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
When are anti-folates most effective?
S-phase; rapid proliferation.
26
What are vinca alkaloids?
Compounds from periwinkle plant that inhibit tubulin polymerization to disrupt the M phase.
27
What are taxanes?
Pacific yew tree derivatives that promote microtubule assembly to inhibit mitosis and cell division.
28
What are camptothecins?
Anti-cancer drugs derived from acuminata tree that bind the transient DNA-topoisomerase 1 complex, leading to accumulation of ssDNA breaks.
29
What are topoisomerases?
Nuclear enzymes that reduce torsional stress in supercoiled DNA through transient strand breaks and reseasling.
30
What phase are comptothecins specific to?
S phase.
31
What are anti-cancer antibiotics derived from?
Streptomyces.
32
What is the function of anti-cancer anti-biotics?
To bind DNA through intercalation and block DNA synthesis/replication.
33
What is the mechanism of anthracyclines?
1. Inhibit topoisomerases. 2. Generate free radicals. 3. High affinity bind to DNA. 4. Bind cellular membrane to alter fluidity and ionic ocmposition.
34
What is the most widely used anti-cancer drug?
Anthracyclines.
35
What are tyrosine-kinase inhibitors?
Inhibit tyrosine kinase domain of the BCR-Abl oncoprotein in leukemia.
36
How does EGRF differ in solid tumors?
Overly expressed, promotes metastasis and proliferation.
37
What is primary resistance?
Resistance developed spontaneously in the absence of prior exposure to anti-cancer drugs.
38
What is acquired resistance?
Resistance developed in response to a given anticancer agen.
39
What are the adverse effects of anti-cancer drugs?
Loss of rapid-synthesis tissue, carcinogenic.