Brainscape's Knowledge GenomeTM

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


See full index

Cancer Biology > Oncogenes > Flashcards

Oncogenes Flashcards

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

What are oncogenes derivatives of?

A

Proto-oncogenes

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

Are oncogene mutations dominant or negative?

A

Dominant - only one allele needs to be mutated

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

What are oncogenes?

A

Positive regulators of cell growth and proliferation

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

What stages in the pathway to proliferation are a potential target for oncogenic transformation?

A

Growth factors
Growth factor receptors
Signal transducers
Nuclear proteins, transcription factors and coactivators

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

Mechanisms of mutations for an oncogene

A 
Point mutations/ deletion 
Chromosomal amplification 
Chromosomal translocation 
Retroviral insertion 
Retroviral transduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Are tumour suppressor genes dominant or negative?

A

Negative

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

2 examples of oncogenes which are caused by deletion or point mutations

A

Ras

Raf

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

2 examples of oncogenes which are caused by gene amplification

A

Abl

Myc

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

Example of an oncogene which are caused by chromosomal rearrangement - inset an enhancer

A

Ig enhancer: Myc

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

What is the chromosomal rearrangement required to produce the Ig enhancer Myc?

A

t[8:14]

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

Example of an oncogene which are caused by chromosomal rearrangement - gene fusion

A

BCR:Abl

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

What is the chromosomal rearrangement required to produce BCR:Abl

A

t[9:22]

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

What does gene fusion cause?

A

Excessive production of hyperactive fusion protein in the cell

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

Give an example of a virus which is inserted into a chromosome to induce insertional mutagenesis

A

ALV

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

3 examples of oncogenes which are caused by retroviral transduction

A

Ras
Abl
ErbB2

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

What causes activation of Ras in cancer making it constitutively active?

A

Viruses

Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 forms of Ras

A

H-
Ki-
N-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When is Ras normally activated in a cell?

A

When it is bound to GTP

19
Q

What are the effectors of Ras?

A

MAPK pathway
PI3K pathway
Rac
Ral

20
Q

How do you activate Ras?

A

Mutations at 12, 13 and 61 - constitutive Ras activation

NF1 deletion - no GAP to convert it back to RasGDP

21
Q

What is NF1?

A

Neurofibromin
negative regulator of Ras
GAP- GTPase activator protein

22
Q

What are the 3 forms of Raf?

A

A-
B-
C-

23
Q

What causes activation of Raf in cancer making it constitutively active?

A

Viruses

Mutations

24
Q

What is Raf?

A

A serine/threonine kinase

25
Q

What is the most common Raf mutation?

A

V600E (85% of mutations)

26
Q

What domain is Raf commonly mutated?

A

Clustered kinase domain

27
Q

What causes activation of c-Abl in cancer making it constitutively active?

A

Viruses
Mutations
Chromosomal translocations

28
Q

What is Abl?

A

a tyrosine kinase

29
Q

What is the philadelphia chromosome?

A

t[9:22]

30
Q

What disease is associated with Abl mutations?

A

Leukaemias

31
Q

How is Abl inactive in normal cells?

A

The N-terminal cap covers the active site of the catalytic domain

32
Q

Why is Abl active in tumour cells?

A

The N-terminal cap is changed to BCR and therefore does not inhibit the active site of the catalytic domain

33
Q

What causes activation of EGFR in cancer making it constitutively active?

A

viruses

mutations

34
Q

what is EGFR?

A

A receptor tyrosine kinase

35
Q

How is EGFR overactivated?

A

Mutated so it does not need EGF

EGF is overexpressed so EGFR is always saturated

36
Q

Where s c-Myc located?

A

Nucleus

37
Q

What causes activation of c-Myc in cancer making it constitutively active?

A

Chromosomal translocation

38
Q

What cancer is associated with c-Myc?

A

Burkitt lymphoma

39
Q

What is c-Myc

A

a transcription factor

also regulates translation

40
Q

How does Myc promote cell cycle progression?

A

Binds to MAX as a heterodimer
binds to the promoter of target genes
activates cyclins
promote cell cycle progression

41
Q

Why is c-Myc only generally a cell proliferation promoter?

A

If it is injected into a fibroblast without serum, it will stimulate apoptosis

42
Q

Give an example drug treatment for BCR:Abl, how it works and for what disease

A

Gleevac
Structural deregulation of the kinase domain in BCR-Abl by binding to it
Chronic myeloid leukaemia

43
Q

Give 2 examples drug treatment for EGFR, how it works and for what disease

A

Getfitinib
Binds to the active site and blocks it in EGFR ErbB2
Non-small cell lung cancer, and other cancers

Herceptin
Ab against the EGF binding site
Currently in clinical use, so no specific cancer

Cancer Biology (13 decks)

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