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WK 9- CANCER CHEMOTHERAPY Flashcards

1
Q

What are the 4 classes of drugs that act on the structure of DNA

A
  1. Topoisomerase inhibitors
  2. Intercalating Agents
  3. Alkylating Agents
  4. Antimetabolites
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2
Q

What is the action of antimetabolites

A

Interfere with the incorporation of nucleic acid bases (C, T, A, G) into the DNA during DNA synthesis: basically like inducing mutations

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3
Q

What are the 2 outcomes of antimetabolites

A
  1. Chemical modification of a nucleic acid to prevent accurate replication
  2. Inhibit reduction of folic acid
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4
Q

What 2 drugs cause chemical modification of a nucleic acid to prevent accurate replication

A

5-fluorouracil (synthetically modified form of uracil- also inhibits thymidine synthetase), gemcitabine (also inhibits ribonucleotide reductase)

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5
Q

What is the action of methotrexate (antimetabolite)

A

inhibit folic acid reduction- folate is essential for the transfer of methyl groups in DNA synthesis) from its inactive dihydrofolate → active tetrahydrofolate (therefore no active tetrahydrofolate is produced)

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6
Q

What is the action of alkylating agents

A

Form methyl cross-bridges between base pairs (A==T; C==G) to prevent the two DNA strands coming apart during mitosis and stop formation of daughter DNA fragments-> basically tie the two DNA strands together and stop cell division

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7
Q

What class does cyclophosphamide belong to

A

Alkylating agents

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8
Q

Why does renal/bladder function need to be monitored in pt taking cyclophosphamide

A

break down of cyclophosphaminde→ forms inactive metabolites and toxic metabolites→ these increase in conc in bladder/kidney and cause side effects

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9
Q

What are intercalating agents

A

Similar to alkylating agents-> Intercalating agents wedge between bases along the DNA (A--T and C--G). The intercalated drug molecules affect the structure of the DNA, preventing polymerase and other DNA binding proteins from functioning properly-> Stops two strands coming apart and stops replication

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10
Q

What specific intercalating agent binds to Guanine to cross link within/across strands

A

Platinum compounds-> cisplatin

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11
Q

True or false, intercalating agents are cytotoxic antibiotics

A

True- anthracyclin is a cytotoxic antibiotic

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12
Q

What is the function of bleomycin-> what class does it belong to

A

Intercalating agents- Partially intercalates to produce direct DNA demage through forming a complex with iron => reactive toxic product

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13
Q

What is the function of topoisomerase

A

Topoisomerase is an enzyme → control tertiary coiling of DNA → topoisomerase enzyme binds to double stranded DNA and cut the phosphate backbone of the DNA strands→ allows the DNA to be untangled or unwound and then the DNA is resealed→ inhibiting this means that mutation continues

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14
Q

What is the function of topoisomerase inhibitors

A

Topoisomerase inhibitors prevent topoisomerase enzymes from being able to fix mutated DNA strands-> allowing damaged cells to continue to proliferate

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15
Q

What are the 2 groups of topoisomerase inhibitors

A

-Topoisomerase I
→ Camptothecin group: Topotecan and irinotecan
-Topoisomerase II
→Podophyllotoxins: Etoposide and teniposide

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16
Q

What 2 classes of drugs act on mitosis

A

Spindle poisons: Vinca alkaloids: vincristine and vinblastine
Taxane group: paclitaxel and docataxel

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17
Q

What are the actions of taxane groups

A

Cause tubulin polymerisation to result in abnormal spindles and cell death

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18
Q

How do signal transduction inhibitors work

A

Inhibition of the tyrosine kinase pathway results in decreased cell growth/proliferation

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19
Q

What drugs are examples of signal transduction inhibitors

A

Imatinib, gefitinibe, sorafenib and sunitinib→ when it ends with ‘ib’ – it is an enzyme inhibitor

20
Q

What is the action of proteosome inhibitors

A

Proteosomes are large protein complexes to regulate and metabolise/remove proteins into small peptide fragments
-If inhibited, the ordered degradation of proteins controlling cell cycle is disrupted → causing apoptosis

21
Q

What is an example of a proteosome inhibitor

A

Bortezomib used in recurrent multiple myeloma

22
Q

How does targeting spindle formation work to treat cancer

A

Mitosis requires spindle formation in the sorting and moving chromosomes following replication at the end of mitosis-> without spindles there cannot be proper cell division

23
Q

What 4 classes of drugs work to target angiogenesis

A
  1. Monoclonal antibody to target VEGF receptors
  2. VEGF receptor tyrosine kinase inhibitor (inhibits receptor
  3. Vascular disrupting agents
  4. Thalidomide and lenalidomide
24
Q

What are 4 types of cancer that are highly sensitive to chemotherapy

A

Leukemia, lymphoma, myeloma, germ cell tumours

25
What are 4 types of cancers that have medium sensitivity to chemotherapy
Breast, colorectal, bladder, ovary
26
What 5 cancers have low sensitivity to chemotherapy
Prostate, kidney, brain, sarcomas, melanomas
27
What are the 6 common limiting toxicities from chemotherapy
Bone marrow suppression, bowel toxicity, renal damage, neurological damage, cardiac, and bladder toxicities
28
What are the 4 mechanisms by which cancer cells can become resistant to drugs
1. Altered biochemical pathways: →Modified folate use to avoid dihydrofolate reductase block by methotrexate 2. Altered cell transport mechanisms; → To prevent drug concentration in cancer cells by reduced uptake or enhanced flux 3. Altered drug metabolism: → Increasing clearance, Reducing drug activation 4. Impaired apoptotic mechanisms
29
How do cancer cells develop resistance to drugs
due to cancer cells being heavily dividing→ there are mutations that constantly occur→ some can benefit the survival of the cells (eg. Getting rid of cytoxic drug from the cell-> allowing cell to survive and continue to replicate)
30
What gene encodes for the transporter that allows for multi-drug resistance
MDR1 gene encodes for a glycoprotein important in cell transport-> aids in extruding foreign molecules from the cell and ridding cytotoxic drugs from within the cells
31
What 2 drugs can be used to overcome multi-drug resistance
Verapamil and cyclosporine→To inhibit efflux of cytotoxic drugs (keep them in cell to concentrate their action)
32
Which types of cancers are; 1. oestrogen sensitive 2. androgen sensitive 3. oestrogen and progesterone sensitive
1. Breast cancer 2. Prostate cancer 3. Endometrial cancer
33
How is hormone therapy used within cancer treatments
If a tumour is hormone sensitive, then it utilises the hormone to grow-> hormone therapy will either work through blocking the hormone receptors on the tumour or through administering hormones to cause down-regulation of receptors and disruption of the hormonal axis
34
What are the 3 treatment methods by which hormonal therapy treats breast cancer and what drug is used for each method
1. Direct binding to estrogen receptor (ER) and blockage of ER activity→ tamoxifene 2. Indirectly by blocking production and peripheral activation of oestrone and oestriol to oestradiol by inhibiting aromatase (oestradiol is most common form of oestrogen)→ anastrozole and letrozole 3. Down-regulation of ER→ decreased sensitivity to oestrogens (2nd or 3rd line treatment)→Medroxyprogesterone (progesterone)
35
What are the side effects of the hormonal therapies used in breast cancer
Artificially create menopause-like situation by blocking or decreasing oestrogen - Anti-oestrogens: hot flushes, fluid retention, vaginal dryness, uterine bleeding, DVT - Aromatase inhibitors: hot flushes, nausea rashes, joint stiffness, vaginal dryness, high cholesterol, osteoporosis - Progesterone: Nausea, fluid retention, weight gain
36
What are the 2 methods by which prostate cancer is treated
1. Direct androgen receptor antagonists | 2. Indirectly through disrupting the HPG (hypothalmic-pituitary-gonadal axis)
37
How is the HPG axis targeted
target LHRH (central regulator) at level of pituitary by using an agonist→ high doses of peptide agonist causes down regulation of receptors (less responsive)
38
What are biological therapies - what are the two types
Chemicals/modified chemicals that are produced by the body in response to injury/infection and include MAB and Alpha-interferon
39
How does alpha interferon aid in killing cancer cells - what 2 cancers is it most commonly used for
Aid in enhancing the body’s natural defence to remove malignant cells -Hairy cell leukemia, renal cancer, melanoma
40
What are monoclonal antibodies
Antibodies that act to carry toxic agents to a cell defined by specific surface antigens against which the antibody is targeted→ are specific for antigens on cancer cells
41
What is the action by which MAB act to kill cancer cells
-Bind to antigen target and induce immune response to eliminate the cells OR they can be used to bind toxic agents and deliver it directly to cancerous cells
42
What is the method by which trastuzumab works and what does it treat
(Herceptin) | -Will bind antigens found on breast cancer cells and ilicit and immune response that will cause killing of the cells
43
What are the 5 types of monoclonal antibody drugs-how do they work
1. Rituximab: CD20 antigen on B-cell lymphomas 2. Ibritumomab: Anti-CD20 antibody tagged with a radioisotope yttrium-90 for follicular lymphoma→ radioisotope is carried directly to cell 3. Trastuzumab: Herceptin: 4. Alentuzumab: Anti-CD52 antibody in chronic lymphocytic leukaemia 5. Bevacizumab: VEGF antibody (tumour vasculature) in colorectal cancer
44
How do tyrosine kinase inhibitors work | -what suffix do the drugs have
Blocking receptors for tyrosine kinase pathways that are abnormally activated in cancers -'ib'
45
what is an MTOR inhibitor
When mTOR is mutated (ie. hyperactivation of mTOR1) it will cause molecules downstream of mTOR to be activated and cause proliferation and growth -inhibiting mTOR enhances antineoplastic therapies through decreasing angiogenesis and tumour cell proliferation and growth
46
What are the 3 mechanisms of antineoplastic antibodies
1. Bind to cyclin dependent antigens on malignant lymphocytes and cause cell lysis 2. Bind to HER2/EGF/VEGFR and inhibit proliferative response--> ie. Trastuzumab (for HER2), Cetuximab (EGFR) and Bevacizumab (VEGFR) 3. Checkpoint (immune) inhibitors
47
How do checkpoint/immune inhibitors work
Bind to CTLA4 (cytotoxic lymphocyte associated antigen 4) and block the interaction between CTLA4 and B7-> when CTLA4 binds to B7 it stops co-stimulation and renders T Cells innactive-> by blocking this connection, T cells are able to be activated and increase the immune response that causes cell death

TIN (14 decks)

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