Cells and molecular biology of cancer Flashcards

(43 cards)

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

21
Q

p53=

A

transcription factor

22
Q

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

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
what do most proto-oncogenes code for
components of the regulatory pathways of growth/ cell division
26
how many mutations can enable oncogenes
1- mutation in one allele
27
how many mutations in tumour suppressors genes to inactivate them
2- mutations in both alleles
28
5 types of gene mutation
1. point mutation 2. gene amplification 3. chromosomal translocation 4. local DNA re-arrangement 5. insetional mutagenesis
29
2 main classes of tumour suppressor genes
caretakers and gatekeepers
30
e.g of 2 gatekeepers
Rb | p53
31
what does Rb control
G1--->S restriction point
32
loss of gatekeeper causes
excessive cell proliferation
33
caretakers--->
maintain genetic stability (e.gDNA repair) but not directly involved in controlling cell proiliferation
34
e.g of caretaker
BRCA1 and 2
35
when a cell detects DNA damage levels of what normally increase
p53
36
where does p21 arrest the cell cycle
G1
37
if there is no p53 what happens
cell will carry on the cell cycle even with DNA damages
38
what instructs the DNA repair proteins to start repairing
ATM
39
what usually keeps p53 at low levels
because its bound to Mdm2 which keeps its levels low via degradation
40
what does Rb regulate
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
what happens in tumours without Rb
transcription factor is always free to bind the DNA---> lots of proliferation
42
what does viral factor E7 produced from HPV do
E7 binds to Rb and keeps it away from the transcription factor
43
what does viral factor E6 produced from HPV do
sequesters p53 so it can no longer stop the cell cycle when DNA needs repair