Tumour Suppressor Genes, Cell Cycle Clock Flashcards

1
Q

What happens to TSGs for cancer to occur?

A

Dysregulated inhibition

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2
Q

During what process can the heterozygosity of Rb be lost?

A

Meiosis

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3
Q

What are some mechanisms for the loss of heterozygosity in Rb?

A

Gene conversion
Hemizygosity - section of chromosome discarded
Nodisjunction- error in segegration of chromosomes during mitosis

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4
Q

Epigenetic mechanism of TSG inactivation

A

Promoter methylation

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5
Q

What induces cell proliferation?

A

Mitogens

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6
Q

What parts in the cell cycle are similar between cancerous and normal cells?

A

S-M

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7
Q

What parts in the cell cycle are different between cancerous and normal cells?

A

Cells responsive to extracellular signals during G1 until R and dysregulation at the R point causes many cancers

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8
Q

What drives the cell cycle clock?

A

CDK-cyclin complexes

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9
Q

Most cyclinsare driven by programmed fluctuations throughout the cell cycle, which cyclin does not?

A

D Cyclins

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10
Q

What controls the levels of D cyclins?

A

Mitogens

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11
Q

What tips cells beyond the R point transition?

A

pRb (Protein of Rb)- Guardian of the Restriction Gate

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12
Q

What 2 cyclins are responsible for phosphorylating pRb and when?

A

D Cyclin-CDK4/6 complexes phosphorylates the protein to do the hypophosphorylated state.
E Cyclin rises during the R point and E Cyclin-CDK2 phosphorylates the protein to the hyperphosphorylated state.

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13
Q

How is pRb disregulated?

A
Mutation of Rb
Methylation of the Rb promoter
Inactivation by viral oncoproteins
Excessive accumulation of cyclin D1
Inhibition of pRb phosphorylation at M/G1 transition by PP1 phosphotase
Inhibition of CKIs
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