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2nd yr- IBMS: Biology and molecular biology of cancer > Biology and molecular biology of cancer II > Flashcards

Biology and molecular biology of cancer II Flashcards

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
Q

What does the c-src gene code for?

A

A protein that is involved in the positive regulation of cell growth and cell division

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26
Q

What functions to PROTO-oncogenes have within the cell?

A
  1. Growth factors
  2. Protein kinases
  3. Membrane associated G-protein
  4. Nuclear DNA- binding/ transcription factors
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27
Q

What role do oncogenes have in the cell?

A
  1. Growth factors
  2. Protein kinases
  3. Receptors
  4. Transcription factors
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28
Q

How are cell activities and interaction regulated?

A

They are tightly regulated via cell signalling

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29
Q

In cancer what happens to cell signalling?

A

Cell signalling is disrupted at several points

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30
Q

Describe how cell signalling is disrupted in cancerous cells

A
  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
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31
Q

What does the c-sis gene encode for?

A

Encodes the PDGF beta chain (the platelet derived growth factor)

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32
Q

What is the PDGF beta chain?

A

the platelet derived growth factor

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33
Q

Where is the v-sis gene found?

A

In the simian sarcoma virus

34
Q

What does the int-2 gene encode for?

A

An FGF- related growth factor

35
Q

What does the KFG gene encode for?

A

An FGF- related growth factor

36
Q

What is another name for the KGF gene?

A

Hst

37
Q

What has the KGF (hst) gene also been identified in ?

A

Gastric carcinoma and kaposis sarcoma cells

38
Q

What is the FGFR gene?

A

The fibroblast growth factor receptor

39
Q

What has the FGFR been been associated with?

A

Many types of cancer

40
Q

What have ERBB2 mutations been linked with?

A

Lung and gastric cancers

41
Q

What is RAS?

A

RAS is a GTPase

42
Q

What is RAF?

A

A serine/threonine kinase

43
Q

What doe KRAS and BRAF have a role in?

A

Colo-rectal cancer

44
Q

What does the RAS-MAPK signalling pathway lead to?

A

Expression of genes involved in proliferation, differentiation and survival

45
Q

What is the CDK4 gene?

A

It is a cyclin dependent kinase

46
Q

What is CDK4 associated with?

A

Associated with melanoma but also breast cancer and myeloma

47
Q

What does the CDK4 protein help with?

A

Helps to control cell division

48
Q

What happens when the CDK4 gene is mutated?

A

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
Q

What has a disrupted c-myc gene found to be involved in?

A

Involved in numerous haematopoietic neoplasias

50
Q

What happens if the c-myc gene is disrupted?

A

Show to result in retroviral integration and transduction as well as chromosomal rearrangements

51
Q

Where was the Myc gene originally identified?

A

In the avian myelctomatosis

52
Q

What is the Fos gene identified as?

A

As the feline osteosarcoma virus

53
Q

What does the fos protein interact with?

A

The protein interacts with a second proto-oncogenic protein, Jun to form a transcriptional regulatory complex (Fos-Jun).

54
Q

What was the p53 gene originally identified as?

A

Asa major nuclear antigen in transformed cells

55
Q

Name the most identified mutant protein in human tumours?

A

The p53 gene

56
Q

What do mutant forms of the p53 gene interact with?

A

Interfere with cell growth suppressor effects of wild type p53 indicating that the p53 gene product is actually a tumour suppressor.

57
Q

How were tumour suppressor genes first identified?

A

By making cell hybrids between tumour and normal cells

58
Q

Name some tumour suppressor genes tat have been identified

A
  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
Q

How does the tumour suppressor P53 gene arise?

A

Due to a loss of of heterozygosity at the short arm of chromosome

60
Q

What has analysis of several murine leukemia cell lines shown?

A

That the p53 locus was lost by either insertion or deletion on both alleles

61
Q

Mutations at the p53 locus occur in which cancers?

A
  1. Colon
  2. Breast
  3. Liver
  4. Lungs
62
Q

What can lead to damage/ mutation of a stable p53 gene?

A
  1. Hyperproliferative signals
  2. DNA damage
  3. Telomere shortening
  4. Hypoxia
63
Q

What can damage/mutation to the p53 gene lead to?

A
  1. Cell cycle arrest
  2. Senscence
  3. Apoptosis
64
Q

What does the p53 gene do?

A

It regulated cell division and prevents cells dividing too fast
Also prevents damaged cells from dividing

65
Q

How does our body protect cells that have been exposed to lethal mutations due to environmental carcinogens?

A

Cells have the ability to repair DNA defects which prevents cancer

66
Q

Name some hereditary cancers

A
  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
Q

How can tumour cells arise due to infections?

A

Tumor cells also can arise through the actions of specific tumor viruses

68
Q

Name the 2 distinct types of tumour viruses?

A
  1. DNA genomes

2. RNA genomes (termed retroviruses)

69
Q

What are RNA tumour viruses common in?

A

Chickens, mice an cats but RARE in humans

70
Q

Name the only known human retroviruses

A
  1. The human T-cell leukemia viruses (HTLVs)

2. the human immunodeficiency virus (HIV).

71
Q

Cellular transformation to cancer by DNA tumor viruses has been shown to be the result of what?

A

Protein protein interactions

72
Q

What are tumour antigens?

A

Proteins encoded by the DNA tumour viruses

73
Q

What can t antigens interact with?

A

Can interact with cellular proteins

74
Q

What can interactions between cellular proteins and T antigens lead to?

A

Can effectively sequester the cellular proteins away from their normal functional locations within the cell

75
Q

Name the predominant types of proteins that are sequestered by viral T antigens

A

Tumour suppressors

76
Q

What causes the cellular transformation of tumour suppressors?

A

It is the loss of their normal suppressor functions

77
Q

What happens when a retrovirus infects a cell?

A
  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
Q

What type of oncogenes do Retroviruses contain?

A

Retroviruses can carry viral versions of cellular proto-oncogenes (v-onc).

79
Q

What type of oncogenes do Retroviruses contain?

A

Retroviruses can carry viral versions of cellular proto-oncogenes (v-onc).

80
Q

What is located at the ends of retroviral genomes?

A

There are powerful transcriptional promoter sequences termed long terminal repeats (LTRs)

81
Q

What can promoter sequences termed long terminal repeats (LTRs) activate?

A

They can activate host genes near to the site of integration.

82
Q

Name the 3 distance pathways by which most people come to oral cancer

A
  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.

2nd yr- IBMS: Biology and molecular biology of cancer (2 decks)

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