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Block 9 Ellen > Cells and molecular biology of cancer > Flashcards

Cells and molecular biology of cancer Flashcards

1
Q

tumour=

A

abnormal growth of tissue that usually forms a mass

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2
Q

what is the cause of all cancer

A

genetic mutations

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3
Q

when do tumours arise

A

when balance between cell division and cell differentiation or death is disrupted

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4
Q

what cells do genetic mutations causing cancer have to be in

A

proliferating cells

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5
Q

what gene mutations are in most tumours

A

genes controlling cell cycle

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6
Q

5 stages of cell cycle

A 
M
G0 
G1
S
G2
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7
Q

interphase=

A

G1, G2, S (synthesis)

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8
Q

Gap 1 (G1)=

A

no visible changes but increase in cell contents (organelles, proteins ect)

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9
Q

Synthesis=

A

replication of DNA occurs, resulting in chromosomes becoming 2 sister chromatids

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10
Q

G2=

A

preparation for division process

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11
Q

g0=

A

not going through cell cycle

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12
Q

what ensures the cell cycle is happening in the right order

A

cyclin- CDK

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13
Q

what does cyclin- CDK do

A

signal stages of the cell cycle to happen

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14
Q

what controls cell cycle progression

A

transition points

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15
Q

what halts the cell cycle if the cell is unsuitable

A

checkpoint pathways

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16
Q

when is cyclin level highest in the cell

A

in mitosis

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17
Q

restriction point at_______

A

G1–> S

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18
Q

3 checkpoints in cell cycle

A
  • DNA damage checkpoint
  • DNA replication checkpoint
  • Mitotic spindle checkpoint
19
Q

what causes external signalling

A

growth factors

20
Q

internal signalling for the cell cycle can happen because of

A

DNA damage

21
Q

p53=

A

transcription factor

22
Q

what 2 proteins have a kinase activity and activate DNA repair and p53

A

ATM and ATR

23
Q

what happens to p53 after DNA damage

A

phosphorylation by ATM making p53 go into the nucleus and stimulate expression of many genes including p21

24
Q

what does p21 do

A

an inhibitor of cyclin and CDK leading to cell-cycle arrest

25
Q

what do most proto-oncogenes code for

A

components of the regulatory pathways of growth/ cell division

26
Q

how many mutations can enable oncogenes

A

1- mutation in one allele

27
Q

how many mutations in tumour suppressors genes to inactivate them

A

2- mutations in both alleles

28
Q

5 types of gene mutation

A
  1. point mutation
  2. gene amplification
  3. chromosomal translocation
  4. local DNA re-arrangement
  5. insetional mutagenesis
29
Q

2 main classes of tumour suppressor genes

A

caretakers and gatekeepers

30
Q

e.g of 2 gatekeepers

A

Rb

p53

31
Q

what does Rb control

A

G1—>S restriction point

32
Q

loss of gatekeeper causes

A

excessive cell proliferation

33
Q

caretakers—>

A

maintain genetic stability (e.gDNA repair) but not directly involved in controlling cell proiliferation

34
Q

e.g of caretaker

A

BRCA1 and 2

35
Q

when a cell detects DNA damage levels of what normally increase

A

p53

36
Q

where does p21 arrest the cell cycle

A

G1

37
Q

if there is no p53 what happens

A

cell will carry on the cell cycle even with DNA damages

38
Q

what instructs the DNA repair proteins to start repairing

A

ATM

39
Q

what usually keeps p53 at low levels

A

because its bound to Mdm2 which keeps its levels low via degradation

40
Q

what does Rb regulate

A

a transcription factor (keeping it away from the nucleus) which would otherwise start the expression of genes making the cell progress into the G1 phase

41
Q

what happens in tumours without Rb

A

transcription factor is always free to bind the DNA—> lots of proliferation

42
Q

what does viral factor E7 produced from HPV do

A

E7 binds to Rb and keeps it away from the transcription factor

43
Q

what does viral factor E6 produced from HPV do

A

sequesters p53 so it can no longer stop the cell cycle when DNA needs repair

Block 9 Ellen (21 decks)

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