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Week 4 - female GU/breast > Cancer chemotherapy > Flashcards

Cancer chemotherapy Flashcards

(43 cards)

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1
Q

What are the special characteristics of cancer cells?

A
  • Uncontrolled proliferation
  • Loss of original function (anaplasia)
  • Invasiveness
  • Metastasis (malignant cells)
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2
Q

When is surgical removal an option for cancer therapy?

A
  • Only for solid tumours
  • The location is suitable
  • If it has not metastasised
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3
Q

What are the two main categories of genetic change in the transformation of cancer cells?

A
  • Inactivation of tumour suppressor genes

* Activation of proto-oncogenes to oncogenes

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4
Q

What are the general toxic effects of chemotherapy?

A
  • Bone marrow suppression (blood cells) i.e. anaemia, immune depression, prone to infection, impaired wound healing
  • Loss of hair
  • Damage to GI epithelium
  • Liver, heart and kidney effects
  • In children, depression of growth
  • Sterility
  • Teratogenicity (damage to embryo)
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5
Q

What are the stages of the cell cycle?

A
  • G1 phase
  • S phase
  • G2 phase
  • Mitosis
  • G0
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6
Q

What happens in s phase?

A

DNA replication

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7
Q

What happens in the mitosis phase?

A

nuclear division and cytokinesis

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8
Q

What happens in the G1 phase?

A

There is a high rate of biosynthesis

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9
Q

What is the significance of the cell cycle with chemotherapy drugs?

A

Drugs that act on a cell cycle will only affect the cells in that stage of the cycle so the patient may need to be on the drugs for a long period of time

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10
Q

What happens if the restriction point after G1 phase is disabled?

A

The cell enters a cycle of uncontrolled proliferation

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11
Q

What is the name for the group of drugs that are active only on dividing cells?

A

Cell cycle specific drugs

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12
Q

What are cell cycle non specific drugs?

A

They are active on the resting (g phase) drugs

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13
Q

What cells do solid tumours consist of?

A
  • Dividing cells - progressing through cell cycle
  • Resting cells - not dividing but could do so
  • Cells which can no longer divide but contribute to the tumour size
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14
Q

Which cells in a solid tumour are most likely to cause relapse?

A

The resting cells as they are not sensitive to many drugs

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15
Q

Why must we aim for a total kill of all cancer cells?

A
  • The host immune system does not destroy the cells that will be left over as it hasn’t already
  • This would cause relapse
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16
Q

What are the main classes of chemotherapy drugs?

A
  • Alkylating agents
  • Antimetabolites
  • Cytotoxic antibodies
  • Microtubule inhibitors
  • Steroid hormones and antagonists
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17
Q

What is the mechanism of action of alkylating agents?

A
  • Form strong covalent bonds with the DNA
  • Interfering with both transcription and replication
  • Most alkylating agents have two reactive groups allowing the drug to cross link either within one strand of DNA or across the two strands of DNA
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18
Q

Where is lomustine active?

19
Q

What is special about Busulphan

Study These Flashcards
A

It has a selective effect on bone marrow

20
Q

What is mechlorethamine?

Study These Flashcards
A
  • Nitrogen mustard

* Was used as a blister agent

21
Q

What is mechlorethamine used to treat?

Study These Flashcards
A
  • Hodgkins lymphoma

* Non Hodgkins lymphoma

22
Q

What is the route of administration of mechlorethamine and why?

Study These Flashcards
A

IV, it kills the cells they encounter

23
Q

What is melphalan

Study These Flashcards
A

Nitrogen mustard

24
Q

What is melphalan used to treat?

Study These Flashcards
A
  • Multiple myeloma
  • Ovarian cancer
  • Breast cancer
25
What is cyclophosphamide?
Nitrogen mustard, it is a prodrug that requires activation by phophoramidase
26
Describe specific targeting with cyclophosphamide
*  Requires activation by phosphoramidase which has high activity in some tumours *  However it is activated in the liver *  But, it is less toxic and aldehyde dehydrogenase protects against the toxicity of the drug (and is in high concentrations in bone marrow cells, hepatocytes and intestinal epithelium
27
What is the mechanism of action of cisplatin?
*  It stops DNA replication | *  Targets N7 of purine nucleotides
28
Where does resistance for cisplatin rise from?
*  Nucleotide excision repair mechanisms | *  Efflux transporters for copper (heavy metals)
29
How do any metabolites work?
They interfere with nucleotide synthesis or DNA synthesis
30
Name 3 antifolates
*  Methotrexate *  Ralitrexed *  Pemetrexed
31
Name 3 nucleotide analogues
*  5-flurouracil *  Cytarabine *  Gemcitabine *  Fludarabine *  Capecitabine
32
Mechanism of action of fluoro-uracil
Prevents thymidine formation
33
Mechanism of action of mercaptopurines
Converted into false nucleotides, disrupts purine nucleotide synthesis and may be incorporated into DNA disrupting the helix
34
What is the mechanism of action of cytarabine?
*  Nucleotide analogue *  Sugar is arabinosine instead of ribose *  undergoes cellular activation to ara-CTP * Inhibits DNA polymerases (so s phase specific) * Incorporation into the DNA causes chain termination)
35
What is dactinomycin?
Cytotoxic antibiotic
36
What is the mechanism of action of dactinomycin?
*  Inserts itself into the minor groove in the DNA helix | *  Disrupts the RNA polymerase function
37
What is doxorubicin?
cytotoxic antibody
38
What is the mechanism of action of doxorubicin?
*  Inserts itself between base pairs | *  Causes local uncorking impairing DNA and RNA synthesis
39
What are vinca alkaloids?
Antibiotic - microtubule inhibitors
40
What is the mechanism of action of vinca alkaloids?
*  Bind to micro tubular protein *  Block tubules polymerisation *  Block normal spindle *  Disrupt the cell division
41
What is prednisone and what does it do?
It is a steroid hormone with is converted to the active form prednisolone in the body which suppresses lymphocyte growth
42
What is tamoxifen and what does it do?
It is an antagonist of the oestrogen receptor. As some breast cancers are oestrogen dependent, oestrogen stimulates their growth
43
Prostate cancer hormonal treatment
*  Most prostate cancers are testosterone dependent *  Testosterone receptor antagonists: flutamide or bicalutamide *  Pituitary downregulators LHRH agonists inhibit LH release which stimulates the testes to produce testosterone

Week 4 - female GU/breast (7 decks)

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