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BMS 114: Stem cells and society > Cancer > Flashcards

Cancer Flashcards

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1
Q

Why must exactly half of the progeny of a stem cell must stay as a stem cell?

A

LESS
- Regenerative capacity of the tissue is compromised

MORE
- Cancer?

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2
Q

What is hypertrophy?

A

Increase in cell size

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3
Q

What is hyperplasia?

A

Increase in cell NUMBER

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4
Q

When does hyperplasia occur?

A
  • In tissues that can divide

- In tissues with abundant stem cells

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5
Q

What is metaplasia?

A
  • Change in cell differentiation
  • Replacement of one MATURE cell type with another MATURE cell type
  • Altered differentiation of stem cell
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6
Q

What is dysplasia?

A
  • Changed in cell differentiation
  • Replacement of one MATURE cell type with a LESS MATURE cell type
  • Disordered
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7
Q

What are the reversible abnormal cellular growth and why?

A
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia

Reversible because they are a result of a STIMULUS

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8
Q

What is an irreversible abnormal cellular growth and why?

A

Neoplasia (resulting from metaplasia –> dysplasia –> neoplasia)

Is a result of an autonomous factor (mutations)

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9
Q

What is cancer?

A

1) Uncontrolled cell proliferation (eg. mitosis)

2) Aberrant differentitation
- Usually balances with proliferation

3) Uncontrolled cell interaction (invasion and metastasis)
- Not in situ
- Can invade other tissues

4) Cancer cell host interactions

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10
Q

What are 4 cancer cell host interactions?

A

1) Angiogenesis
- Tumour cells need blood supply

  • Hormone dependency
  • Hormone production
  • Immune response
    Tumours are ‘foreign’
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11
Q

What are benign tumours?

A
  • Confined

- Well defined structures

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12
Q

What are the stages in malignant tumour formation?

A

1) Dysplasia
2) Anaplasia (severe dysplasia)
3) Invasion
4) Metastasis

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13
Q

How do spread (metastasis)?

A
  • Break through the basement membrane
  • Into the blood vessels
  • Travel to a distant site in the blood vessel
  • Fuse with the vessel wall, through the vessel wall
  • Colonise distant sites
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14
Q

What are the 4 carcinogenic factors that cause cancer?

A

1) Chemical
- Smoking

2) Parasites

3) Radiation
- UV
- Ionising radiation

4) Viruses
- insert into the genome

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15
Q

What are the genetic causes of cancer?

A
  • Loss of function in tumor suppressor genes (recessive)
  • Gain of function of oncogenes (dominant)
  • Need MULTIPLE mutations to initiate neoplasia
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16
Q

Examples of tumor suppressor genes?

A

Rb

p53

17
Q

Examples of oncogenes?

A

myc
ras
abl

18
Q

What does the stochastic model suggest about cancer?

A
  • Cells have unlimited proliferative capacity
  • ALL the cells of a tumour are tumour-initiating so therefore ALL cells can be targets for anti-cancer treatments
  • Mutating cells transform growth
  • Heterogeneity of cellular composition is limited
19
Q

What are the problems with the stochastic model?

A

1) Tumours when treated can recur

2) Tumours are heterogeneous in cellular composition

20
Q

What do tumours contain?

A
  • Lots of differentiated cells

- High degrees of heterogeneity

21
Q

In a tumour, where does heterogeneity extend to?

A
  • Differentiation rates
  • Proliferation rates
  • Migratory and invasive capacity
  • Size
  • Therapeutic response
22
Q

What do functional assays show about cancer cells?

A
  • Only a small subset of cancer cells are capable of extensive proliferation
  • Only some populations of cells in a tumor can reform tumours in secondary transplantation assays
  • Implying there is a hierarchy in a tumours tissue architecture
    (only SOME cells are tumour initiating)
23
Q

What are the implications of tumour heterogeneity?

A

1) Not every cell in a tumour is the same
- Hard to treat

2) Only some cells n give rise to cells with higher proliferative targets
3) Only SOME cells appear capable of re-initiating the tumours

24
Q

When treating tumours, what cells do we want to target mostly?

A

The ‘dormant’ cells which are not highly proliferative but give rise to the highly proliferative cells

25
Q

What is the ‘cancer stem cell’ model?

A

Only a small, definable subset of cancer cells are the tumour initiating cells that have the ability to proliferate indefinitely

26
Q

What does the ‘cancer stem cell’ model suggest?

A
  • Heterogeneity is from differentiation
    (A stem cell structure)
  • Only some cells are targets for anti-cancer treatments as only some cells are tumor initiating
27
Q

What are ‘cancer stem cells’?

A

Rare cells within tumours with the ability to self-renew and give rise to the phenotypically diverse tumor cell population

28
Q

What are the propertires shared between normal stem cells and cancer stem cells?

A
  • Assymetric division

- Regulated by similar pathways

29
Q

Which cells in the hierachy are cancer stem cells? Why?

A 
Any of the three:
- Stem cell
- Progenitor cell 
- Oligolineage precursors 
Could act as cancer stem cells
  • A cancer stem cell is not necessarily derived from a stem cell but it is the ACQUISITION of stem cell PROPERTIES
30
Q 
What cancer stem cell marker is shared between:
Colon
Lung
Liver
Pancreas
A

CD133+

31
Q

What are the implications of cancer stem cells?

A
  • CSCs may be dormant in G0

- Tumours can grow back after the proliferating cells are removed

32
Q

How does control of differentiation offer approaches to therapy?

A
  • Deliver something to the tumour which causes differentiation of malignant stem cells to non-malignant derivatives
33
Q

What are the problems with the CSC model of tumour growth?

A

1) Testing the CSC model relies of xenotransplantation
- What if the model is not correct because the model is unsuccessful?

2) Testing CSC model often relies upon purification using markers
- Are they shared by other cells?

3) Some tumours loose heterogeneity
- Caused by further mutation and selection

  • May evolve intot he stochastic model

BMS 114: Stem cells and society (15 decks)

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