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Year 2 > Biology and molecular biology of cancer II > Flashcards

Biology and molecular biology of cancer II Flashcards

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1
Q

What is an oncogene?

A

An oncogene is a gene that has the potential to cause cancer

An overactivity mutation of one gene creates an oncogene

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2
Q

What is a tumour suppressor gene?

A

is a gene that regulates a cell during cell division and replication. If the cell grows uncontrollably, it will result in cancer.
2 inactivating mutations functionally eliminates the tumour suppressor gene promoting cell transformation

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3
Q

Which type of mutation leads to an oncogene being formed?

A

An overactivity mutation

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4
Q

What is an overactivity mutation?

A

A function is gained

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5
Q

Which type of mutation leads to a tumour suppressor gene being formed being formed?

A

An under activity mutation

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6
Q

What is an under activity mutation?

A

Loss of a function

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7
Q

Define oncogenesis

A

The process of activation of photo oncogenes to oncogenes

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8
Q

What can oncogenesis include?

A
  1. Retroviral integration
  2. Point mutations
  3. Insertion mutations
  4. Gene amplification
  5. Chromosomal translocation
  6. Protein-protein interactions
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9
Q

What are proto oncogenes?

A

They are a group of geese that cause notable cells to become cancerous when they are mutated

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10
Q

Are Proto-oncogene mutations usually dominant or recessive?

A

Typically dominant

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11
Q

What is the mutated version of a Proto-oncogene called?

A

An oncogene

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12
Q

What do Proto-oncogenes encode?

A

They encode proteins that function to stimulate cell division, inhibit cell differentiation and halt cell death

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13
Q

Why are photo oncogenes important

A

They code proteins that function to stimulate cdll division, inhibit cell differentiation and halt cell health which are all important processes to maintain tissues and organs

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14
Q

What do oncogenes code for?

A

They encode for the same proteins as proto-oncogenes but the production of these proteins is at an increased rate
This leads to increased cell division, decreased cell differentiation and inhibition cell death

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15
Q

How many men are estimated to develop cancer inter lifetime ?

A

Approx 1 out of every 2 men

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16
Q

How many women are estimated to develop cancer inter lifetime?

A

Approx 1 out of 3 women

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17
Q

Out of the current list of known cancer genes how many are associated with germlinemutations?

A

70 genes

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18
Q

Out of the current list of known cancer genes how many are associated with somatic mutations?

A

342

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19
Q

What are germline mutations?

A

Inherited mutations

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20
Q

What are somatic mutations?

A

Spontaneous mutations

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21
Q

Generally speaking name the 2 basic classes of genes that if mutated can lead to cancer?

A
  1. proto-oncogenes

2. tumour suppressor genes-

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22
Q

Who discovered the first tumour causing virus?

A

Peyton Rous

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23
Q

Name the first tumour causing virus

A

The rous sarcoma virus

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24
Q

What was the road sarcoma viral gene responsible fro and how did it lead to cancer?

A

Caused cancer as the host cell proto-oncogene (c-src) was hijacked by the viruses viral oncogene (v-src)
So following infection the v-src oncogene was depressed at high levels in the host cells leading to uncontrolled host cell growth

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25
What does the c-src gene code for?
A protein that is involved in the positive regulation of cell growth and cell division
26
What functions to PROTO-oncogenes have within the cell?
1. Growth factors 2. Protein kinases 3. Membrane associated G-protein 4. Nuclear DNA- binding/ transcription factors
27
What role do oncogenes have in the cell?
1. Growth factors 2. Protein kinases 3. Receptors 4. Transcription factors
28
How are cell activities and interaction regulated?
They are tightly regulated via cell signalling
29
In cancer what happens to cell signalling?
Cell signalling is disrupted at several points
30
Describe how cell signalling is disrupted in cancerous cells
1. The growth facto receptor is amplified or mutated 2. So the signalling molecule is locked in its active configuration 3. Deletion or methylation induced silencing of genes occurs due to negate regulators 4. As the signalling molecule is locked in its active configuration the transcription factor gene is amplified 5. So the target gene is activated when it shouldn't be or inactivated when it should be
31
What does the c-sis gene encode for?
Encodes the PDGF beta chain (the platelet derived growth factor)
32
What is the PDGF beta chain?
the platelet derived growth factor
33
Where is the v-sis gene found?
In the simian sarcoma virus
34
What does the int-2 gene encode for?
An FGF- related growth factor
35
What does the KFG gene encode for?
An FGF- related growth factor
36
What is another name for the KGF gene?
Hst
37
What has the KGF (hst) gene also been identified in ?
Gastric carcinoma and kaposis sarcoma cells
38
What is the FGFR gene?
The fibroblast growth factor receptor
39
What has the FGFR been been associated with?
Many types of cancer
40
What have ERBB2 mutations been linked with?
Lung and gastric cancers
41
What is RAS?
RAS is a GTPase
42
What is RAF?
A serine/threonine kinase
43
What doe KRAS and BRAF have a role in?
Colo-rectal cancer
44
What does the RAS-MAPK signalling pathway lead to?
Expression of genes involved in proliferation, differentiation and survival
45
What is the CDK4 gene?
It is a cyclin dependent kinase
46
What is CDK4 associated with?
Associated with melanoma but also breast cancer and myeloma
47
What does the CDK4 protein help with?
Helps to control cell division
48
What happens when the CDK4 gene is mutated?
It makes an abnormal CDK4 protein that is too active | This abnormal protein makes cells divide abnormally fast which could lead to tour formation
49
What has a disrupted c-myc gene found to be involved in?
Involved in numerous haematopoietic neoplasias
50
What happens if the c-myc gene is disrupted?
Show to result in retroviral integration and transduction as well as chromosomal rearrangements
51
Where was the Myc gene originally identified?
In the avian myelctomatosis
52
What is the Fos gene identified as?
As the feline osteosarcoma virus
53
What does the fos protein interact with?
The protein interacts with a second proto-oncogenic protein, Jun to form a transcriptional regulatory complex (Fos-Jun).
54
What was the p53 gene originally identified as?
Asa major nuclear antigen in transformed cells
55
Name the most identified mutant protein in human tumours?
The p53 gene
56
What do mutant forms of the p53 gene interact with?
Interfere with cell growth suppressor effects of wild type p53 indicating that the p53 gene product is actually a tumour suppressor.
57
How were tumour suppressor genes first identified?
By making cell hybrids between tumour and normal cells
58
Name some tumour suppressor genes tat have been identified
1. Retinoblastoma susceptibility gene (RB1), 2. Wilms' tumours (WT1), 3. neurofibromatosis type-1 (NF1), 4. Familial adenomatosis polyposis coli (APC or FAP), 5. p53 which was originally thought to be a proto-oncogene
59
How does the tumour suppressor P53 gene arise?
Due to a loss of of heterozygosity at the short arm of chromosome
60
What has analysis of several murine leukemia cell lines shown?
That the p53 locus was lost by either insertion or deletion on both alleles
61
Mutations at the p53 locus occur in which cancers?
1. Colon 2. Breast 3. Liver 4. Lungs
62
What can lead to damage/ mutation of a stable p53 gene?
1. Hyperproliferative signals 2. DNA damage 3. Telomere shortening 4. Hypoxia
63
What can damage/mutation to the p53 gene lead to?
1. Cell cycle arrest 2. Senscence 3. Apoptosis
64
What does the p53 gene do?
It regulated cell division and prevents cells dividing too fast Also prevents damaged cells from dividing
65
How does our body protect cells that have been exposed to lethal mutations due to environmental carcinogens?
Cells have the ability to repair DNA defects which prevents cancer
66
Name some hereditary cancers
1. Hereditary nonpolypbosis colorectal cancer (Colon, ovaries) 2. Xeroderma pigmentosum (skin carcinomas, melanomas) 3. Blooms syndrome (Carcinomas, leukaemia, lymphomas) 4. Fanconi anemia (acute myeloid leukaemia. squamous cell carcinomas) 5. Hereditary breast cancer (breast and ovarian caner)
67
How can tumour cells arise due to infections?
Tumor cells also can arise through the actions of specific tumor viruses
68
Name the 2 distinct types of tumour viruses?
1. DNA genomes | 2. RNA genomes (termed retroviruses)
69
What are RNA tumour viruses common in?
Chickens, mice an cats but RARE in humans
70
Name the only known human retroviruses
1. The human T-cell leukemia viruses (HTLVs) | 2. the human immunodeficiency virus (HIV).
71
Cellular transformation to cancer by DNA tumor viruses has been shown to be the result of what?
Protein protein interactions
72
What are tumour antigens?
Proteins encoded by the DNA tumour viruses
73
What can t antigens interact with?
Can interact with cellular proteins
74
What can interactions between cellular proteins and T antigens lead to?
Can effectively sequester the cellular proteins away from their normal functional locations within the cell
75
Name the predominant types of proteins that are sequestered by viral T antigens
Tumour suppressors
76
What causes the cellular transformation of tumour suppressors?
It is the loss of their normal suppressor functions
77
What happens when a retrovirus infects a cell?
1. When a retrovirus infects a cell its RNA genome is converted into DNA by an RNA-dependent DNA polymerase (reverse transcriptase) 2. The DNA then integrates into the genome of the host cell where it can remain being copied as the host genome is duplicated during the process of cellular division.
78
What type of oncogenes do Retroviruses contain?
Retroviruses can carry viral versions of cellular proto-oncogenes (v-onc).
79
What type of oncogenes do Retroviruses contain?
Retroviruses can carry viral versions of cellular proto-oncogenes (v-onc).
80
What is located at the ends of retroviral genomes?
There are powerful transcriptional promoter sequences termed long terminal repeats (LTRs)
81
What can promoter sequences termed long terminal repeats (LTRs) activate?
They can activate host genes near to the site of integration.
82
Name the 3 distance pathways by which most people come to oral cancer
1. Tobacco and alcohol use 2. Exposure to the HPV-16 virus 3. Under 7% of people can get get oral cancers from no currently identified cause thought to be some genetic predisposition.

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