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BMS 114: Stem cells > Lecture 16: Cancer > Flashcards

Lecture 16: Cancer Flashcards

1
Q

What is the significance of cancer?

A
  • is a significant disease
  • about 25% of UK deaths
  • Cancer is MOSTLY a disease of old age
  • 5 year survival improving but is not 100%
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2
Q

Tissue repair: small air ways (bronchioles)

A

Damage results in loss of basal stem cells –> dedifferentiated of clara cells.
-Process of repair has to be controlled to replace just the tissue (cells) required

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3
Q

adult stem cells: asymmetric division

A

stem cell = 1 stem cell, 1 progeny

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4
Q

Stochastic or Directed division:

A

stem cell = 2 stem cells (or 2 progeny)

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5
Q

Exactly half of the progeny of a stem cell must stay as a stem cell: less & more

A

Less = regenerative capacity of the tissue is compromised

MORE - CANCER?

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6
Q

Hypertrophy:

A

increase in cell size

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7
Q

Hyperplasia:

A

increase in cell number

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8
Q

Metaplasia:

A

change in cell differentiation (mature 4 mature)

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9
Q

Dysplasia:

A

change in cell differentiation (mature 4 less mature)

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10
Q

whats the difference between hypertrophy, hyperplasia, metaplasia , dysplasia + Neoplasia

A

NEOPLASIA IS IRREVERSIBLE BECAUSE IT IS AUTONOMOUS.

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11
Q

Neoplasia

A

CANCER

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12
Q

chronic irritation from cigarette smoke leads to

A

METAPLASIA reversible to dysplasia reversible also.

But on its way to neoplasia - IRREVERSIBLE

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13
Q

What is Cancer?

A

1) uncontrolled cell proliferation i.e. mitosis
2) Aberrant differentiation
3) uncontrolled cell interaction -invasion&metastasis
4) Cancer cell host interactions

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14
Q

Aberrant differentiation:

A

Normally there is a balance between cell proliferation & differentiation

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15
Q

Cancer cell host interactions:

A
  • Angiogenesis
  • -tumour cells need blood supply
  • Hormone dependency
  • hormone production
  • immune response
  • immune response
  • protection can be damaging
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16
Q

2 types of tumours

A

benign + malignant

17
Q

benign =

A

confined, well defined structures

18
Q

malignant tumours:

A

(Early)

  • dsyplasia
  • anaplasia (sever dysphasia)
  • invasion
  • metastasis
    (late)

ALL IRREVERSIBLE

19
Q

what causes cancer?Major carcinogenic factors

A
  • chemical (smoking)
  • Parasites
  • Radiation
  • Viruses
20
Q

what causes cancer? Genetic changes

A
  • oncogenes
  • loss or inactivation of RECESSIVE inhibitory genes (tumour suppressor genes)
  • need multiple mutations to cause cancer
21
Q

A general model for cancer

A
  • Stochastic model
    ALWAYS:
    1 becomes 3, 2 survive. join become 2, divide & become 4, join
    -All cancer cells are potential tumour initiating cells but have a low probability of proliferation in clonogenic assays
22
Q

tumour heterogeneity

A
  • display high degree of heterogeneity
  • tumours contain lots of differentiated cells
  • this extends to virtually all measurable properties of cancer cells
23
Q

implications oh tumour heterogeneity

A
  • not every cell in a tumour is the same
  • only some cels can give rise to cells with higher proliferative capacity
  • only some cells appear to be capable of re-initiating the tumours, i.e. are TUMOUR INITIATING CELLS
24
Q

“Cancer stem cell” model?

A
  • Only a small definable subset of cancer cells are tumour initiating cells that have the ability to proliferate indefinitely.
  • heterogeneity is from differentiation (i.e.stem cell)
  • only some these cells are tumour-initiating & therefore can be targets for anti-cancer treatments
  • BUT remember that further mutation & selection will be happening
25
Q

Normal stem cells:

A

Rare cells within organs with the ability to self-renew and give rise to all types of cells within the organ to drive organogenesis

26
Q

Cancer stem cells:

A

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

27
Q

properties shade by normal stem cells & cancer stem cells

A
  • assymetric division
  • -self renewal
  • -differentiation into phenotypically diverse mature cell types
  • regulated by similar pathways
28
Q

which of these could act as cancer stem cells?

A
  • stem cell
  • progenitor cell
  • oligolineage precursors

ANY, it is the acquisition of stem cell properties NOT necessarily being derived from a stem cell that defines a cancer stem cell

29
Q

why might there be cancer stem cells?

A

1) stem cells are relatively few in number - smaller target?
2) stem cells mostly quiescent - less chance for mutation?
3) Immortal strand hypothesis - is newly synthesised DNA strand in dividing stem cells always passed to differentiation progeny cells?

BMS 114: Stem cells (16 decks)

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