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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
Q

Explain the role of receptor over-expression in cancer

A

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
Q

Explain the relationship with overexpression of growth factor receptor ligands and cancer

A

Vascular Endothelial Growth Factor is overexpressed:

prostate cancer, kidney cancer, breast cancer

–> leading to increased Kinase cascade and signal amplification

–> angiogenisis in cancer

27
Q

Explain the role of Constitutive (ligand independent) receptor activation in cancer

A

EGFR (lung cancer) epidermal growth factor receptor

FGFR (head and neck cancers, myeloma)

Leading to. Kinase cascade and signal amplification

28
Q

What is the advantage of monoclonal cancers therapeutically?

A

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
Q

What is the MOA of a dual kinase inhibitor?

A

Inhibit 2 protein kinases to prevent cancer cells switching to other pathways (which needs another kinase)

But: are also more toxic

30
Q

What do normal cells require in order to grow and poliferate?

How is that different from cancer cells?

A

Normall cells need growth factors to proliferate

Cancer cells don’t need them/ develop strategies to get higher stimmulation

31
Q

What is the general target of monochlonal antibodies in the treatment of cancer?

A

They are normally designed to target + inhibit growth factor receptors

32
Q

Explain the MOA of the use of monochlonal antibodies in cancer treatment

A

They are designes to stop the

  • Groth Factor receptor system
    • neutralise the ligand
    • inhibit dimerisation
    • cause internilisation
  • might induce phagocytosis + cytolysis
33
Q

What are the types of targeted cancer treatment?

A
  1. Monoclonal antibodies
  2. Small molecule inhibitors
34
Q

Explain the MOA of small molecule inhibitors

A

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
Q

What is the overall principle of targeted cancer treatment?

A

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
Q

What are the main disadvantages of targetet therapy of cancer?

A

Resistance

37
Q

What are the main resistance mechanism in targeted cancer therapy?

A
  • 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
Q

What are the endings used to classify different antibodies (e.g. used in anti-cancer treatment)

A
  • -momab (derived from mouse antibodies)
  • -ximab (chimeric) e.g cetuximab
  • -zumab (humanised) e.g. bevacizumab trastuzumab
  • -mumab (fully human) e.g. panitumumab
39
Q

Explain the MOA of glivec

In which type of disease is it used?

A

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
Q

Explain the use of anti-sense oligonucleiotides in cancer treatment

A
  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
Q

Explain the use of RNA interference in cancer treatment

A
  • SS complementary RNA
  • (lagging behind oligosense nucleotides)

Year 2 MCD Cancer (17 decks)

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