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Cellular Pathology > Cellular Growth Regulation > Flashcards

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
Q

What direction in new DNA synthesised in?

A

5’ to 3’

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26
Q

How is new DNA synthesised?

A

From a deoxynucleotide triphosphate precursor at a replication fork by a multicomplex enzyme

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27
Q

What is Fidelity?
AND
How is it Determined?

A

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
Q

Synthesis of the new DNA strand uses an RNA primer and occurs continuously on which strand?
Discontinuously on which strand?

A

Continuously on the LEADING STRAND

Discontinuously strand on the TRAILING STRAND

29
Q

What does the trailing strand give rise to?

A

Okazaki fragments
RNA primer removed
Okazaki fragments ligated together

30
Q

What are the 4 main stages of Mitosis?

A

1) Prophase
2) Metaphase
3)Anaphase
4)Telophase
and then its not a phase but cytokinesis

31
Q

What occurs during Prophase?

A
  • Nucleus becomes less definite
  • Micro-tubular spindle apparatus assembles
  • Centrioles migrate to poles
32
Q

What occurs between prophase and metaphase but isn’t a phase itself?

A

Prometaphase

  • Nuclear membrane breaks down
  • Kinetochores attach to spindle in nuclear region
33
Q

What occurs in metaphase?

A

-Chromosomes align in the equatorial plane

34
Q

What occurs in Anaphase?

A

-Chromatids separate and migrate to opposite poles

35
Q

What occurs in Telophase?

A

Daughter nuclei form

36
Q

What happens after telophase?

A

Cytokinesis

  • Division of cytoplasm
  • Chromosomes decondense
37
Q

What are 2 drugs that act in the S phase ( S phase active)?

A

5-Fluorouracil

Bromodeoxyuridine

38
Q

What does 5-Fluorouracil do?

A

An analogue of thymidine

Blocks thymidylate synthesis

39
Q

What does Bromodeoxyuridine

A

Analogue of thymidine

Can be incorporated into DNA –> Detected by antibodies –>Identify cells that have passed through the S-Phase

40
Q

What are 3 drugs that act in the M Phase (M Phase Active)?

A

1) Colchicine
2) Vinca Alkaloids
3) Paclitaxel

41
Q

What does Colchicine and Vinca Alkaloids do?

A

-Stabilises free tubulin
-Prevents microtubule polymerisation
-Arresting cells in mitosis
Used in Karyotype Analysis

42
Q

What does Paclitaxel/Taxol do?

A
  • Stabilises Microtubules

- Prevents de-polymerization

43
Q

What are 4 drugs you can use in the treatment of cancer?

A

5-Flurouracil
Paclitaxel
Vinca Alkaloids
Tamoxifen

44
Q

What are cell cycle checkpoints?

A

Controls (involving specific protein kinases and phosphatases) ensure the strict alternation of mitosis and DNA replication

45
Q

What is the cell cycle checkpoints before?
-S Phase
-M Phase
And during metaphase

A

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
Q

Which phase is the only phase in which cells can respond to extracellular molecules eg mitogens

A

G1

47
Q

Explain the regulation of cyclin-CDK Activity?

A

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
Q

What do active Cyclin-CDK complex do?

A

Phosphorylate specific substrates

49
Q

How many genes in the CDK subunit and Cyclin regulatory subunit?

A 
CDK = 10 Genes
Cyclin = > 20 Genes
50
Q 
Match up 
-CDK
-Cyclin
TO:
-Regulatory
-Catalytic
A

CDK - Catalytic Subunit (10 genees)

Cyclin - Regulatory Subunit (<20 genes)

51
Q

How do you dephosphorylate substrates ?

A

Binding of CDK inhibitors

52
Q

Pick one of the following the best describes the action of the retinoblastoma protein:

  • Tumour Activation
  • Tumour Suppressing
  • Transcription Factor
A

Tumor Suppressing

53
Q

What does tumour suppressor mean in terms of retinoblastoma?

A

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
Q

In the absence of D-CDK’s , how does Retinoblastoma act?

A

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
Q

In the presence of D-CDK’s, how does retinoblastoma act?

A

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
Q

What types of the cyclin are needed for CDK4 and CDK2 (these are the CDK’s used to phosphorylate RB)?

A

Cyclin D- CDK4
Cyclin E- CDK2
Remember this because the transcription factor is E2f, so cyclin E must match with CDK2

57
Q

What two families of CDK inhibitors are there?

A

1) CIP/KIP , now called CDKN1

2) INK4 , now called CDKN2

58
Q

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?
A
  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
Q

This question relates to CDKN2 only?

  1. What is it stimulated by?
  2. Which CDK-Cyclin complexes does it inhibit
A
  1. TFGbeta

2. Specifically inhibit G1 CDK’s

60
Q

Explain how an increase in mitogens results in an increase in cyclin expression?

A
  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
Q

What activates :

  • G1 CDK’s
  • Late CDK’s
A

G1 CDK’s are activated in response to environmental signals

Late CDK’s are activated in responses to preceding kinase activities

62
Q

What dephosphorylates hyperphosphorylated RB?

A

Protein phosphatase 1

63
Q

Out of G1 CDK’s and late CDK’s which ones hyperphosphorylate and hypophosphorylate ?

A

G1 CDK’s HYPOphosphorylate

Late CDK’s HYPERphosphorylate

64
Q

Explain the sequence of events triggered by growth factors that help the cell get through S-phase and mitosis

A
  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
Q

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?
A
  • Detected at checkpoints
  • Triggers Apoptosis
  • If repaired = re-enters cell cycle
  • If not repaired = Apoptosis
66
Q

Explain how TP53 responds to DNA Damage?

A
  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
  4. Express genes required for DNA repair
    (IF cant repair - APOPTOSIS)

Cellular Pathology (13 decks)

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