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Concepts of Disease > Cancer 2 > Flashcards

Cancer 2 Flashcards

1
Q

What do tumour cells need to do in order to spread?

(1 mark)

A

Break cell-cell and cell-ECM attatchment

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2
Q

What is Organotropism and why can it happen?

A
  • Where cancer spreads to specific part of the body.
  • May be due to:
    • direction of blood flow
    • so tumour cells can get trapped in capillary beds
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3
Q

What is the ‘Seed and soil hypothesis’?

Apply it to a specific tumour.

A
  • The need to match with optimum environment to grow - by Paget
  • Kidney tumour likes to grow in the thyroid gland
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4
Q

What is a pre-metastic niche? Give an example. (2 marks)

A
  • When a distant site is prepared by molecules released by tumour
  • E.g. prostrate cancer secretes molecules that breakdown bone and prepapre it for metastic cells
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5
Q

What happens in each of the stages below: (6 marks)

  • Invasion
  • Intravasion
  • Transport
  • Extravasion
  • Metastasis
A
  • Invasion: introduction of EMT to get mobile cells
  • Intravasion: tumour into blood vessel AKA circulating tumour cell. Only need one to survive to form a metastatic tumour
  • Transport: transport in blood stream
  • Extravasion: exit blood and swithc on angiogenesis can grow exponentially
  • Metastasis: metastatic colonisation and angiogenesis
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6
Q

What is an ‘invadeapodia’ and how does it assist the formation of tumour cells? How is it formed? (2 marks)

A

Secretes molecules that breaks down basement membrane to allow tumour cells to get through.

Formed by cells breaking through basement membrane to underlying tissue

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7
Q

What is metastatic colonisation? (3 marks)

A
  • Establishment of a progressively growing tumour at a distant site
  • Involves formation of new blood vessels - an essential process to provide nutrients and oxygen
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8
Q

What does a tumour need to produce to degrade the basement membrane?

A

Proteases and enzymes whihc degrade the peptide bonds between amino acids

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9
Q

Why is Src a good target for drug therapy? (2 marks)

A
  • In tumours Src helps mediate breakdown of cell:cell and cell:ECM contacts.
  • Targeting this will decrease motility of tumour
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10
Q

What does EMT stand for? What does it do? (5 marks)

A
  • Epithelial mesenchymal transition (EMT)
  1. Static epithelial cells transformed into mesenchymal cells
  2. Stroma make signals to drive EMT - cancer cells hijack TGF-ß to make more mobile
  3. Loss of cell adhesion molecules
  4. Increase in mesenchymal markers
  5. Use of SNAIL and TWIST
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11
Q

What do SNAIL and TWIST do in metastasis? (5 marks)

A
  • Both control genes needed to trigger EMT

TWIST:

  • Key regulator of metastasis - inhibit and see loss in metastasis steps
  • TF activated from receptor kinase

SNAIL:

  • Binds to E box sequences in epithelial genes and recruits polypeptide
  • So causes histone modifications and epigenetic regulation to repress gene expression
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12
Q

What are the EMERGING hallmarks of cancer? (2 marks)

A
  1. Ability of tumour cell to completely reprogramme metabolism
  2. Ability cancer cells to avoid being destroyed
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13
Q

What is the Warburg effect? (3 marks)

A
  • Increase in rate of glucose uptake and preferential production of lactate despite being in the presence of oxygen
  • Cancer cells do this as they need energy much quicker than normal cells for their rapid growth
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14
Q

Why do cancer cells utilise aerobic glycolysis? (2 marks)

A
  • Angiogenesis in tumour is quite leaky so if were not to use aerobic glcolysis a lot of it would be hypoxic (the ferment)
  • Tumour cells have dependency on glucose
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15
Q

What is immune surveillance?

A

Where the immune system can recognise and kill tumour cells. People on immunosuprressants after organ transplant more susceptible to cancer

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16
Q

How does the immune system recognise and kill cancer cells?

(4 marks)

A
  • Cancer cells have cancer specific antigens
  • Cell dies, it is presented to T cell so can recognise the antigen
  • T cell infiltrates the tumour and binds to tumour cells and kills it
  • Thus releasing more antigen for recognition
17
Q

How does a T cell kill a cancer cell?

A
  • Injects granzyme and its target is effector caspases - granzyme will cleave these into their active form
  • Or bind to death ligand on cell surface which locks onto death receptors and triggers apoptosis
18
Q

How can cancer cells negatively affect T cell priming?

(5 marks)

(Think of avoiding immune destruction)

A
  • Can decrease tumour antigens
  • Cause down regulation of antigen presenting molecules
  • Over express main checkpoint proteins
  • Tumour produces lots of PD-L1 to trick T cell into thinking it’s dying when it actually isn’t
  • Cancer cells an change immune cells recruited to their microenvironment e.g. anti-inflammatory cytokines

PD-L1 is a ‘programmed death’ ligand

19
Q

What do macrophages produce that the tumour can use as growth molecules?

A

Cytokines

20
Q

How is chronic inflammation related to cancer? (1 mark)

A

Lots of chronic inflammation present in disregulated fat - increased amount of cytokines in inflammation which can be sed as a growth tool by tumours e.g. Type 2 diabetes

21
Q

What benefit do cancer stem cells have?

A
  • Infinite replication potential as can maintain telomere length (doesn’t have to break off)
  • Self-renew and differentiate into anything
22
Q

What is present at the bottom of the crypts of villi in the intestine? How does this contribute to carcinoma formation?

(2 marks)

A
  • Stem cells that migrate and differentiate at top of crypt where they die by apoptosis
  • Secretory epithelial cells more prone to mutations and carcinoma formation
23
Q

What are cancer stem cells responsible for? (2 marks)

A

Tumour plasticity

Migratory abilities

24
Q

What is ‘heterogeneity in tumours’? (1 mark)

A
  • Due to cancer stem cells, can renew themselves adn give rise to cells that differentiate into different types of cells
  • Good target for drug therapy
25
Q
A

Concepts of Disease (20 decks)

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