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Cellular Growth Regulation Flashcards

1
Q

What is the difference between hyperplasia and hypertrophy?

A 
Hyperplasia= increase in cell NUMBER
Hypertrophy= increase in cell SIZE
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2
Q

Give an example of cellular hypertrophy?

A

Exercising—>Bigger Heart–>Increase in cell size NOT number

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3
Q

The growth of a population of cells depends on the integration of what?

A

Intra and extracellular signals

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4
Q

What do intra and extracellular signals check? (4 examples)

A

1) Cellular Pathology
2) Growth
3) Inhibitory Factors
4) Cell Adhesion

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5
Q

What is one key difference between growth at cellular level and a population of cells in terms of hyperplasia and hypertrophy?

A

At growth at the cellular level (cell cycle) it is due to increase in size (hypertrophy) and cell division.
Growth of a population of the cells you have to distinguish between hyperplasia and hypertrophy.

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6
Q

List the cell cycle phases?

A

G1, S,G2,M

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7
Q

What is the progression of the cell cycle controlled by?

A

Three key checkpoints- restriction points

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8
Q

Define Apoptosis?

A

A coordinated program of cell dismantling ending in phagocytosis

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9
Q

Define Necrosis?

Is apoptosis similar to necrosis or not?

A

Necrosis is the death of most/all cells due to injury or poor blood supply. Apoptosis is distinct from necrosis

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10
Q

Necrosis occurs as a response to injury or blood loss.

What does apoptosis respond to?

A

DNA damage and viral infection

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11
Q

What are mitogens?

A

Proteins that stimulate proliferation

triggers mitosis , hence the name

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12
Q

What do growth factors, cytokines and interleukins do?

A
  • Stimulate Proliferation
  • Maintain Survival
  • Stimulate Differentiation
  • Inhibit Proliferation
  • Induce Apoptosis
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13
Q

What is a growth factor that?

  • Inhibits Proliferation
  • Induces Apoptosis
A
  • TGFbeta

- TNFalpha and other members of the TNF family

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14
Q

What are the three broad classes of growth factors, cytokines and interleukins

A

1) Paracrine
2) Autocrine
3) Endocrine

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15
Q

Briefly describe the differences between paracrine, autocrine and endocrine?

A 
Paracrine= Stimulates proliferation of a diff cell type with correct receptor
Autocrine = When a cell signals to itself 
Endocrine= Distant signals (hormones that act on distant target cells)
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16
Q 
On a graph where you're measuring the log of cell number over days 
What effect would 
-GF addition
-GF removal
-Growth Inhibitor
-Death signal
-Protein running out
A
  • Addition = cell number increasing
  • Removal = Graph will plateau
  • Inhibitor = Graph will plateau
  • Death signal = Graph will decline
  • Protein running out = Graph will plateau
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17
Q

Give an example of a growth factor and inhibitor

A

Growth factor = PDGF

Growth Inhibitor = TGFbeta

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18
Q

What occurs in the interphase of the cell cycle?

A

Cell GROWS in size
Make more cytoskeleton to grow
Macromolecules synthesised continuously

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19
Q

What occurs in the S phase of the cell cycle?

A

DNA Replication
Incorporate Thymidine
2n—>4n for G2 and M

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20
Q

What occurs in the G0 phase in the cell cycle?

A

Quiescent Cells - Cells that are not dividing but some can re-enter the cell cycle or some go through terminal differentiation

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21
Q

What occurs after terminal differentiation?

A

Cell shredding- APOPTOSIS

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22
Q

What is a fluorescence activated cell sorter analysis used for?

A

Used to check whether cells are growing and what stage they are in

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23
Q

Explain the steps in using a fluorescence activated cell sorter analysis

A

1) Take cells and label DNA with dye
2) Dye read by laser- laser indicates how intense DNA content is
3) Machine determines how fluorescent the nuclei of cells are in each phase
4) Cells not growing that fast = G1
5) Cells can be treated with GF’s to see effects

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24
Q

“DNA is replicated semi-conservatively”

What does this mean?

A

Daughter cells inherit one parental and one new strand

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25
What direction in new DNA synthesised in?
5' to 3'
26
How is new DNA synthesised?
From a deoxynucleotide triphosphate precursor at a replication fork by a multicomplex enzyme
27
What is Fidelity? AND How is it Determined?
Fidelity= how much of a exact copy something is Determined by two things: 1)Base Pairing 2)Presence of proof reading enzyme in DNA Pol
28
Synthesis of the new DNA strand uses an RNA primer and occurs continuously on which strand? Discontinuously on which strand?
Continuously on the LEADING STRAND Discontinuously strand on the TRAILING STRAND
29
What does the trailing strand give rise to?
Okazaki fragments RNA primer removed Okazaki fragments ligated together
30
What are the 4 main stages of Mitosis?
1) Prophase 2) Metaphase 3)Anaphase 4)Telophase and then its not a phase but cytokinesis
31
What occurs during Prophase?
- Nucleus becomes less definite - Micro-tubular spindle apparatus assembles - Centrioles migrate to poles
32
What occurs between prophase and metaphase but isn't a phase itself?
Prometaphase - Nuclear membrane breaks down - Kinetochores attach to spindle in nuclear region
33
What occurs in metaphase?
-Chromosomes align in the equatorial plane
34
What occurs in Anaphase?
-Chromatids separate and migrate to opposite poles
35
What occurs in Telophase?
Daughter nuclei form
36
What happens after telophase?
Cytokinesis - Division of cytoplasm - Chromosomes decondense
37
What are 2 drugs that act in the S phase ( S phase active)?
5-Fluorouracil | Bromodeoxyuridine
38
What does 5-Fluorouracil do?
An analogue of thymidine | Blocks thymidylate synthesis
39
What does Bromodeoxyuridine
Analogue of thymidine | Can be incorporated into DNA --> Detected by antibodies -->Identify cells that have passed through the S-Phase
40
What are 3 drugs that act in the M Phase (M Phase Active)?
1) Colchicine 2) Vinca Alkaloids 3) Paclitaxel
41
What does Colchicine and Vinca Alkaloids do?
-Stabilises free tubulin -Prevents microtubule polymerisation -Arresting cells in mitosis Used in Karyotype Analysis
42
What does Paclitaxel/Taxol do?
- Stabilises Microtubules | - Prevents de-polymerization
43
What are 4 drugs you can use in the treatment of cancer?
5-Flurouracil Paclitaxel Vinca Alkaloids Tamoxifen
44
What are cell cycle checkpoints?
Controls (involving specific protein kinases and phosphatases) ensure the strict alternation of mitosis and DNA replication
45
What is the cell cycle checkpoints before? -S Phase -M Phase And during metaphase
Before S phase = DNA not damaged, Cell Size and Metabolite Before M Phase = DNA completely replicated and DNA not damaged During Metaphase = Chromosomes alligned on spindle
46
Which phase is the only phase in which cells can respond to extracellular molecules eg mitogens
G1
47
Explain the regulation of cyclin-CDK Activity?
Balance between Cyclical Synthesis (Gene expression) and Destruction (By Proteasome) Post translational modification by phosphorylation - depending on the modifications site it could result in activation, inhibition or destruction.
48
What do active Cyclin-CDK complex do?
Phosphorylate specific substrates
49
How many genes in the CDK subunit and Cyclin regulatory subunit?
``` CDK = 10 Genes Cyclin = > 20 Genes ```
50
``` Match up -CDK -Cyclin TO: -Regulatory -Catalytic ```
CDK - Catalytic Subunit (10 genees) | Cyclin - Regulatory Subunit (<20 genes)
51
How do you dephosphorylate substrates ?
Binding of CDK inhibitors
52
Pick one of the following the best describes the action of the retinoblastoma protein: - Tumour Activation - Tumour Suppressing - Transcription Factor
Tumor Suppressing
53
What does tumour suppressor mean in terms of retinoblastoma?
It inhibits the progression of the cell cycle It acts in the G0 and G1 phase to decide if a cell is ready to move to the S phase If the DNA is damaged (ie tumour) retinoblastoma would inhibit the cell from progressing in the cell cycle and therefore suppresses the tumour
54
In the absence of D-CDK's , how does Retinoblastoma act?
In their absence, RB wont be phosphorylated which means it can bind to the transcription factor E2F, this inactivates the TF so that the cell cycle progression is inhibited
55
In the presence of D-CDK's, how does retinoblastoma act?
As D-CDK's are KINASES, they phosphorylate, so they phosphorylate RB and it can no longer bind to E2F. E2F is released from the complex , makes more cyclin E (needed for the CDK's to work) and S-Phase proteins. As E2F is a TF- it makes components needed for cell growth
56
What types of the cyclin are needed for CDK4 and CDK2 (these are the CDK's used to phosphorylate RB)?
Cyclin D- CDK4 Cyclin E- CDK2 Remember this because the transcription factor is E2f, so cyclin E must match with CDK2
57
What two families of CDK inhibitors are there?
1) CIP/KIP , now called CDKN1 | 2) INK4 , now called CDKN2
58
This question relates to CDKN1 only 1. What is it weakly stimulated by? 2. What is it strongly stimulated by? 3. What CDK-cylin complexes does it inhibit? 4. Which stage in the cell cycle is it sequestered and how?
1. TGFbeta 2. DNA Damage 3. All other CDK-Cyclin complexes 4. Gradually sequestered by G1 CDK's so later CDK's are activated
59
This question relates to CDKN2 only? 1. What is it stimulated by? 2. Which CDK-Cyclin complexes does it inhibit
1. TFGbeta | 2. Specifically inhibit G1 CDK's
60
Explain how an increase in mitogens results in an increase in cyclin expression?
1. Mitogens induce GF to bind to GFr 2. This results in signal transducers being activated 3. There is a kinase cascade 4. (Nucleus) Transcription begin begins, codes for proteins
61
What activates : - G1 CDK's - Late CDK's
G1 CDK's are activated in response to environmental signals | Late CDK's are activated in responses to preceding kinase activities
62
What dephosphorylates hyperphosphorylated RB?
Protein phosphatase 1
63
Out of G1 CDK's and late CDK's which ones hyperphosphorylate and hypophosphorylate ?
G1 CDK's HYPOphosphorylate | Late CDK's HYPERphosphorylate
64
Explain the sequence of events triggered by growth factors that help the cell get through S-phase and mitosis
1. Growth factor signalling activates early gene expression 2. Early gene products stimulate delayed gene expression (includes Cyclin D, CDK2/4 and E2F) 3. E2F sequestered by binding to unphosphorylated RB 4. G1 cyclin-CDK complexes hypophosphorylate RB and then G1/S cyclin-CDK complexes hyperphosphorylate RB releasing E2F 5. E2F stimulates expression of more Cyclin E and S-phase proteins (e.g. DNA polymerase, thymidine kinase, Proliferating Cell Nuclear Antigen etc.)  6. S-phase cyclin-CDK and G2/M cyclin-CDK complexes build up in inactive forms. These switches are activated by post-translational modification or removal of inhibitors, driving the cell through S-phase and mitosis.
65
This question is about DNA Damage: - How is it detected? - What does it trigger? - If you attempt to repair DNA damage , and it works what will happen? What will happen if you cant repair it?
- Detected at checkpoints - Triggers Apoptosis - If repaired = re-enters cell cycle - If not repaired = Apoptosis
66
Explain how TP53 responds to DNA Damage?
1. There is a mutation in DNA 2. This damage is detected by kinases (ATM , ATR) 3. Kinases activate checkpoint 2 4.P53 is phosphorylated so cant be degraded 5.P53 becomes a stabilised protein - bind to promoters of TFs 6. Express genes required for DNA repair (IF cant repair - APOPTOSIS)

Cellular Pathology (13 decks)

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