

A

S phase

51
Q

What are 5 adverse effects of antimetabolites?

A
  • Immunosuppresant
  • GI lesions
  • Alopecia
  • Bone marrow depression
  • Skin rash
52
Q

What other conditions may antimetabolites be used to treat?

A

Autoimmune diseases such as RA

53
Q

What antimetabolite targets folic acid?

A

Methotrexate

54
Q

What antimetabolite targets purine synthesis?

A

Mercaptopurine

55
Q

What antimetabolite targets pyrimidine synthesis?

A

Fluorouracil

56
Q

What plant are vinca alkaloids derived from?

A

Periwinkle plant

57
Q

What phase of the cell cycle do vinca alkaloids act on?

A

M phase

58
Q

What types of cancer are vinca alkaloids use din?

A
  • Breast cancer

- Choriocarcinoma

59
Q

What are 4 adverse effects of vinca alkaloids?

A
  • Bone marrow suppresion
  • Alopecia
  • GI lesions
  • Neurotoxicity
60
Q

What are 2 vinca alkaloids?

A
  • Vincristine

- Vinblastine

61
Q

What is the MOA of cytotoxic antibiotics and synthetics?

A
  • Bind to DNA to inhibit RNA synthesis
62
Q

What cell phase do cytotoxic antibiotics and synthetics act on?

A

G2 phase

63
Q

What are adverse effects of cytotoxic antibiotics and synthetics?

A
  • Visual toxicity

- Unique, drug-specific side effects

64
Q

What antibiotic/ synthetic drug is used to treat lung fibrosis?

A

Bleomycin

65
Q

What is an example of anti-estrogen drug? What is it used for?

A
  • Tamoxifen

- Treats breast cancer

66
Q

What are other TYPES of hormonal drug therapies?

A
  • Androgens for breast cancer
  • Anti-androgens for prostatic cancer
  • Progestins for advanced breast cancer or endometrial carcinomas
67
Q

What drugs block cancer cell signaling?

A
  • Tyrosine Kinase Inhibitors
  • Monoclonal Antibodies
  • Cox-2 inhibitors
  • Thalidomide
68
Q

What signals do Tyrosine Kinase Receptors transduce?

A
  • Growth
  • Division
  • Migration
  • Synthesis
  • Apotosis
69
Q

What type of protein are Tyrosine Kinases?

A

An enzyme

70
Q

What does Tyrosine Kinase act on? What do they do?

A

Phosphorylates tyrosine residues

71
Q

What cells do tyrosine kinase receptors become active in?

A

Cancer cells

72
Q

What are some major TKR families?

A
  • Epidermal growth factor receptor & family
  • Vascular endothelial growth factor receptor & family
  • Insulin receptor and family
  • etc…
73
Q

What types of cancer demonstrate high epidermal growth factor receptor expression?

A
  • NSCLC
  • Prostate
  • Gastric
  • Breast
  • Colorectal
  • Pancreatic
  • Ovarian
74
Q

What is high expression of EGFR associated with?

A
  • Invasion
  • Metastasis
  • Late-stage disease
  • Chemotherapy resistance
  • Hormone-therapy resistance
  • Poor outcome
75
Q

What is VEGFR increased in patients with growing tumors?

A

Large tumors require blood vessels to grow instead of relying on diffusion from nearby blood vessels.
- Tumors release VEGF to stimulate growth of new vessels into the tumor

76
Q

How large can a tumor grow without a blood supply?

A

1 - 2 mm^3

77
Q

What is angiogenesis?

A

Growth of new blood vessels

78
Q

Do tyrosine kinase inhibitors act inside or outside of the cell?

A

Inside

79
Q

What is a tyrosine kinase inhibitor that is specific to Bcr-Ab which is active in CMLl?

A

Gleevec

80
Q

What organ does tyrosine kinase inhibitors adversely affect?

A

Skin

81
Q

What is CML?

A

Chromosomal rearrangement that fuses two genes together.

- Produces oncogene, which encodes a form of tyrosine kinase (BCR-ABL)

82
Q

What type of TKR inhibitor can act outside of the cell?

A

Monoclonal antibodies

83
Q

What monoclonal antibody targets breast cancer?

A

Herceptin (Trastuzumab)

84
Q

What monoclonal antibody is the only one that targets blood vessels?

A

Avastin (Bevacizumab)

85
Q

What type of cancer is Avastin used to treat?

A
  • Colorectal carcinoma
86
Q

What are 3 adverse effects of Herceptin?

A
  • Cardiomyopathy
  • Anemia/ leukopenia
  • Rashes
87
Q

What are 4 adverse effects of Avastin?

A
  • Thrombosis
  • Hypertension
  • Proteinuria
  • Bleeding
88
Q

How does Cox-2 facilitate tumor development?

A

Cancer cells overexpress Cox-2, causing an expression of VEGF through production of PGE2

89
Q

How is Cox-2 treated?

A
  • Cox-2 inhibitors downregulate angiogenesis causing factors such as VEGF
90
Q

What does Thalidomide block angiogensis?

A
  • Blocks VEGF through a decrease in the cell’s ability to induce COX2 expression
91
Q

What type of cancer is Thalidomide best suited towards treated?

A

Multiple Myeloma (plasma cell disorder)

92
Q

What is the limitation of antiangiogenic therapy when compared with other chemotherapies?

A
  • Inhibits tumor growth instead of regressing established tumors
93
Q

What is the clinical value of antiangiogenic therapy?

A
  • Prolongs acute conditions to chronic

- Gives individuals extra time (extra month)

Pharmacology (9 decks)

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