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Principles of tumour biology for FRCR CO1 > 1.3 Normal and Aberrant Mechanisms of Cell Growth and Control > Flashcards

1.3 Normal and Aberrant Mechanisms of Cell Growth and Control Flashcards

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1
Q

What is cell growth?

A

Increase in mass of cell

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2
Q

What is cell proliferation?

A

Increase in cell numbers , repeated cell divisions (mitosis)

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3
Q

What are growth factors?

A

Signalling molecules/proteins which induce a specific response within a cell

e.g. survival, migration, proliferation, differentiation

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4
Q

Where do autocrine GF act?

A

on the cell produced from

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5
Q

Where do paracrine GFs act?

A

Neighbouring cell

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6
Q

Where do endocrine GFs act?

A

Distant cell

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7
Q

What gene mutations lead to aletered gene expression and result in abnormal cell growth?

A
  • Chromosome gain/loss
  • Structual alterations e.g. translocations or inversions
  • Somatic Copy Number Alterations (SCNAs) - amplifications/deletions
  • Somatic mutations - base insertions/ substitutions/ deletions
  • Histone acetylation
  • Methylation
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8
Q

What is a somatic cell?

A

Any cell in the body excluding gametes

Somatic mutations are not passed on to offspring

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9
Q

Give 2 examples of Epidermal Growth Factors

A
  • EGF
  • TGFalpha
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10
Q

Give 2 examples of Epidermal Growth factor receptors

A
  • ErbB
  • HER1
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11
Q

What do Epidermal Growth Factors do?

A

Cause epithelial proliferation

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12
Q

Name a Fibroblast Growth Factor

A

FGF1

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13
Q

Name a Fibroblast Growth Factor receptor

A

FGFR1

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14
Q

What do Fibroblast Growth Factors do?

A

wound healing and tissue repair

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15
Q

Name an insulin like growth factor

A

IGF1

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16
Q

Name an insulin like growth factor receptor

A

IGF1R

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17
Q

What does insulin like growth factor do?

A

Mediates growth hormone

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18
Q

What is an example of platelet derived growth factor

A

PDGF1

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19
Q

What is an example of a platelet derived growth factor receptor

A

PDGFalpha and PDGFbeta

20
Q

What does platelet derived growth factor do?

A

fibroblast/smooth muscle proliferation

21
Q

What is an example of a Vascular Endothelial Growth Factor?

A

VEGFA

22
Q

What are some examples of Vascular Endothelial Growth Factor receptor?

A

VEGFR1 and VEGFR2

23
Q

What do VEGFs do?

A

angiogenesis

24
Q

What are the steps in signal transduction?

A

Signal is converted to a response

  1. Signal binds to a receptor and initiates signal transduction
  2. The signal undergoes transduction where it is amplified, diversified and integrated
  3. The cells forms a response from the outcome of the pathway
25
Q

What dysregulates signalling pathways?

A

Alterations in oncogenes or tumour suppressor genes

26
Q

How can transduction pathways be targeted clinically?

A

Encorafenib
Binimetinib
Cetuximab

27
Q

What are the main types of receptors in signal transduction pathways?

A
  1. Transmembrane enzyme-linked
  2. G protein coupled receptor
28
Q

What are some examples of transmembrane enzyme-linked receptors?

A

Tyrosikne Kinase Receptor (TKR)

Ser/thr kinase

29
Q

What are the 3 parts of a transmembrane receptor?

A
  • Ligand binding domain
  • Transmembrane domain
  • Intracellular TK domain
30
Q

What happens when a ligand binds to a TKR?

A
  1. Ligand binds
  2. Receptor undergoes dimerisation and phosphorylation

This results in activation of the signalling pathway

31
Q

What are some examples of GPCRs?

A
  1. Adrenaline
  2. Chemokines CXCR4
32
Q

What is the structure of a GPCR?

A

Passes through the cell membrane 7 times

GDP-inactive
GTP-active (phosphorylated)

33
Q

What are the two types of G protein and what do they signal with?

A
  1. Gq - Protein Kinase C
  2. Ga - cAMP + Protein Kinase A
34
Q

What occurs during Transduction in the signalling pathway?

A
  1. Post-translocation modifications of proteins e.g. phosphorylation cascade
  2. Secondary messengers are produced e.g.:
    - ATP -> cAMP -> AMP
    - PIP2 -> PIP3 -> AKT (Inhibited by PTEN)
35
Q

What occurs during response in signal transduction?

A
  • Regulation of gene expression
  • Regulation of cellular events

Cell changes its phenotype by:
- Changing protein levels by transcription or translation
- Modifying available proteins by changing their localisation or function

36
Q

What are some signal transduction pathway examples in cancer biology?

A
  • MAP Kinase
  • PI3 Kinase/mTOR
  • Wnt/Beta catenin
  • Rb/E2F
  • Hedgehog
37
Q

What are the steps in the MAP Kinase pathway?

A
  1. Growth factor binds to domains I and III on Receptor Tyrosine Kinase on the cell surface
  2. RTK dimerises and autophosphorylates making a docking site for EGRB2 inside the cell
  3. EGRB2 recruits SOS (guanine exchange factor) which activates RAS by swapping GDP for GTP
  4. This initiates the MAPK cascade:
    - RAS -> RAF (ser/thr kinase)
    - RAF -> MEK
    - MEK -> ERK
  5. ERK - Extracellular Receptor Kinase increases transcription of c-fos, c-jun
  6. Cyclin D transcribed causing cell to enter cell cycle
38
Q

What are the steps in the PI3Kinase/mTOR pathway?

A
  1. PI3K activated by TKR/GPCR/RAS
  2. PI3K converts PIP2 -> PIP3
  3. PIP3 activates AKT
  4. AKT activates mTOR and cell enters cell cycle
    AKT inhibits Bad, p21, p27 and this inhibits apoptosis
39
Q

What reverses PI3K?

A

PTEN

Dephosphorylates PIP3 -> PIP2

(antagonising of PI3K)

40
Q

What are the steps in the Wnt/Beta Catenin pathway?

A
  1. Increase in beta catenin
  2. Wnt binds to frizzled receptor and LRP5/6 and activates it
  3. DVL binds to LRP and is activated
  4. DVL inhibits the beta-catenin destruction complex preventing phosphorylation and degradation
  5. Beta-catenin accumulates in the cytoplasm
  6. BC interacts with TCF activating target genes for cell proligeration, differentiation and stem cell reneweal
41
Q

What inhibits the Wnt pathway?

A

When Wnt is low the destruction complex phosphorylates beta-catenin marking it for ubiquitination and proteosomal degredation

In the absence of beta-catenin Groncho binds to TCF and inhibits the pathway

42
Q

What are the steps in the Rb/E2F pathway?

A
  1. Early in G1 CyclinD-CDK4/6 phosphorylates Rb protein - partially inactivates it 2. This causes a coformational change which releases Histone Deacetylases (HDACs)
  2. Cyclin E/CDK2 causes another conformation change which releases E2F/DP
  3. This allows histone acetylation. chromatin relaxation, and transcription of E2F target genes allowing S phase progression
43
Q

What are the proteins and genes in the hedgehog pathway?

A

Transmembrane proteins: Patched and Smoothened

Tumour Suppressor gene = patched

44
Q

What is the pathway if hedgehog is absent?

A
  1. Patched proteins remain in the cilia and smoothened are therefore inhibtied
  2. Transcription factor Gli is cleaved by proteosomes
  3. This inhibits the genes expressed by hedgehog
45
Q

What is the pathway if hedgehog present?

A
  1. Hedgehog binds to patched which translocates it out of the cilia
  2. SMoothened protein can move into cilia
  3. Protein complex dissociates and releases Gli
  4. Gli is translocated into the nucleus and causes expressiion of hedgehog target genes e.g. Cyclin D, Bcl2, VEGF and NSAIL

Principles of tumour biology for FRCR CO1 (4 decks)

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