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Cancer CE & VP > CE L4 Stem cells > Flashcards

CE L4 Stem cells Flashcards

1
Q

is it easier to target over or underactive?

A

over

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2
Q

Is any cell as likely to mutate as another?

A

Initially we thought this bu actually no

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3
Q

What is the future for cancer prognosis?

A

we wold get an individualised map of mutations to predict prognosis and response to therapy etc.

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4
Q

development of and organism relies on a balance between (3 processes)

A

differentiation
proliferation
apoptosis

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5
Q

development of and organism relies on a balance between (3 processes)

A

differentiation
proliferation
apoptosis

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6
Q

Why cant cancer cells carry out normal function?

A

They become undifferentiated

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7
Q

Why cant cancer cells carry out normal function?

A

They become undifferentiated

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8
Q

PROBLEM

Tumour masses look like they are made of many/few cell types?

A

Many - but cancers are clonal (arising from a single cell)

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9
Q

PROBLEM

Can all cancer cells recolonise?

A

No - only a small number can when implanted into a secondary site

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10
Q

PROBLEM

Cancer is a disease of proliferating cells - but…

A

but most mature cells don’t proliferate

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11
Q

PROBLEM

Cancers are caused by the accumulation of 3+ mutations - but

A

most cells have a finite lifetime and don’t live long enough to acquire this

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12
Q

4 evidences that cancer arrises from stem cells?

A
  1. Clonal
  2. Can recolonise
  3. Live long enough to get 3 mutations
  4. Proliferating cells
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13
Q

4 evidences that cancer arrises from stem cells?

A
  1. Clonal
  2. Can recolonise
  3. Live long enough to get 3 mutations
  4. Disease of proliferating cells
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14
Q

Stem cells are…

A

unspecified cells that reproduce themselves and/or generate more specialised cells indefinately

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15
Q

Specialised cells carry out a specialized function but often cannot…

A

divide

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16
Q

Changes in cell state are ………….. regulated

A

transcriptionally

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17
Q

What are progenitor cells

A

Unipotent e.g. haemopoetic- can only become one type of cell

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18
Q

What is asymmetrical stem cell

A

a

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19
Q

What is asymmetrical stem cell

A

Each time the cell divides it produces one daughter cell that is more differentiated and one identical.

Stem cell -> Restricted stem cell -> Progenitor cell

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20
Q

What are adult stem cells present for?

A

Healing and normal cell turnover (producing new blood cells etc.)

21
Q

Problems studying adult stem cells

A

difficult to isolate and identify

22
Q

What does recolonisation of adult stem cells suggest?

A

If you implant an adult stem cell in other tissues in some cases it forms a tumour. If you do this with differentiated cells the don’t

They would need to dedifferetiate first to acquire ability to proliferate.

23
Q

Where are adult stem cells held?

A

In a stem cell niche - encapsulated environment, suppresses growth. Only allowed to proliferate to replace damaged cells.

24
Q

What happens to the stem cell niche in cancer?

A

Cancer cell becomes independent of niche or have changes so the niche can not longer suppress them

25
Q

Proliferation of adult stem cells is high so when mutations occur….

A

they are rapidly spread to many daughter cells

26
Q

Proliferation of adult stem cells is high so when mutations occur….

A

they are rapidly spread to many daughter cells

27
Q

Stem cells live longer giving the opportunity for

A

many mutations to accumulate

28
Q

Many signalling pathways involved in …………………. have been shown to be mutated in cancer cells

A

self renewal

29
Q

How do stem cells become independant on niceh

A
  1. Expasion of niche allows expansion of cancer cells
  2. Adaption to a different niche allowing their expanion
  3. Niche independance
  4. Shift in the programmed declined replication potential
30
Q

Wnt is a …………………………… found in what cancers

A

protooncogene

colon

31
Q

Telomeres are

A

repeats found at the end of chromosomes that aid chromosomal replication

32
Q

Do mature cells in the body express telmerase enzymes?

A

no - but cancers do. It has to be reactivated, so was it never switched off if the cancer is from a stem cell?

It’s been a target for therapy as different to self

33
Q

What is the function of telomeres?

A

Enzymes used to copy DNA need something to sit on so they don’t fall off before reaching the end

34
Q

What happens to telomeres in each cell division?

A

Shorten - because DNA polymerase cannot copy right to the end.

35
Q

What happens when the telomere is too short?

A

recognised as damaged DNA

p53 is activated - senescense or even apoptosis

36
Q

What does measuring telomerase activity tell us about cancer?

What else do we measure with this?

A

Prognosis

N-myc

(high is poor)

37
Q

What are telomerase enzymes?

A

Reverse transcriptase enzymes containing RNA template to add TTAGGG repeats onto the chromosomal ends

38
Q

What is the benefit for the cancer cell of expressing telomerases?

A

Able to repair telomeres and so extend life

39
Q
  1. exmples of a theoretical anti telomerase therapy
A

telomerase antisence

or

telomerase with mutated DNA template

40
Q
  1. exmples of a theoretical anti telomerase therapy
A

telomerase antisence

or

telomerase with mutated DNA template

41
Q

Patched is a

A

tumour supressor

42
Q

Describe the patched pathway

A

Hh binds to patched, when bound it releases smoothened.

This releases Gli
Gli (transcription factor) - drives proliferation

43
Q

2 Problems in the patched pathway that may cause cancer

A

Over expression oh Hh

loss of function of patched

44
Q

~Describe the wnt pathway

A

wnt binds to frizzled .

When bound the complex draws GSK3 out of normal complex and binds to receptor.

This releases beta catenin (TF)
Drives c-myc(TF) + cyclin D expression

Drives G1 and cell cycle

45
Q

How many forms of Hh are there

A

3 - sonic, desert and indian

46
Q

What is in the normal complex with GSK3 in the Wnt pathway

A

APC
Axin
CKI
GSK3

47
Q

Problem in Wnt pathway causing colon cancer?

A

loss of function of APC (so the normal complex can’t form)

48
Q

WHAT IS THE ULTIMATE OUTCOME OF WNT AND Hh PAATHWAYS -

HOW DOES THIS RELATETO STEM CELLS

A

drives proliferation

Cancer CE & VP (15 decks)

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