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BMS247 Stem Cells > L12 - Oncogenes > Flashcards

L12 - Oncogenes Flashcards

1
Q

What quantity of tumours are induced by viruses

A

Minority

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2
Q

How many genes do viral genomes have

A

Few genes

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3
Q

What can be said about the few genes that viruses do contain

A

They are enough to drive the tumour phenotype

  • Extremely potent genes which perturb the complex regulatory circuit of the host cells that they infext
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4
Q

RSV

A

Rous Sarcoma Virus

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5
Q

How was the carcinogenic agent in RSV discovered

A

Chicken with sarcoma in breast
Sarcoma removed and ground with sand
Collect filtrate that had passed through a fine-pore filter
Inject filtrate into a young chicken
Observe the formation of a sarcoma in the injected chicken

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6
Q

What are foci

A

Clusters of tumour cells which appear after infection

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7
Q

Describe the morphology of the foci and how they grow

A

Rounded cells that grow one on top of the other

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8
Q

What characteristics of the foci is similar to the cells of the tumour

A

Have similar metabolism

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9
Q

Define cell transformation

A

Converstion of a normal cell into a cancer cell

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10
Q

Describe the transmission of the cancer between the cells of the foci

A

Transformed phenotype was transmitted from the initially infected cells to its descendents

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11
Q

What is a TS RSV mutant

A

RSV virus which carries a temperature sensisitve mutation

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12
Q

Describe how the TS RSV mutant functions

A

Proteins are able to function at the permissive temperature (37) if raised about this the proteins don’t have TW function

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13
Q

What can be said of the dependence of the transformed phenotype on the virus

A

Viral transforming gene is required to initiate and maintain the transformed phenotype of the infected cells

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14
Q

Properties of transformed cells

A 
Altered morphology 
Loss of contact inhibition 
Ability to grow w/o attachment 
Ability to proliferate indefintely 
Reduced requirement for MGFs 
High saturation density 
Inability to halt proliferation in the absence of GFs 
Increased uptake of glucose 
Tumorigenicity
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15
Q

How many genes in the RSV virus

A

4

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16
Q

What are the four genes in RSV

A

Gag, Pol, Env, C

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17
Q

What is the effect of the removal of Gag, Pol and Env

A

Virus is unable to replicate but is still able to transform other cells

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18
Q

What is the effect of the removal of X

A

Virus is able to replicate but is unable to induce cell transformation

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19
Q

The single gene required for transformation is known as

A

Src

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20
Q

How many genes are required for replication of the RSV virus

A

3,

Gag, pol and env

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21
Q

What is the derivations behind the name Src

A

Ability to induce a sarcoma in the chicken

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22
Q

What can be used to understand the origin and functions of Src especially useful to be able to follow it in infected cells

A

Src specific DNA probe

23
Q

Src when it is normally found in organisms is known as

A

C-Src

24
Q

What type of Src is found in viruses

What can it act as

A

V-Src

Potent oncogene

25
Q

What is an oncogene

A

Gene which is able to transform a normal cell into a tumour one

26
Q

What type of gene is C-src

What is it a precurrsor to

A

Proto-oncogene

Precursor of an active oncogene

27
Q

What are the two hypothesies to describe how oncogenes become activated

A

Through endogenous retroviruses

Induction through mutants

28
Q

Describe how you would be able to identify wether chemicall transformed cells are able to carry mutated genes

A

TRANSFECTION STUDIES
Chemically transform mouse fibroblasts
Isolate DNA - transfect using calcium phosphate
Inject into normal mouse fibroblasts
Formation of a focus of morphologically transformed cells
Injection of morphologically transformed cells into mouse host
Formation of a tumour

29
Q

What was the overall conclusion of the transfection studies

A

Donor tumour DNA carried by one or several genetic elements is able to convert a normal cells into a tumorigenic one

30
Q

Oncogenes detected by transfection were derived from ____

A

Pre-existing normal cellualr genes which lack previously lacked oncogenic function - similar scenario to the viral oncogenes

31
Q

Give an example of an oncgoene detected in human bladder carcinoma

A

H-Ras

32
Q

Is H-Ras expressed through gene amplification

A

No - mutation present in only the one copy

33
Q

What is the mutation which must occur in order for h-Ras to become oncogenic

A

Point mutation at residue 12

Glycine –> Valine

34
Q

Describe the method which is used to identify the sequence which has changed

A

Creation of hybrids - 1/2 and 1/2 of the known cancer and normal
If the hybride can transform you know thar THE CANCER HALF CONTAINS THE MUTATED SEQUENCE
Perform again

35
Q

What are the 3 Ras proteins

What do they have in common

A

H, K and N Ras

Point mutations are able to convert from protooncogenes to oncogenes

36
Q

Describe the cycling seen in small GTPases

A

cycle between the active form - with GTP bound
AND
The inactive form with GDP bound

37
Q

What is required to activated Ras

A

GEF

38
Q

What is required to cause a cessation in the signalling of Ras

A

GAPS

39
Q

What is significant about Ras G12V (Glycine –> Valine at position 12)

A

It is unable to hydrolyse GTP

Protein is consituitively active

40
Q

In the presence of no growth factor describe the activity of the Ras G12V

A

ONCOGENIC RAS

No growth factor but mutant RAS is always ON
Leading to cell division and proliferation

41
Q

What are the four immediate downstream targets of Ras

A

RAF
PI3K
RALGDS
PLC

42
Q

How many mechanisms are there which would lead to the activation of the myc oncogene

A

3

43
Q

What are the three mechanisms leading to oncogenic transformation of myc

A

1) Expression driven by normal promoter but gene is amplifyed
2) Chromosomal translocation
3) Pro-virus integration causing an insertional mutagenesis

44
Q

How does Expression driven by normal promoter but gene is amplifyed arise?

A

More than 2 copies => high levels of gene product

45
Q

What can be said about the prognosis of myc at the various copy levels

A

With a higer myc copy number the prognosis for patients is worse

46
Q

How many chromosomal translocation cause oncogenic activation of Mtc

A

C-myc would be under the control of a foreign promoter

**Most common to have Myc expressed under a Ig (immunoglobin) promoter

47
Q

During a chromosomal translocation is there any change to the strucutre of myc

A

NO

Strucutall normal but is expressed at high ammounts

48
Q

Wht type of lymphoma is caused by a chromosomal translocation affecting myc

A

Burkitt lymphoma

49
Q

What is ALV

A

Avian leukosis virus

50
Q

Describe how pro-virus integration may lead to elevated myc expression

A

Virus integrates immeidatly adjacent to the myc gene so expression of myc is now driven by the active viral promoter leads to an INCREASE IN GENE PRODUCT

51
Q

Describe how changes in the EGF receptor may form ocogenees

A

Trucation of the EC ligand bidning domain results in a consituitively active receptor

52
Q

What is the normal structure and mechanism of activation of the EGF receptor

A

EC ligand binding domain - when a growth factor binds here the IC domain is able to signal

53
Q

What are 4 ways in which EGF signalling could be manipulated to oncogenic levels

A

Over expression of EGF ligand
Overexpression of the receptor
Ligand independent dimerisation (dimerisation in the absence of ligand biinding)
Mutations resulting in the formation of a constituitvelt active receptor

BMS247 Stem Cells (14 decks)

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