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2a- Pathology > The molecular pathology of newer anti-cancer agents > Flashcards

The molecular pathology of newer anti-cancer agents Flashcards

1
Q

What are examples of conventional chemotherapies?

A
  • Vinblastine
  • Etoposide
  • Ifosamide
  • Cisplatin
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2
Q

What are examples of conventional chemotherapies that stop DNA replication?

A
  • Vinblastine: antimicrotubule agent
  • Etoposide: inhibits topoisomerase 2
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3
Q

What are examples of conventional chemotherapies that bind directly to DNA?

A
  • Ifosamide
  • Cisplatin
    Both inhibit DNA synthesis by cross linking
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4
Q

What are cons of conventional chemotherapy?

A
  • Not selective for tumour cells
  • Usually hits cells that are dividing
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5
Q

What can conventional chemotherapy lead to?

A
  • myelosuppression - a decrease in bone marrow activity that results in reduced production of blood cells
  • hair loss
  • diarrhoea
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6
Q

What are reasons for increase in tumour size?

A
  • Cell division
  • Lack of cell death (apoptosis)
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7
Q

What type of tumour is conventional chemotherapy good for?

A
  • Good for fast dividing tumours
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8
Q

What are some examples of fast dividing tumours?

A
  • germ cell tumours of testis
  • acute leukaemias
  • lymphomas
  • embryonal paediatric tumours
  • choriocarcinoma
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9
Q

What is targeted chemotherapy?

A

Exploits some difference between cancer cells and normal cells to target drugs to the cancer cells

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10
Q

What are some advantages of targeted chemotherapy?

A
  • more effective
  • less side effects
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11
Q

How can you differentiate between normal cells and cancer cells?

A
  • Gene arrays
  • Proteomics
  • Tissue microarrays
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12
Q

What are examples of monoclonal antibodies that target growth factor receptors?

A
  • Cetuximab
  • Herceptin
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13
Q

What is cetuximab?

A

Monoclonal antibody inhibiting epidermal growth factor receptor (EGFR)

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14
Q

How does cetuximab work?

A
  • chimeric IgG humanised monoclonal antibody
  • binds competitively to extracellular domain of EGFR
  • antitumour activity in xenograft models
  • blocks production of VEGF, interleukin 8, bFGF
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15
Q

How do we select patients for Cetuximab therapy?

A

Immunohistochemistry

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16
Q

What is herceptin?

A

Monoclonal antibody against human epidermal growth factor receptor 2: Her-2

17
Q

What is seen in Her-2 in breast cancer?

A

Overexpression

18
Q

How does herceptin work?

A
  • Removal of Her-2 by endocytosis
  • Or lymphocytes can bind to herceptin then kill Her-2
19
Q

What is her-2 associated with?

A
  • large size
  • high grade
  • aneuploidy
  • negative oestrogen receptor status
  • independent adverse prognostic factor
20
Q

How do we detect HER-2 amplification?

A
  • Fluorescent in situ hybridisation (FISH)
    • Chr 17 are green dots where Her-2
      genes are
    • Timeconsuming
  • Immunohistochemistry
21
Q

What is another example of monoclonal antibody therapy?

A
  • Anti-PD1 (programmed cell death protein 1)
    • Pembrolizumab
    • Nivolumab
22
Q

What is programmed cell death protein 1?

A
  • Immune checkpoint
  • Inhibits T cell response
  • In normal physiology prevents auto-immunity
  • PD1 over-expression in tumours
23
Q

What are examples of small molecular inhibitors?

A
  • Gleevec
  • Gefitinib
24
Q

How does gleevec work?

A
  • Tablet that can shrink tumour, not totally cure
  • Small molecular inhibitor of c-kit (tyrosine kinase)
  • Mutation in c-kit protein meaning its always on
25
Q

How does gefitinib (iressa for astrazeneca) work?

A
  • small molecular inhibitor of EGFR TK (tyrosine kinase)
  • works best when mutation in EGFR leads to overactivity of internal tyrosine kinase leading to lack of apoptosis
26
Q

What is CAR-T therapy?

A

Chimeric antigen receptor T cell

27
Q

How does CAR-T therapy work?

A
  1. Blood taken from patient
  2. Filter out immune T cells
  3. Harmless virus used to deliver genes to T cells modifies them causes them to recognise and target cancer cells
  4. Modified cells duplicated in lab
  5. Modified CAR-T cells injected back into patient
28
Q

What are some disadvantages of CAR-T therapy?

A
  • Labour intensive
    • Different for every patient
  • Some patients died in trials as some normal cells causing a ‘cytokine storm’ and system failure
    • Now have safety mechanism of 2 receptors
    • 2nd receptor to inhibit activation

2a- Pathology (16 decks)

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