Session 7

Question 1

What determines the size of a cell population?

Answer 1

Depends on rate of cell proliferation, cell
differentiation and cell death by apoptosis. (Increased numbers are seen with increased
proliferation or decreased cell death).

Question 2

When can cells no longer divide?

Answer 2

Once they’re terminally differentiated.

Question 3

What regulates normal cell proliferation?

+ Problem if it’s not regulated?

Answer 3

• Proto-oncogenes regulate normal cell proliferation.
• Excessive physiological stimulation can become pathological, e.g., prostatic hypertrophy. (Cell proliferation occurs in physiological and pathological conditions.A cell may be producing hormones in excess, the cell function is physiological but the amount is pathological.)

Question 4

How is cell proliferation controlled?

Answer 4

• Largely by chemical signals from the
  microenvironment which either stimulate or
  inhibit cell proliferation.
• When a signalling molecule binds to a receptor it results in the modulation of gene expression.
• Receptors usually in cell membrane but can be in the cytoplasm or nucleus (e.g., steroid receptors).

Question 5

What can the chemical signals make the cell do? (4)

Answer 5

Survive – resist apoptosis

Divide – enter cell cycle

Differentiate – take on specialised form and function

Die – undergo apoptosis

(Complicated process but limited number of outcomes)

Question 6

Increased population growth occurs by: (2)

Answer 6

• Shortening the cell cycle

* Conversion of quiescent cells to proliferating cells by making them enter the cell cycle.

Question 7

When does a cell permanently exit from the cell cycle?

Answer 7

When it is terminally differentiated.

Question 8

What part of the cell cycle can’t be seen under the light microscope?

Answer 8

Interphase.

Question 9

What information can be gained from counting mitoses?

Answer 9

It gives the grade of the cancer (how dangerous that cancer is/how it’ll behave).

Question 10

What prevents cells with damaged DNA from replicating?

Name one way in which this defence is bypassed by cancerous cells?

Answer 10

• Checkpoints in cell cycle: damaged DNA or all of DNA not present -> cell will try to fix it -> if unable to do so, cell is pushed into apoptosis.
• The checkpoint alters.

Question 11

What is the restriction (R) point?

Answer 11

• Near the end of G1.
• Most critical checkpoint.
• Majority of cells that pass R point will complete cell cycle (Up until this point, the cell needs external stimulators in order to push it around the cycle but this point onwards, it can continue independently).
• Most commonly altered checkpoint in cancer cells (which allows cells with abnormal DNA to continue the cell cycle.)
• Checkpoint activation delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53.

Question 12

Which molecules control the cell cycle?

Answer 12

• Cyclin dependent kinases (CDKs) become active by binding with cyclins.
• CDK’s then phosphorylate another molecule and this allows the cell to go around the cell cycle.
• There are also inhibitors of CDKs
• Different cyclins produced at varying parts of the cell cycle. Must be produced in the correct order to ensure correct cell cycle. (See graph from notes)

(Often in cancers, mutations produce abnormal cyclins, CDK or CDK inhibitors –> problems with controlling of cell cycle)

Question 13

Describe how Cyclin works.

Answer 13

Cyclin binds to the enzyme and also to the substrate of the enzyme
Cyclin activates CDK
CDK phosphorylate said the target protein.