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MBD/MI (Wothaya) > Cell Growth And Differentiation > Flashcards

Cell Growth And Differentiation Flashcards

1
Q

What are the three main groups of disease?

A

Developmental conditions, neoplasia and others

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2
Q

What are developmental conditions?

A

Related to cell growth or differentiation

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3
Q

What are neoplasia (and metaplasia)?

A

Cancers and tumours

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4
Q

What are the two main groups of cell growth?

A

Hypertrophy and hyperplasia

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5
Q

What is hypertrophy?

A

Bigger cells (more proteins and membrane)

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6
Q

What drives hypertrophy?

A

Elevated protein synthesis

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7
Q

What is hyperplasia?

A

More cells

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8
Q

What is hyperplasia caused by?

A

Cell division or proliferation

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9
Q

What does cell differentiation begin with?

A

Exit from the cell cycle

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10
Q

What are the three broad classes of extracellular signals?

A

Paracrine, autocrine, endocrine

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11
Q

What do paracrine signals do?

A

Stimulate proliferation of a different cell type that has the appropriate cell surface receptor

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12
Q

Where are paracrine factors produced?

A

Locally

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13
Q

What are autocrine signals produced by?

A

Cell that also expresses the appropriate cell surface receptor

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14
Q

How do endocrine signals work?

A

Released systematically for distant effects

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15
Q

What are the type of proteins used in cell growth and differentiation?

A

Proteins that:
Stimulate proliferation and promote survival
induce differentiation and inhibit proliferation
Induce apoptosis

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16
Q

What do mitogens do?

A

Stimulate proliferation and promote survival

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17
Q

What are the phases of the cell cycle?

A

Mitosis, G1, S phase, G2

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18
Q

What are quiescent cells and what phase are they in?

A

Cells that have left the cell cycle- G0

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19
Q

Can quiescent cells rejoin the cell cycle?

A

Yes

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20
Q

What is FACS used to measure?

A

DNA content of every cell in a population

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21
Q

What are the controls of the cell cycle checkpoints?

A

Specific protein kinases and phosphatases

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22
Q

What do the controls of the cell cycle checkpoints ensure?

A

Strict alteration of mitosis and DNA replication

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23
Q

What are the three cell cycle checkpoints (and when do they happen)?

A 
Restriction point (end of G1)
G2/M phase checkpoint 
Mitotic checkpoint
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24
Q

What is checked at the restriction point?

A

DNA not damaged
Cell size
Metabolite/nutrient stores

25
What does the G2/M checkpoint check?
DNA completely replicated | DNA not damaged
26
What is colchicine used for?
Immune supression
27
What is checked at the mitotic checkpoint?
Chromosomes aligned on the spindle
28
When do extrinsic factors act on the cell cycle?
G1
29
What does CDK stand for?
Cyclin dependent kinases
30
What does CDK do?
Catalytic subunit
31
What does cyclin do?
Regulatory subunit
32
What is cyclin expression induced by?
Growth factors
33
What does an active cyclin-CDK complex do?
Phosphorylates specific substrates
34
What destroys the cyclin-CDK complex?
Proteasomes
35
What does post-translational phosphorylation result in?
Activation, inhibition or destruction
36
What is the retinoblastoma protein (RB)?
Key substrate of G1 and G1/S cyclin dependent kinases
37
How does RB normally work?
Unphosphorylated RB binds E2F transcription factor preventing its stimulation of S-phase protein expression - > RB is phosphorylated and E2F dissociates in the presence of cyclin D-CDK4 and cyclin E-CDK2 - > E2F stimulates expression of more cyclin E and S phase proteins - > DNA replication starts
38
What are some cyclin E and S phase promoters?
DNA polymerase, thymidine kinase, PCNA
39
What are some sequential activites in the cell cycle?
Mitogens in G1 phase signal to the nucleus - > drives early gene expression - > encode delayed genes - > cyclin D able to form active complexes with CDK4/6 - > hypophosphorylates RB - > allows some cyclin E expression which causes hyperphorphorylation of RB - > activation of E2F responsive genes - > cyclin E and CDK 2 phosphorylates and activates cyclin A and CDK 1 - > same happens to cyclin B and CDK1 - > RB dephosphorylation mediated by PP1
40
What does DNA damage trigger?
Cell cycle arrest or apoptosis
41
What is stopping of the cell cycle driven by?
CDKI genes
42
What things attempt DNA repair?
Nucleotide or base excision enzymes, mismatch repair etc
43
What causes programmed cell death?
BCL2 family or caspases
44
What happens if the cell senses DNA damage?
Cell cycle stops, DNA repair attempted, if not possible -> programmes cell death
45
What happens to TP53 in the normal cell?
Completely and continously destroyed by a proteasome
46
What happens to TP53 if there is DNA damage?
Kinases are activated - > phosphorylates TP53 - > phosphorylated TP53 can’t be destroyed by proteasome - > phosphorylated TP53 then accumulates
47
What are the functions of TP53?
Expression of CKI causing cell cycle arrest | DNA repair - if not possible it causes apoptosis
48
What mutations are the most frequent in cancer?
TP53 loss of function
49
What are the ways in which TP53 loss of function mutations cause cancer?
Prevent cell cycle arrest, apoptosis and DNA repair
50
How does the prevention of DNA repair lead to cancer?
More mutations -> more heterogenity -> more adaptation -> cancer progression
51
What are the types of chemo drugs?
S phase, M phase and colchicine
52
What do S phase drugs do?
DNA damage
53
What do M phase drugs do?
Mess up the mitotic spindle
54
What are the types of M phase drugs?
Vinca alkaloids, paclitaxel
55
What do vinca alkaloids do?
Stabalise free tubulin Prevent microtubule polymerisation Arrest cells in mitosis
56
What does paclitaxel do?
Stabalise microtubules Prevents depolymerisation Arrest cell in mitosis
57
What are the two types of S phase drugs?
5-fluorouracil and cisplatin
58
How does 5-fluorouracil work?
Prevents synthesis of thymidine
59
How does cisplatin work?
Binds to DNA causing damage and blocking repair

MBD/MI (Wothaya) (57 decks)

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