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Pharmacology > Anti Cancer Drugs > Flashcards

Anti Cancer Drugs Flashcards

1
Q

Oncogenes

A

-Normally: tightly regulated growth and differentiation of cells (ex. Bcl-2)

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2
Q

Tumour Suppressor Genes

A

Normally: suppress overgrowth of cells

ex. p53

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3
Q

Explain the 3 stages of cancer pathophysiology with a diagram.

A

-antineoplastics lecture

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4
Q

Describe the stages of cancer

A

Stage 0-early cancer, not detectable
Stage I-III-higher number reflects increase size and spread
Stage IV-invasion of other tissues and metastasis

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5
Q

Explain traditional and newer anti cancer drugs

A

traditional-target the cell cycle and kill rapidly dividing cells
newer-target specific proteins/processes unregulated in tumors

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6
Q

What are 3 principles of chemotherapy

A
  1. chosen agent must be tolerable, administer MTD
  2. use combinations to increase likelihood of killing tumour cells
  3. Dose and regimen must be chosen to max effectiveness –>cyclic therapy
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7
Q

What are the 4 classes of traditional antineoplastic agents?

A
  • alkylating and platinum agents
  • topoisomerase inhibitors and antibiotics
  • antimetabolites
  • vinca alkaloids and taxanes
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8
Q

Cyclophosphamide

A
  • alkylating agent
  • prodrug-activated by cyto P450 in the liver
  • cross links 2 guanines, disrupts DNA structure and causes strand breaks
  • can also bind to similar functional groups (SH, OH, NH-lipids, proteins, etc)
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9
Q

Cisplatin

A
  • platinum containing agents

- cause inter and intra DNA strand cross linking in cells (similar to alkylating agents

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10
Q

Topotecan

A
  • binds to topoI- makes ss breaks, untangles and ligates back together)
  • prevents religation of strand breaks
  • prevents movement of rep complex
  • halting these processes signals cell death
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11
Q

Doxorubicin

A
  • topoII inhibitor, prevents religation of ds breaks–>cell death pathways
  • natural product isolated from strep
  • intercalates b/w strands
  • form free radicals causing additional cytotoxicity
  • cardiotoxicity
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12
Q

Mercaptopurine

A
  • purine antagonists
  • structurally similar to adenine
  • interacts with enzymes involved in purine nucleotide synthesis
  • incorporated into DNA like adenine, unable to make correct base pair
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13
Q

Fluorouracil (5-FU)

A
  • pyrimidine antagonist
  • similar structure to uracil and thymine
  • binds to thymidylate synthase preventing further synthesis of thymidine nucleotides
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14
Q

Methotrexate

A
  • inhibits dihydrofolate reductase

- prevents purine nucleotide synthesis

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15
Q

Antimetabolites

A
  • similar in structure to endogenous compounds (folic acid, nucleotide bases)
  • prevent DNA synthesis
  • cells deficient in building blocks undergo cell death
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16
Q

Vinca alkaloids-vincristine

A
  • from rosy periwrinkle
  • prevent microtubule formation of mitotic spindles
  • inhibit cell division
  • neurotoxicity and neuropathy is a common adverse effect
17
Q

Docetaxel

A
  • taxanes
  • made semi synthetically from natural products derived from a different yew species
  • stabilizes microtubules so they can’t disassemble
18
Q

What are the adverse effects of traditional antineoplastic drugs?

A
  • do not differentiate b/w cancerous and non cancerous cells
  • cells with a high turnover rate are more susceptible to damage
19
Q

4 considerations when choosing a combo therapy

A
  1. efficacy-each drug must be effective alone
  2. toxicity-choose drugs with different side effects to avoid additive adverse effects
    - sometimes lower doses can be given when using combos
  3. scheduling-use shortest recovery interval possible to increase killing efficacy
  4. choose drugs with different MOA- to increase tumour killing efficacy, decrease resistance
20
Q

CAV combination regimen

A
  • used in lung cancer
  • cyclophasphamide
  • adriamycin (doxorubicin)
  • vincristine
21
Q

What is the problem with traditional antineoplastics?

A

-the cell targets are common to ALL cells in the body

22
Q

Rituximab

A
  • mAb targeted to CD20
  • flags B cells for destruction by immune system
  • results in death of CD20 positive B cells
  • normal B cells are regenerated from stem cells
23
Q

Tositumomab

A
  • mAb conjugated radioactive isotopes

- targets radioactivity to tissues expressing antigen

24
Q

Sipuleucel-T

A
  • virus expressing tumour antigen
  • vaccines administered to initiate a host immune response against the tumour
  • remove cells from patients tumour or blood, manipulate and re-inject into patients
25
Q

Bevacizumab

A
  • mAb targeted against VEGF

- binds circulating VEGF

26
Q

Sorafenib

A
  • small molecule TK inhibitors
  • bind to intracellular domain of VEGFR
  • prevent initiation of signalling cascade by inhibiting phosphorylation
27
Q

What are 2 drug targets that interfere with growth and proliferation?

A
  • Epidermal growth factor (EGF)-stimulates cell growth and proliferation
  • HER2-TK R, upregulated in breast cancer
28
Q

Trastuzumab

A
  • specifically targets HER2
  • binds to the TK R and blocks ligand bind
  • flags for the immune system
29
Q

Gefitinib

A
  • small molecule TK inhibitor
  • bind to intracell domain of EGFR
  • prevent R activation
30
Q

Imatinib

A
  • small molecule TK inhibitor
  • inhibit the intracellular TK R, BCR-ABL
  • prevents the up regulation of Bcl-2
  • competitively binds to active site
31
Q

What are the 2 types of drug resistance?

A

Primary-drug is ineffective on first attempt
-most commonly related to impaired responses to cell death signals in tumour cells (p53 inactivation)
Acquired-drug worked at first then became ineffective
-related to adaptation and mutation of tumour cells

32
Q

How might cells alter expression of proteins in tumour cells to promote drug resistance?

A
  • increase DNA repair mechanisms (i.e. resistant to alkylating agents, radiation)
  • alterations in drug targets (i.e. upreg of enzyme targeted by methotrexate
  • removal of drug from target cells (up regulation of p glycoprotein pumps)
33
Q

Leuroprolide

A
  • synthetic analogue of GnRH
  • overtime decreases FSH, LH production=decreased estrogen
  • also decreases testosterone
34
Q

Letrozole

A

-inhibits the aromatase enzyme necessary for the conversion of androgens to estrogen

35
Q

Tamoxifen

A
  • estrogen antagonist

- competes for estrogen R binding in tumour cells

Pharmacology (9 decks)

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