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SCRA > 9. cancer stem cells > Flashcards

9. cancer stem cells Flashcards

1
Q

what makes stem cells good possible cancer initiating cells?

A
  • they are long lived and so can accumulate mutations over time
  • they are already have the potential to proliferate indefinitely
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2
Q

what makes progenitors good possible cancer initiating cells?

A

they are more highly proliferate than stem cells

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3
Q

what cell type does CML probably arise from and why?

A

stem cells are it progression is low

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4
Q

what cell type does AML probably arise from and why?

A

this progress much faster and so probably arises from progenitors

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5
Q

why might a patient relapse after surgery and therapy?

A

some of the residual tumour was left behind

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6
Q

what is the cancer stem cell hypothesis?

A
  • cancer contain a hierarchical organisation of cells

- cancer stem cells can replenish the tumour and are resistant to chemotherapy

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7
Q

what is the therapeutic consequence of the cancer stem cell hypothesis?

A

in order to eradicate the tumour we must target and kill cancer stem cells

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8
Q

give an example cancer where cancer stem cells have been proved to exist

A

AML cancer stem cells were shown to give rise to themselves and bulk leukaemia

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9
Q

what happens when cells isolated from AML with surface markers of identified cancer stem cells are injected into mice?

A

some engraft and some do not

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10
Q

how did they prove that human colon cancer contains cancer stem cells?

A

cells from human colon cancer were able to give rise to cancer in immunocompromised mice

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11
Q

why will we never fully be able to prove that human cancer stem cells exist?

A

we cannot inject cancer stem cells into humans to see if they give rise to cancer and so we will have to rely on mouse models - tumour formation in these are slightly different from humans - they are hard to generate and need to be started by more than one cell

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12
Q

what is one variation seen between human tumour samples?

A

number of cancer initiating cells

this variation is also seen between tumours of the same class

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13
Q

what can influence the determination of how many cancer initiating cells are in a sample?

A

the type of assay used

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14
Q

genetic instability in cancer cells allows them to undergo what process?

A

clonal evolution

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15
Q

how are stem cells different from cancer initiating cells?

A
  • they are very stable
  • they don’t proliferate much
  • they give rise to consistent progeny
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16
Q

what process generates stem cell like cells in epithelial tumours? and what does this process allow?

A

epithelial to mesenchymal transition allow cells to metastasise

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17
Q

what process occurs to these stem cell like cells once they have reached a distal location?

A

they undergo mesenchymal to epithelial transition

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18
Q

if we eliminate cancer stem cells in a tumour what may occur? and why?

A
  • other cancer cells may become cancer stem cells
  • killing CSC may open up an environment, for example like by blood vessel, which allow other less proliferative cells to become proliferative and allow them to evolve
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19
Q

how are cancer stem cells are stem cell similar?

A

they both give rise to themselves and progeny

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20
Q

how are cancer stem cells and stem cell dissimilar?

A
  • CSC are not necessarily rare like SCs
  • CSC are not necessarily quiescent
  • CSC have heterogeneous karyotypes
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21
Q

do cancer stem cells always arise from stem cells?

A

no

22
Q

mutations that have the potential to result in cancer occur in people that do not have cancer, give an example of this and what does this tell us

A
  • the rearrangement of BCR and BAL gene is a hallmark of CML, yet this is seen in many old people who do not have CML
  • this shows us that cancer is not driven by a single mutation
23
Q

why might a change in mutated cells environment lead to cancer? and what does this explain?

A
  • the change in the environment may allow cells to proliferate and develop into cancer
  • this explain why only so people with a certain mutation develop cancer
24
Q

give an example of a change in a mutated cells environment that may lead to cancer

A

inflammation

25
Q

what are the three present challenges in the cancer stem cell field?

A
  1. identification of whether tumours have a cell hierarchy
  2. identification adequate experimental analysis to asses CSC
  3. determining better ways of detecting and eliminating CSC
26
Q

cancer stem cells may not always be the chemoresisatnt cells yet a patient may still relapse, why?

A

a non-cancer stem cell may be chemoresistant. because there are now no other cells around it can fill the role of the cancer stem cell and give rise to the cancer again.

27
Q

what might the cancer stem niche promote?

A

it may promote the formation of cancer stem cells

28
Q

cancer stem cells are identical to the stem cells of the tissue they arose in, TURE or FALSE

A

FALSE

29
Q

what is the hardest type of cells for cancer stem cells to arise from?

A

very differentiated cells

30
Q

what is the term for cells that are abnormal and persistent?

A

neoplastic cells

31
Q

define malignant cells

A

these are cells that are able to spread and occupy the tissue more than neoplastic cells

32
Q

what did a paper in 2008 that shook the cancer stem cell field show?

A

they showed that depending on how you assayed a tumour determined how many cancer stem cells could be identified

33
Q

what was the first paper thing that this 2008 paper showed?

A

depending on what type of immunocompromised mice the tumour cells were injected resulted in a different frequency of tumour formation
- the more immunocompromised the mouse the faster more efficient tumour formation

34
Q

what is the difference between NOD/SCID and NOD/SCID Il2g-/- mice?

A
  • NOD/SCID mice lack B and T cells

- NOD/SCID Il2g-/- mice also lack NK cells

35
Q

what was the second thing the 2008 paper showed?

A

if cells were injected into NOD/SCID Il2g-/- mice with matrigel to support and anchor the cells then tumours were much more aggressive

36
Q

how did the 2008 paper show that this was also true for non-cancer cells?

A

they used human cord blood to show that the more immunocompromised the mouse, the better the engraftment

37
Q

how can the CIC frequency of a tumour be assess?

A

single cell transplantation

38
Q

when single cells are injected with the addition of matrigel what is observed?

A

the frequency of cancer initiating cells is very high

1 in 4 cells gave rise to melanomas in mice

39
Q

what was the last thing that this 2008 paper showed?

A

up until this point the field has considered CD133+ cells to be cancer stem cells, they showed that CD133 did not define the cancer initiating cell population

40
Q

how do sub-clones arise and what do they do in an tumour?

A

sub-clones arise from genetic instability, they try and out compete other clones

41
Q

how is it possible to try and recreate the history of a tumour by looking a mutations in sub-clones?

A

the mutations that arose in the first clone will be present in all clones, mutations that arose in the most recent clones will only be present in that clone population

42
Q

how can we confirm that a patient who has a tumour after treatment has relapsed?

A

relapsed tumour will have a number of mutations in common with the original tumour

43
Q

when a tumour cell enter circulation and is able to create another tumour at a secondary location, what does this suggest about the tumour cell?

A

it might be a cancer stem cell as it is able to generate a tumour at a secondary location

44
Q

which cells in a tumour are most likely to metastasise and how has this been observed?

A

cells close to the vessel

this has been observed using time lapse microscopy of solid tumours

45
Q

specific cancer types preferentially metastasize to certain locations, give an example of this and a reason for why it occurs

A

breast cancer normally metastasises to the bone
breast cancer cells express CXCR4, a receptor for the chemokine SDF1 which is produced by osteoblasts at high levels in the BM

46
Q

what are the microvesicles produced by cancer cells called and what is their function?

A

exosomes enter circulation and target specific tissues, they generate a pro-inflammatory environment which is favourable for tumour formation

47
Q

when a cell metastasise to another tissue, what is it capable of doing?

A

lying dormant in a tissue for a long amount of time

48
Q

what is often seen in people that die from breast cancer?

A

lots more micro-metastasis (single cells) in the bone marrow than was initially thought

49
Q

what does a large number or circulating tumour cells suggest?

A

a worse prognosis

50
Q

what is a worse prognostic marker than single circulating tumour cells?

A

circulating clusters

51
Q

what might a circulating tumour cell be?

A

a cancer stem cell

SCRA (19 decks)

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