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Lecture 5 Flashcards

Ch.5 The cell cycle (52 cards)

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1
Q

What was Rudolf Virchow the first one to propose?

A

That all cells arise from pre-existing cells

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2
Q

What phases does the interphase include?

A

Everything except of the M-phase

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3
Q

What is the order of the phases?

A

G1, S, G2, M, G0

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4
Q

What happens in the S-phase?

A

Replication, where cohesin holds the sister chromatids toghether

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5
Q

What happens in the M-phase?

A

The creation of 2 cells with the mitotic spindle

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6
Q

What is the order of the phases that can be found within the M-phase?

A

Pro/prometaphase, metaphase (neatly alligned chr.), anaphase (separate chr.), telophase/cytokinesis (pinch off the 2 cells)

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7
Q

What is the function of the G1 phase?

A

Growing, make nucleotides and prepare for DNA synthesis

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8
Q

What is the function of the G2 phase?

A

Prepare for mitoses and growing

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9
Q

What is the function of CDK’s and when are they active?

A

They control the cell cycle and are active when cyclin is bound

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10
Q

Which CDK and cyclin match with the G1 phase?

A

CDK4/6 and cyclin D

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11
Q

Which CDK and cyclin match with the S phase?

A

CDK2 and cyclin A and E

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12
Q

What is the function of CDK2?

A

Phosphorylating factors that are needed for DNA replication

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13
Q

Which CDK and cyclin match with the G2/M phase?

A

CDK1 and cyclin B

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14
Q

What is the function of CDK1?

A

To proceed the cell from the G2 to the M phase

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15
Q

What happens with the cyclin levels in the cell?

A

They fluctuate and set the stage (phase) that the cell is in

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16
Q

How are the cyclin levels controlled?

A

With the use of transcription and proteolytic degradation (Ubiquitin-mediated)

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17
Q

What happens with Cycling B and how does that happen?

A

It is high until the metaphase and quickly declines before the anaphase with the use of ubiquitin-mediated proteolysis by APC/C

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18
Q

What is the result of less cyclin B?

A

There is less CDK1, which then triggers mitotic progression

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19
Q

What is the function of CDKi’s?

A

These are proteins that inhibit CDK activity (eg p21, p16)

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20
Q

Which molecules are involved in the phosphoregulation of CDK?

A

Wee1/Myt1 : phosphorylate to inactivate
Cdc25 : dephosphorylate to activate
CAK : phosphorylates to activate

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21
Q

Which two ways are there for CDKi’s to inhibit?

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A

Either by binding to the place of cyclin or inhibit the already assembled complex

22
Q

What is checked in the G1-S checkpoint?

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A

Whether the conditions are favourable to enter the S phase and whether the DNA is intact enough

23
Q

What is the function of E2F in the G1-S checkpoint?

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A

It drives a program that is required for the S-phase

24
Q

What is the result of inhibiting E2F via Rb?

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A

It prevents the S-phase genes from being expressed.

25
How is the inhibition done of E2F via Rb?
Rb bind to E2F and HDAC is recruited
26
What is the result of Rb phosphorylation by cyclin D/CDK 4?
HDAC is released and there is transcription of cyclin E
27
What is the result of Rb phosphorylation by cyclin E/CDK 2?
If this is done after cyclin D/CDK 4 it also gives cyclin E transcription and full E2F activation so the cell can go into the S phase
28
What is the result of genotoxic stress?
p53 in activated, which activates p21, which inhibits CDK2, so there is no progression into the S-phase
29
What is the purpose of the G2-M checkpoint?
Mitosis is prevented if the DNA is damaged
30
What are the key component of the G2-M checkpoint?
ATM and ATR kinases, they inhibit CDK activity via phosphorylation
31
What is ATM (and CHK2) signaling also required for?
For inducing p53/p21 in G1 phase
32
What is the purpose of the mitotic checkpoint?
To check whether all chr. are properly attached to the spindle
33
What are important mediators of the mitotic checkpoint?
Aurora kinases
34
What is the result if not all the chr. are attached properly?
It is arrested in the metaphase, due to inhibition of cyclin B ubiquitination (thus degradation)
35
Where can most checkpoint defects be found?
In the G1-S phase
36
What cancers are a consequence of upregulation of cyclin D1?
It can lead to breast, head and neck and esophagul cancer
37
What cancers are a consequence of the loss of Rb?
Prostate, bladder, lung, breast cancer, retinoblastoma and osteosarcoma
38
What cancers are a consequence of ATM kinase mutation?
Neurodegenerative diseases, higher risk of lymphoma and leukemia
39
What cancers are a consequence of p53 mutation?
Li-Fraumeni syndrome, high risk of sarcoma, leukemia and breast cancer
40
What cancers are a consequence of aurora kinase mutations?
Amplification, mitotic defect, aneuploidy, high risk of breast, colon and pancreatic cancer
41
What is the role of aneuploidy in cancer?
It is very common in cancer. But it is uncertain whether it is the driver or a consequence
42
In which checkpoint are mutations rarely found?
In the mitotic checkpoint
43
What is the function of DNA damaging agents in cancer treatment?
To activate the DNA integrity checkpoints (eg with the use of radiation, doxorubucin and PARP inhibitor)
44
Which drug does mitotic checkpoint activation?
Taxol
45
What does Taxol do?
It takes away the mitotic spindles, thus there is mitotic arrest (cells curl up)
46
What other type of treatment is used for cancers?
Targeting the cell cycle kinases
47
What are the master regulators of DNA damage checkpoints?
ATM and ATR, their targeting for treatment is explored
48
What is the ultimate treatment plan?
Combining ATM/ATR inhibition with radiation or cytostatic treatment
49
What is the drug Palbociclib used for?
It is a CDK4/6 inhibitor that is used for breast cancer (arrest cells in G1), is not useful in all cancers and some are resistant
50
What is the reason that not all cells are sensitive to Palbociclib?
There is a mutation in Rb, E2F etc which lowers the sensitivity
51
What study was done to see whether any genes were involved with this insensitivity or higher sensitivity?
Some cells were treated with palbociclib and it was found that a less of the ARMBRA1 gene leads to more cyclin D1, so enter the G1/S, thus you need less CDK4/6
52
The inhibition of which gene is detrimental to cells that overexpress cyclin E?
The inhibition of PKMYT1 (which regulates CDK phosphorylation)

Oncology (8 decks)

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