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PMCOL 200 > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

What is metastasis?

A

Abnormal cell growth in which cells spread to other parts of the body.

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2
Q

What are the causes of cancer?

A
  1. Environmental and genetics (BRCA1)
  2. Tobacco, ionizing radiation, pollution.
  3. Viral infections.
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3
Q

What are the five phases of the cell cycle?

A
  1. G1
  2. S
  3. G2
  4. M
  5. G0
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4
Q

What is the G1 phase?

A

Checkpoint to ensure cell is ready for DNA syntheses.

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5
Q

What is the S phase?

A

DNA synthesis

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6
Q

What is the G2 phase?

A

Checkpoint to ensure cell is ready for mitosis.

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7
Q

What is the M phase?

A

Mitotic phase

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8
Q

What is the G0 phase?

A

Quiescent state

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9
Q

What are tumor suppressor genes?

A

Genes that encode for proteins that repress cell cycle or promote apoptosis.

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10
Q

How to TMGs repress cell cycles or promote apoptosis?

A
  1. Inhibit cell division.
  2. Initiate apoptosis following irreversible DNA damage.
  3. Repair damaged DNA (BRCA)
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11
Q

What is p53?

A

Tumor suppressor protein that is usually mutated in all tumors.

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12
Q

What are proto-oncogenes?

A

Normal genes involved in cell growth and proliferation or inhibition of apoptosis.

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13
Q

What are the two forms of mutations?

A
  1. Point mutations: small scale.

2. Chromosomal translocation: large scale.

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14
Q

What is Philadelphia chromosome?

A

Specific genetic abnormality on chromosome 22 found in leukemia cancer cells.

Creates gene BCR-ABL leading to unregulated tyrosine kinase activity.

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15
Q

What does unregulated tyrosine kinase activity lead to?

A

Unregulated cell cycle and cell division.

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16
Q

What two stages of the cell cycle do anti-cancer drugs typically act at?

A

S and M phase.

17
Q

What tissue is susceptible to damage from cytotoxic anti-cancer drugs (radiation)?

A

Tissues that proliferate rapidly (bone marrow, hair, intestinal epithelium).

18
Q

What are pyrimidine analogues?

A

Anti-cancer drug that competes with normal pyrimidine precursors for the enzyme thymidylate synthase, which alters the generation of dTMP.

19
Q

What is phophoribosyl pyrophosphate amidotransferase (PRPP amidotransferase)?

A

Enzyme that catalyzes purine nucleotide synthesis.

20
Q

What are alkylating agents?

A

Highly reactive compounds which covalently link to chemical groups commonly found in nucleic acid. Leads to cross-linking between DNA and breakage.

21
Q

What atom is particularly susceptible to formation of covalent bonds with alkylating agents?

A

N7 atom of guanine.

22
Q

What drug are cancer cells most susceptible to in late G1/S phases?

A

Alkylating agents

23
Q

What is folic acid?

A

Dietary factor converted to FH4 cofactors that synthesize precursors for RNA/DNA.

24
Q

What are folic acid analogues?

A

Interfere with FH4 metabolism thereby inhibiting DNA replication.

25
Q

When are anti-folates most effective?

A

S-phase; rapid proliferation.

26
Q

What are vinca alkaloids?

A

Compounds from periwinkle plant that inhibit tubulin polymerization to disrupt the M phase.

27
Q

What are taxanes?

A

Pacific yew tree derivatives that promote microtubule assembly to inhibit mitosis and cell division.

28
Q

What are camptothecins?

A

Anti-cancer drugs derived from acuminata tree that bind the transient DNA-topoisomerase 1 complex, leading to accumulation of ssDNA breaks.

29
Q

What are topoisomerases?

A

Nuclear enzymes that reduce torsional stress in supercoiled DNA through transient strand breaks and reseasling.

30
Q

What phase are comptothecins specific to?

A

S phase.

31
Q

What are anti-cancer antibiotics derived from?

A

Streptomyces.

32
Q

What is the function of anti-cancer anti-biotics?

A

To bind DNA through intercalation and block DNA synthesis/replication.

33
Q

What is the mechanism of anthracyclines?

A
  1. Inhibit topoisomerases.
  2. Generate free radicals.
  3. High affinity bind to DNA.
  4. Bind cellular membrane to alter fluidity and ionic ocmposition.
34
Q

What is the most widely used anti-cancer drug?

A

Anthracyclines.

35
Q

What are tyrosine-kinase inhibitors?

A

Inhibit tyrosine kinase domain of the BCR-Abl oncoprotein in leukemia.

36
Q

How does EGRF differ in solid tumors?

A

Overly expressed, promotes metastasis and proliferation.

37
Q

What is primary resistance?

A

Resistance developed spontaneously in the absence of prior exposure to anti-cancer drugs.

38
Q

What is acquired resistance?

A

Resistance developed in response to a given anticancer agen.

39
Q

What are the adverse effects of anti-cancer drugs?

A

Loss of rapid-synthesis tissue, carcinogenic.

PMCOL 200 (19 decks)

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