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Veterinary Pharmacology > Anti-Neoplastic Drugs, Pt. 2 > Flashcards

Anti-Neoplastic Drugs, Pt. 2 Flashcards

1
Q

What 4 dog breeds are at the highest risk of developing cancer? What kind of cancer is each most susceptible to?

A
  1. Boxers - lymphoma, lymphosarcoma, brain tumors, mast cell tumors
  2. Golden Retrievers - hemangiosarcoma, lymphoma
  3. Bernese Mountain Dogs - lymphoma, lymphosarcoma
  4. Rottweilers - lymphoma, bone cancer, soft tissue sarcoma, blader carcinoma, angiosarcoma
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2
Q

What 5 environmental factors contribute to the development of cancer?

A
  1. UV rays (sun)
  2. chemical carcinogens (herbicides, insecticides, pesticides)
  3. asbestose, cadmium, vinyl chloride, benzene, uranium, nickel
  4. second-hand tobacco smoke
  5. air pollution
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3
Q

Why does advanced age predispose to cancer?

A
  • weakening of the immune system
  • longer exposure to environmental carcinogens
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4
Q

What 2 types of viruses have been linked to cancer development?

A
  1. FeLV - lymphoma
  2. papilloma virus - oral papilloma in dogs
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5
Q

What type of cancer is sexually transmitted in dogs? What can be caused by vaccination?

A

canine transmissible venereal tumor

injection site sarcomas

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6
Q

What is squamous cell carcinoma associated with?

A

UV light in white (unpigmented skin) cats, dogs, and horses

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7
Q

What are the 3 causes of cancer on the genetic level?

A
  1. SPORADIC (90%) - accumulation of mutations in somatic cells over a lifetime with development at older age and in certain cells
  2. HEREDITARY (5-10%) - inherited susceptibility through germline mutation giving the tumor a “head start” allowing it to develop at a younger age
  3. RANDOM ERRORS (66%) - environmental factors multiply errors
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8
Q

What is the point to understanding the type of mutation a patient has that is causing their cancer?

A

affects treatment —> find the mutation that is driving tumor and inhibit the pathway to slow down or stop tumor growth

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9
Q

What 2 groups of genes have been linked to serious mutations that cause hereditary cancer risk?

A
  1. BRCA1 and BRCA2 - DNA repair molecules responsible for genetic stability (typically only passed on from one parent, since an embryo with 2 mutated copies would likely die)
  2. p10 and p53 - tumor suppressor genes
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10
Q

What cat breed is most susceptible to developing cancer? What 3 types?

A

Siamese

  1. lymphoma
  2. lymphosarcoma
  3. thymoma
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11
Q

What is the molecular basis of cancer?

A

cancer is a cell growth disease where cells undergo division many more times than normal, making the cells prone to replication errors accumulating mutations that are not repaired

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12
Q

How do normal cells usually maintain homeostasis?

A
  • growth factors induce cell proliferation
  • death signals induce controlled cell death (apoptosis)

homeostasis balances cell proliferation and cell death

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13
Q

How do normal cells become cancerous?

A

unbalanced proliferation and apoptosis leads to survival of cells with mutations that are able to accumulate

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14
Q

How does the disruption of normal tissue homeostasis cause cancer?

A
  • overexpressed oncogenes induce proliferation of cancer cells and tumor formation
  • inhibition, mutation, or mutation of tumor suppressor genes (p53, p10) block apoptosis of cancer cells
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15
Q

What are the 5 stages of the cell cycle?

A
  1. G0 = resting
  2. G1 = growth
  3. S = DNA synthesis
  4. G2 = growth and preparation for mitosis
  5. M = mitosis (cell division)
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16
Q

What are checkpoints? Which 4 exist in the cell cycle?

A

control mechanisms in cells that ensure proper division

  1. DNA damage checkpoint at the end of G1
  2. DNA damage checkpoint in the middle of S
  3. DNA replication and damage checkpoint at the end of G2
  4. spindle assembly formation at the beginning of M
17
Q

What happens during checkpoint failure?

A

genetic instability, which is a major factor in the development of cancer

18
Q

What forms the DNA damage and replication checkpoints? What are 2 examples?

A

network of proteins

  1. cyclins
  2. cyclin-dependent kinases (Cdks)
19
Q

Carcinogenesis and DNA damage:

A

cancer is most common in proliferative tissues where the increased turn-over leads to more chances of mutations

20
Q

What is the Cental Dogma of Molecular Biology?

A

DNA is transcripted into mRNA, which is translated into protein

(at each level something can go wrong and allows for cancer drug targeting)

21
Q

What are the 2 types of nitrogenous bases?

A
  1. PURINES = double-ring structure
    - adenine
    - guanine
  2. PYRIMIDINES = single-ring structure
    - thymine
    - uracil
    - cytosine
22
Q

What must happen before a cell can divide? What will each new DNA molecule consist of?

A

DNA in the nucleus must be duplicated

one old strand and a new complementary strand

23
Q

How do helicases and DNA polymerases function in DNA replication?

A

HELICASE = unzips double-stranded DNA

DNA POLYMERASE = adds complementary nucleotides to the unwound DNA

24
Q

What do topoisomerases do? What 2 partake in DNA replication?

A

overwinding or underwinding of DNA (act on 3D topology of DNA

  1. TOPOISOMERASE I: cut and religate single DNA strand of double helix
  2. TOPOISOMERASE II: cut both strands of DNA double helix
25
Q

What is DNA damage? What are the 6 types?

A

alteration of DNA, which is the aim in cancer treatment (DNA damage-inducing drugs block DNA repair in cancer cells)

  1. single-strand break
  2. mis-match
  3. damaged base
  4. double-strand break
  5. intra-strand crosslink
  6. inter-strand crosslink
26
Q

What do BRCA1 and BRCA2 do?

A

promote efficient and precise repair of mis-match and double-stranded breaks

(germline mutation = accumulation of DNA damageand neoplastic transformation)

27
Q

What are the 6 types of anti-cancer therapy?

A
  1. chemotherapy - cytotoxic, DNA damage
  2. targeted therapy - monoclonal antibody against over-expressed oncogenes, small molecules
  3. endocrine therapy - estrogen receptors, androgen receptors, hormones
  4. immune therapy - immune system activation
  5. epigenetic therapy - DNA methylation, histone acetylation
  6. chemoprevention - dietary products and supplementation
28
Q

What are the 3 major challenges to anti-cancer therapy?

A
  1. need to develop new targeted and tailored therapies
  2. chemoprevention
  3. combination therapies need to have synergistic efficacy and minimum toxicity
29
Q

Why do chemotherapeutic drugs typically cause adverse effects?

A

cannot distinguish between cancer cells and normal cells

30
Q

How are cancers categorized? What is necessary to do this? What causes the low overall therapy success in the past 3 decades?

A

tissues of origin and stages in clinical progression - histopathology

distinct subcategories within one cancer with different molecular signatures —> can’t treat all breast cancers the same

31
Q

What 2 types of cancer are most commonly treated with endocrine therapy?

A
  1. breast cancer
  2. prostate cancer

targets estrogen and androgen receptors

32
Q

What are the best steps for chemoprevention?

A

dietary products and supplementation

  • better to prevent cancer than treat it

Veterinary Pharmacology (35 decks)

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