Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cancer Biology > DNA Repair and Oncogene- Induced Replication Stress > Flashcards

DNA Repair and Oncogene- Induced Replication Stress Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

What is neoplasia?

A

Tissue composed of cells with the ability to grow beyond their normal confines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is genomic instability linked to?

A

DNA damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is gammaH2AX?

A

A phosphorylated form of histones which is generated when DNA damage occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is ATM?

A

A DNA damage response kinase which signals in the presence of DNA breaks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Chk2?

A

A DNA damage response kinase which signals in response to DNA damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is p53?

A

A tumour suppressor which activates a DNA damage induced checkpoint, promoting apoptosis and senescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is increased DNA damage correlated with?

A

More 53BP1 foci which is correlated with increased p53 mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the stages of cancer progression?

A

Normal -> Hyperplastic -> Dysplastic -> Neoplastic -> Metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is hyperplasia?

A

The tissue appears normal but there are too many cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is dysplasia?

A

The cells appear abnormal and the relative number of different cell types are abnormal
Precancerous state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What two factors may be the cause of DNA damage in precancerous cells?

A

Telomere shortening and defects in the DNA repair proteins

Expression of oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In precancerous cells, what is the general trend?

A

The cells responding to DNA damage increase

Apoptosis increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In cancerous cells, what is the general trend?

A

Less cells respond to DNA damage than precancerous cells but more than normal cells
Apoptosis decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the less aggressive nature of precancerous lesions a result of?

A

Tumourigenesis barrier imposed by the DNA damage checkpoint (p53)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is responsible for the continuous levels of DNA damage in precancerous cells?

A

Oncogenes deregulate DNA replication -> leads to collapsed replication forks and DNA breaks which initiate DDR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the process of replication stress?

A

DNA replication -> Replication fork stalling due to anything which block replication e.g. bulky DNA lesions -> Replication fork collapse -> one-ended break

17
Q

How does transcription-replication collisions occur?

A

In a codirectional encounter - upregulation of transcription makes the replication fork catch up with the RNA polymerase and causes a collision
Head on encounters - The replication fork and the RNA polymerase hit each other head on

18
Q

In terms of replication, what do oncogenes cause?

A

Shortened G1 phase

Replication origins to fire in intragenic regions

19
Q

What is intragenic origin firing related to?

A

Increased transcription-replication collisions and formation of DNA breaks

20
Q

Why can R-loops be harmful?

A

They block DNA replication

21
Q

What prevents R loops?

A

RNA binding proteins

22
Q

What is SFPQ?

A

A splicing factor

23
Q

What happens if the splicing factor is removed?

A

Increase in single stranded DNA and DNA-RNA hybrid
Increased DNA replication
Increased DNA breaks due to collapse of replication forks
Increase DNA damage signalling
- Increased phosphorylation of H2AX
- Increased phosphorylation of Chk1

24
Q

What does SFPQ interact with?

A

DHX9 and RNA Pol II

25
Q

What is DHX9?

A

A DNA helicase (unwinds DNA)

26
Q

What does DHX9 loss cause?

A

DNA replication rescue

27
Q

In terms of R-loops, what does DHX9 KO cause?

A

No effect on R loops

28
Q

In terms of R-loops, what does DHX9 + SFPQ KO cause?

A

Reduction in R loops

29
Q

In terms of R-loops, what does SPFQ KO cause?

A

Gain in R loops

30
Q

If RNA pol II is phosphorylated on serine 2, what will it do?

A

Terminate RNA pol II

31
Q

If RNA pol II is phosphorylated on serine 5, what will it do?

A

Initiate RNA pol II

32
Q

If RNA pol II is phosphorylated on serine 2 and serine 5, what will it do?

A

Elongate RNA pol II

33
Q

How are R loops formed?

A

without splicing factors, DHX9 binds to the phosphorylated serine 2 of RNA pol I and doesn’t leave in the beginning like it is supposed to

34
Q

Where does DHX9 bind to RNA pol II in normal cells?

A

Serine 5

35
Q

What do R loops cause RNA pol II to do?

A

Be stuck on the DNA

36
Q

What is the pull down of splicing factors dependent on?

A

DHX9 and RNA

37
Q

How does DXH9 cause splicing factors to bid to RNA pol II?

A

DHX9 binds RNA secondary structures and unwinds the nascent transcript -> RNA binding proteins bind nascent RNA to form ribonuclear protein

38
Q

What happens if there is no DXH9?

A

RNA secondary structures persist, preventing the formation of RNA-DNA hybrid

39
Q

What happens if there is no RNA binding proteins?

A

Nascent RNA can pair with DNA complement to form RNA-DNA hybrid -> RNA pol II is trapped -> increased transcription-replication conflicts and genomic instability

Cancer Biology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions