Tissue renewal, stem cells + cancer Flashcards

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1
Q

Cancer cells have defects in which 2 types of gene?

A

Activating mutations in porto-oncogenes
–> oncogenes

Inactivation of anti-proliferation genes
–> tumour suppressors

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2
Q

Give 2 examples of tumour suppressors

What happens if they’re lost/inactivated?

A

Rb
CIP

Results in inappropriate progress into S phase

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3
Q

In the skin, which direction do cells move when they become more specialised?

A

From the dermis towards the epidermis

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4
Q

Which layer of the skin is a continually renewing barrier?

A

Epidermis

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5
Q

What are the 3 key factors to maintain tissue organisation?

A

Cell communication
Selective cell-cell adhesion
Cell memory

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6
Q

What is selective cell-cell adhesion?

A

Presence of specific cell adhesion molecules allow organisation of cell layers

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7
Q

What is cell memory?

A

Cell has a ‘memory’ of its developmental history

- dictates which set of genes it expresses + this allows it to perform its specialised function

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8
Q
Which cells are renewed...
> never?
> yearly?
> monthly?
> daily?
A

Neuron

Bone

Epidermal + erythrocyte

Gut epithelial

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9
Q

How do stem cells proliferate to renew tissues?

A

> Self-renewal

> Generate intermediate precursor cells that divide a few times before producing differentiated cells

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10
Q

Where in a blastocyst are embryonic stem cells found?

A

Inner cell mass

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11
Q

What are oligopotent stem cells?

A

Cells that give rise to a few terminally differentiated cell types

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12
Q

Describe the structure of epidermis

A

Basal cells - including stem cells + dividing precursors - sit on basal lamina above the dermis

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13
Q

Describe how epidermis is renewed

A

Dividing precursors divide 2-3 time before they differentiate
- gain expression of adhesion molecules specific to the supra-basal layer

–> pulled up into supra-basal layer + lose capacity to divide

  • > continue to move upwards, become flattened + dehydrated
  • nucleus etc. breaks down

Cells sloughed off at surface

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14
Q

Describe the structure of gut epithelium

A

Single cell layer

Folded into crypts + villi

Stem cells reside at base of crypt

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15
Q

Describe the renewal of gut epithelium

A

Stem cells at base of crypt give rise to dividing precursor cells

  • > slide up towards villus tips
  • > differentiate to form secretory + absorptive cell types needed

Cells lost at tips of villi

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16
Q

What is the name of the pathway that controls stem cell renewal + production of diff cell types?

What happens when this pathway is active + inactive?

A

Wnt pathway

Active = cell proliferation

Inactive = no cell proliferation

17
Q

What do all blood cells come from?

A

A single type of multipoint hematopoietic stem cell in bone marrow

18
Q

What have stem cell therapies been used to treat?

How is this carried out?

A

Blood disorders
e.g. leukaemia

Destroy patients own bone marrow cells by radio-/chemotherapy

-> replace bone marrow by transplantation of donor bone marrow

= replaces blood stem cell pool

19
Q

What are iPS cells?

A

Differentiated cells reprogrammed into stem cell state using TFs

20
Q

What are human iPS cells used for?

A

Providing an ethical replacement for hES cells:
> disease remodelling + toxicology
> regenerative medicine

21
Q

What are the 3 key genes that can convert a differentiated cell into an iPS cell?

A

Sox2
Klf4
Oct4

22
Q

Describe how a benign tumour forms

How is a malignant tumour formed?

A
  1. Mutation gives 1 cell a growth advantage
  2. 2nd mutation increases the advantage
  3. 3rd mutation increases advantage further + makes cell invasive

Cells invade surrounding tissues
-> leads to damage that may be life-threatening

23
Q

What are metastasis?

A

Development of secondary malignant growths at a distance from a primary site of cancer

24
Q

How can a polyp in the gut epithelium lead to malignant cancer?

A
1. Tumour suppressor gene (APC) lost 
= excessive epithelial proliferation
2. Oncogene (Ras) activated
=small tumour
3. Another TS gene lost
= large tumour
4. 3rd TS gene (p53) lost
= tumour becomes invasive
4. Rapid accumulation of mutations
= metastasis