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Year 2 MCD Cancer > 3: Biology of Cancer Treatment > Flashcards

3: Biology of Cancer Treatment Flashcards

1
Q

What are the four main modalities for cancer treatment?

A
  1. Surgery
  2. Chemotherapy
  3. Radiotherapy
  4. Immunotherapy
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2
Q

Which type of genetic mutations might cause cancer?

A
  • Chromosome translocation
  • Gene amplification (copy number variation)
  • Point mutations within promoter or enhancer regions of genes
  • Deletions or insertions
  • Epigenetic alterations to gene expression
    • Mutations Can be inherited
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3
Q

What are the overall characteristics of systemically administerd chemotherapeutic agents?

A
  1. IV or PO administration
  2. Non “targeted” – affects all rapidly dividing cells in the body –> causes many of the side-effects
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4
Q

How do you call a chemotherapeutic agent administerd post-surgery?

A

adjuvant

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5
Q

How do you call a chemotherapeutic agent administered pre-operatively?

A

Neoajuvant

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6
Q

What is the MOA of Akylating Agents?

A

Interfere with DNA synthesis

  • Add alkyl groups to guanine residues in DNA
    • Cross-link (intra, inter, DNA-protein) DNA strands and prevents DNA from uncoiling at replication
  • Trigger apoptosis (via checkpoint pathway)
  • Encourage miss-pairing - oncogenic
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7
Q

What is the MOA of pseudo-alkylating agents?

A

Add platinum to guanine in DNA, otherwise causes the same effect as Alkylating agents

  • Cross-link (intra, inter, DNA-protein) DNA strands and prevents DNA from uncoiling at replication
  • Trigger apoptosis (via checkpoint pathway)
  • Encourage miss-pairing - oncogenic
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8
Q

Which drug class do

Chlorambucil, cyclophosphamide, dacarbazine, temozolomide

belong to?

A

Alkylating agents

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9
Q

Which drug class to

carboplatin, cisplatin, oxaliplatin

belong to?

A

Pseudo-alkylating agents (add platinum group)

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10
Q

What are the side-effect of alkylating and pseudoalkylating agents?

A
  • hair loss (not carboplatin),
  • nephrotoxicity,
  • neurotoxicity,
  • ototoxicity (platinums)
  • nausea, vomiting
  • diarrhoea
  • immunosuppression
  • tiredness
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11
Q

Explain the MOA of Anti-metabolites

A

Interfere with DNA synthesis by

  • Masquerade as purine or pyrimidine residues leading to
    • inhibition of DNA synthesis,
    • DNA double strand breaks
    • apoptosis
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12
Q

Which drug class do

methotrexate, 6-mercaptopurine, decarbazine and fludarabine, 5-fluorouracil, capecitabine, gemcitabine

belong to?

A

Anti-metabolites

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13
Q

What are the side-effects of anti-metabolites?

A
  • Hair loss (alopecia) – not 5FU or capecitabine
  • Bone marrow suppression causing anaemia, neutropenia and thrombocytopenia
  • Increased risk of neutropenic sepsis (and death) or bleeding
  • Nausea and vomiting
  • Mucositis and diarrhoea
  • Palmar-plantar erythrodysesthesia (PPE)
  • Fatigue
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14
Q

Explain the MOA of Anthracyclines

A
  • Inhibit transcription and replication by intercalating (i.e. inserting between) nucleotides within the DNA/RNA strand
    • thereby: inhibit Tropoisomerase II
  • Also block DNA repair - mutagenic
  • Create free oxygen radiacals that damage DNA and cell membrane

*

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15
Q

Which drug class do

doxorubicin, epirubicin

belong to?

A

Anthracyclines

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16
Q

What are the side effects of Anthracyclines?

A
  • Cardiac toxicity (arrythmias, heart failure) – probably due to damage induced by free radicals
  • Alopecia= spot hair loss
  • Neutropenia
  • Nausea and Vomiting
  • Fatigue
  • Skin changes
  • Red urine (doxorubicin “the red devil”)
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17
Q

Explain the MOA of Vinca Alkaloids and taxanes

A

Microtubule inhibiting drugs–> leading to mitotic arrest in mitosis by

  1. inhibiting assembly (vinca alkaloids)
  2. disassembly (taxanes) of mitotic microtubules
18
Q

Which drug type are the micrutubule targeting drugs?

A

Vinka alkaloids and taxanes

19
Q

What are the side-effects of vinka alkaloids and taxanes?

A
  • Nerve damage: peripheral neuropathy, autonomic neuropathy
  • Hair loss
  • Nausea
  • Vomiting
  • Bone marrow suppression (neutropenia, anaemia etc)
  • Arthralgia (joint pain)
  • Allergy
20
Q

Explain the MOA o fTopoisomerase inhibitors

A

Topoisomerase is responsible for adding/removing supercoils during DNA replication + protect the free ends of DNA from aberrant( abweichenden, verwirrenden) recombination events

–> alter binding of the complex to DNA and allow permanent DNA breaks

21
Q

Which class of drug do

Topotecan, irinotecan, etoposide

belong to?

A

Topoisormerase inhibitors

Topotecan and irinotecan (topo I)

and etoposide (topoII)

22
Q

What are the side effects of Topoisomerase inhibitors?

A
  • (irinotecan): Acute cholinergic type syndrome – diarrhoea, abdominal cramps and diaphoresis (sweating). Therefore given with atropine
  • Hair loss
  • Nausea, vomiting
  • Fatigue
  • Bone marrow suppression

•

•

23
Q

Through which mechanims might cancer cells develop resistance against the treatment?

A
  • Upregulation of DNA repair mechanisms and DNA damage is repaired
  • DNA adducts replaced by Base Excision repair (using PARP) –> specific repair mechanism
  • Drug effluxed from the cell by ATP-binding cassette (ABC) transporters
24
Q

What are the main characteristics of cancer cells?

(Hallmarks of cancer)

A
  1. Self –sufficient
  2. Insensitive to anti-growth signals
  3. Anti-apoptotic
  4. Pro-invasive and metastatic
  5. Pro-angiogenic
  6. Non-senescent
  7. Dysregulated metabolism
  8. Evades the immune system
  9. Unstable DNA
  10. Inflammation
25
Explain the role of receptor over-expression in cancer
Over-expression of some receptors (expecially growth factor receptors) can be seen in many cancers: * HER2 – amplified and over-expressed in 25% breast cancer * EGFR – over-expressed in breast and colorectal cancer * PDGFR- glioma (brain cancer)
26
Explain the relationship with overexpression of growth factor receptor ligands and cancer
Vascular Endothelial Growth Factor is overexpressed: prostate cancer, kidney cancer, breast cancer --\> leading to increased Kinase cascade and signal amplification --\> angiogenisis in cancer
27
Explain the role of Constitutive (ligand independent) receptor activation in cancer
EGFR (lung cancer) epidermal growth factor receptor FGFR (head and neck cancers, myeloma) Leading to. Kinase cascade and signal amplification
28
What is the advantage of monoclonal cancers therapeutically?
A single "wire cutting", inhibition of cellular pathway might be enough to kill the cell But: only works for some cancers, other might regulate other pathways up
29
What is the MOA of a dual kinase inhibitor?
Inhibit 2 protein kinases to prevent cancer cells switching to other pathways (which needs another kinase) But: are also more toxic
30
What do normal cells require in order to grow and poliferate? How is that different from cancer cells?
Normall cells need growth factors to proliferate Cancer cells don't need them/ develop strategies to get higher stimmulation
31
What is the general target of monochlonal antibodies in the treatment of cancer?
They are normally designed to target + inhibit growth factor receptors
32
Explain the MOA of the use of monochlonal antibodies in cancer treatment
They are designes to stop the * Groth Factor receptor system * neutralise the ligand * inhibit dimerisation * cause internilisation * might induce phagocytosis + cytolysis
33
What are the types of targeted cancer treatment?
1. Monoclonal antibodies 2. Small molecule inhibitors
34
Explain the MOA of small molecule inhibitors
It is a type of targeted cancer treatment * bind to kinase domain of tyrosine kinase * can also bind to intracellular kinase pathways * block autophosphorilation and downstream regulation * e.g. Gleevac
35
What is the overall principle of targeted cancer treatment?
Normally: targeted treatment acts on receptors and modulates cancer halmarks * VEGF alters blood flow to tumor * AKT inhibitors block reisistance to apoptosis --\> without toxicity of other treatments observed
36
What are the main disadvantages of targetet therapy of cancer?
**Resistance**
37
What are the main resistance mechanism in targeted cancer therapy?
* Mutations in ATP-binding domain * Intrinsic resistance * Different gene mutations/ that might not make the targeted receptor/pathway responsible * Intragenic mutations * Upregulation of downstream or parallel pathways
38
What are the endings used to classify different antibodies (e.g. used in anti-cancer treatment)
* -momab (derived from mouse antibodies) * -ximab (chimeric) e.g cetuximab * -zumab (humanised) e.g. bevacizumab trastuzumab * -mumab (fully human) e.g. panitumumab
39
Explain the MOA of glivec In which type of disease is it used?
Glivec is a small molecule inhibitor and targets the ATP binding region within the kinase domain, inhibiting kinase activity of ABL1 --\> Used in the treatment of specific form of CML
40
Explain the use of anti-sense oligonucleiotides in cancer treatment
1. Single Stranded, DNA like molecole (17-22 nucleotides long) 2. Binds to target mRNA hinders translation of proteins by break down of mRNA
41
Explain the use of RNA interference in cancer treatment
* SS complementary RNA * (lagging behind oligosense nucleotides)

Year 2 MCD Cancer (17 decks)

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