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IBMS SR > Biology and the molecular biology of cancer II > Flashcards

Biology and the molecular biology of cancer II Flashcards

Aim-To try to understand the molecular mechanisms leading to cancer. Objectives: To identify common oncogenes To examine different classes of oncogenes. The link with specific types of cancer. The role of viruses in cancer.

1
Q

what occurs in an overactivity mutation

A

a normal cell undergoes a single mutation event and creates an oncogene
this allows for the oncogene to promote cell transformation

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2
Q

what is an overactivity mutation

A

a gain of a function

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3
Q

what is a underactivity mutation

A

a loss of a function

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4
Q

what occurs in a under activity mutation

A

a normal cell undergoes a mutation event= inactivates tumour suppressor gene and this leads for no effect of mutation in one gene copy in the second mutation event it inactivates the second gene copy leading to elimination of the TSG promoting cell transformation

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5
Q

what is oncogenesis

A

The process of activation of proto-oncogenes to oncogenes can include retroviral integration , point mutations, insertion mutations, gene amplification, chromosomal translocation and/or protein-protein interactions.

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6
Q

what interactions can be involved in oncogenesis

A 
retroviral integration 
point mutations
insertion mutations
gene amplification 
chromosomal translocation 
and or protein/protein interactions
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7
Q

what are photo oncogenes

A

group of genes that cause normal cells to become cancerous when they’re mutated

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8
Q

what nature are mutations in proto oncogenes

A

typically dominant

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9
Q

what is the mutated version of a proto oncogene

A

oncogene

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10
Q

what kind of proteins do protoncogenes encode

A

stimulate cell division
inhibit differentiation
halt cell death

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11
Q

what do oncogenes do

A

increased production of proteins so
increased cell division
decreased cell differentiation
inhibit cell deathxt

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12
Q

what are the ACS studies for the numbers of men getting cancer in their lifetime

A

1 out of every 2 men

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13
Q

what are the ACS studies for the numbers of women getting cancer in their lifetime

A

1 out of every 3 women

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14
Q

how many cancer genes are associated with germline( inherited) mutations

A

70

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15
Q

what is the mutation from protooncogene to oncogene

A

a dominant mutation

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16
Q

how many cancer genes are associated with somatic( spontaneous) mutations

A

342

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17
Q

what is contact inhibition

A

if normal cells are taken and placed on a petri dish they will continue growing until they touch other cells and will grow in a monolayer

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18
Q

who discovered the first tutor causing virus

A

Peyton Rous

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19
Q

who is Payton Rous and why is he important

A

he discovered the first tutor causing virus

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20
Q

what was the virus called that Payton discovered

A

Rous sarcoma virus

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21
Q

when was the Rous sarcoma virus discovered

A

early 20th century

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22
Q

what was Rous studying

A

the transmission of tumours in chickens, He found that he could induce tumour formation in a once-healthy chicken by injecting small pieces of a tumour taken from a cancer-prone chicken

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23
Q

what can we see histologically in cancer cells when growing on a petri dish

A

we lose the contact inhibition and the cells start growing on one another

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24
Q

what did Rous filter

A

extracts of chicken tumours through membranes which allowed the virus to pass through but not bacteria

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25
Q

what was allowed to pass through the membrane in Rous experiment

A

the virus but not the bacteria- this was also seen to induce tumour formation in healthy chickens

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26
Q

what was allowed to pass through the membrane in Rous’ experiment

A

the virus but not the bacteria- this was also seen to induce tumour formation in healthy chickens

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27
Q

what type of virus is Rous sarcoma virus

A

a retrovirus

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28
Q

what was later discovered about the rods sarcoma viral gene

A

it was a host gene which had been hijacked by a virus

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29
Q

what was the host cell protooncogene called

A

c-src

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30
Q

what was the rous sarcoma viral oncogene called

A

V-SRC

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31
Q

what is the c-src gene involved in

A

the positive regulation of cell growth and cell division

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32
Q

what functions can protooncogenes carry out

A
  1. Growth Factors
  2. Protein Kinases
  3. Membrane Associated G-Proteins
  4. Nuclear DNA-Binding/Transcription Factors
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33
Q

what are the role on oncogenes in cells

A

growth factor
protein kinases
receptors
transcription factor

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34
Q

what are vascular epithelium growth factors responsible for

A

formation of new blood vessels

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35
Q

what is one way can a growth factor can show mutation

A

much more overactive than previously

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36
Q

what is the difference of v-src and c-src in the body

A

the difference of their origin and the gene dosage- the gene dosage of v-src is much higher

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37
Q

what are protein kinases

A

they are associated with the receptors recognise the growth factor-

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38
Q

what are membrane associated g proteins

A

also from the family of signal transduction proteins which relay the signal from outside the cell to inside and changes gene expression

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39
Q

what is the signal transduction cascade

A

the signalling molecule from the outside of the cell binds to the receptor
leads to a cascade where intracellular affector region and secondary messengers involved which changes gene expression

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40
Q

what is one way of treating colorectal cancer

A

blocking the epidermal growth factor signal- block with an antibody and disrupt the signalling pathway

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41
Q

how do protein kinases work

A

protein which can attach a phosphate to another protein-intracellular cell transduction works

  1. the growth factor binds to the receptor
  2. receptor changes the 3D structure
  3. causes the relay of the phosphorylation signal passed by different protein to the nucleus where the change in gene transcription happens
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42
Q

what are protein kinases

A

protein which can attach a phosphate to another protein-intracellular cell transduction works

43
Q

how can protein kinases become mutated to become oncogenes

A

by continuing to bind to the receptor and therefore the phosphorylation signal keeps on happening allowing for the change in gene transcription

44
Q

how are cell activities and interactions tightly regulated

A

by cell signalling

45
Q

what does disruption of cell signalling ultimately lead to

A

cancer

46
Q

what does the c sis gene encode for

A

the PDGF beta chain

47
Q

what does PDGF beta chain stand for

A

the platelet derived growth factor

48
Q

where is the v sis gene found

A

in the simian sarcoma virus

49
Q

give examples of growth factor oncogenes

A

c sis gene
v sis gene
int-2 gene
KGF/Hst gene

50
Q

what does the int-2 gene encode for

A

FGF related growth factor

51
Q

what does the KGF gene encode for

A

FGF related growth factor ( fibroblasts growth factor)

52
Q

where was the KGF gene identified

A

in gastric carcinoma and Kaposis sarcoma cells

53
Q

what does KGF Stand for

A

Keratinocyte growth factor

54
Q

in which population is karposi’s sarcoma seen

A

in people which suffer from AIDS

55
Q

what is important about the signalling pathways

A

they are all interconnected and we are still learning about them

56
Q

what are RTK

A

receptor tyrosine kinases

57
Q

how do receptor tyrosine kinases work

A
  1. the receptor binds to the growth factor
  2. kinase activity is stimulated and the tyrosine kinases move closer to one another
  3. tyrosines inside the cytosol are phosphorylated
  4. intracellular proteins bind to the phospho tyrosine docking sites
58
Q

which type of mutations have been linked to lung and gastric cancer

A

ERBB2

59
Q

what is erbb2

A

a specific receptor tyrosine kinase

60
Q

how might cancer be caused

A

by the mutation in the FGFR( fibroblast growth factor receptor)

61
Q

give example of a GTPase

A

RAS

62
Q

WHAT IS RAF

A

a serine/threonine kinase

63
Q

what is CDK4

A

cyclin dependant kinase

64
Q

what is CDK4 associated with

A

breast cancer
myeloma
melanoma

65
Q

what does CDK4 help with

A

control cell division

66
Q

what happens when CDK4 is mutated

A

makes an abnormal protein which is too active and this makes cells divide abnormally fast which could lead to tumour formation

67
Q

give examples of transcription factors

A

Myc gene
Fos gene
P53 gene

68
Q

describe the Myc transcription factor gene

A

A disrupted human c- myc gene has been involved in haematopoietic neoplasias

69
Q

where was Myc gene originally found

A

in avian myelocytomatosis virus

70
Q

what does disruption of the c-myc gene cause

A

haemotopoietic neoplasms and has been linked to retroviral integration and transduction as well as chromosomal rearrangements

71
Q

Where was the fos gene identified

A

In the feline osteosarcoma virus

72
Q

What complex is formed with fos

A

A transcriptional regulatory complex- fos jun complex

73
Q

What joins with fos to form the transcriptional regulatory complex

A

A second protooncogene called Jun

74
Q

Where was p53 first identified

A

As a major nuclear antigen I’m transformed cells

75
Q

What is the most identified mutant protein in human tumours

A

P53

76
Q

what is the gene product of the p53 gene

A

a tumour supressor gene

77
Q

how were tumour suppressor genes first identified

A

by making cell hybrids between tumour and normal cells

78
Q

give examples of of tumour suppressor genes

A

retinoblastoma susceptibility gene (RB1),
Wilms’ tumours (WT1),
neurofibromatosis type-1 (NF1),
familial adenomatosis polyposis coli (APC or FAP), and those identified through loss of heterozygosity such as in colorectal carcinomas (called DCC for deleted in colon carcinoma)
p53 which was originally thought to be a proto-oncogene.

79
Q

what is the function of p53 genes

A

to check if there is damage in the DNA and then if there is proteins are produced to repair that Damaged DNa

80
Q

what has been associated with tumours of the lung colon and breast

A

the loss of heterozygosity in the short arm of chromosome 17 which includes p53 gene

81
Q

what has seen to be lost in chromosome 17

A

the loss of heterozygosity in the short arm- this is where p53 is located

82
Q

when we analysed murine leukemia cell lines what was shown

A

the p53 locus was lost by insertions or deletion of both alleles

83
Q

what can p53 detect

A

senses DNA damage: hyperproliferative signals
dna damage
telemere shortening
hypoxia

84
Q

describe p53

A

p53 is a protein that regulates cell division.
It prevents cells dividing too fast.
It also prevents cells dividing if there is DNA damage.
If the DNA damage cannot be repaired, p53 signals for apoptosis/cell death to be activated

85
Q

what can p53 do when it detects a damage

A

cell cycle arrest
senescence- not killed but doesnt do much
apoptosis

86
Q

what are cells exposed to

A

environmental carcinogens

87
Q

what bacteria is linked to stomach cancer

A

helicobacter pylori

88
Q

which parasite is linked to bladder cancer

A

SCHISTOSOMA HAEMATOBIUM

89
Q

which parasite is linked to billary cancer
pancreatic cancer
and gallbadder cancer

A

Clonorchis sinensis AND

opisthorchis viverrini

90
Q

what are the two distinct types of tumour viruses

A

DNA genomes papilloma and adenovirus

RNA genomes retrovirus

91
Q

what are rna tumours common in

A

chickens
cats
mice

92
Q

what is the known human retrovirus

A

human t cell leukemia virus and HIV

93
Q

how does the transformation of DNA tumour viruses into cancer occur

A

by protein protein interaction

94
Q

describe t antigens

A
  1. proteins encoded by the dna tumour viruses/ t antigens can interact with cellular proteins
  2. this moves away the cellular proteins from their nromal functions
95
Q

how can oncogenesis by retrovirus occur

A

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

Contained within the sequences at the ends of the retroviral genome are powerful transcriptional promoter sequences termed long terminal repeats (LTRs). These can activate host genes near to the site of integration.

96
Q

what virus is involved in stomach cancer

hodgkin and non hodgkin lymphomas and nasopharyngeal cancer

A

epstein barr virus

97
Q

what virus is associated with hepatocellular carcinoma

A

hep b/C- causes liver inflammation

98
Q

what virus is associated with karposi sarcoma and non hodgkin lymphoma

A

HIV

99
Q

what virus is associated with cervical anogenital head neck and oral cancers

A

HPV- AKA an std

some strains are high risk strains

100
Q

what cancer is associated with merkel cell polyomavirus

A

skin cancer

101
Q

what cancer is associated with human t cell lymphotrophic virus type 1

A

t cell leukemia and lymphoma

102
Q

how do people get oral cancer

HELP- the two pathways

A

The use of tobacco (smoking, snuff and chewing paan) and alcohol (beers, wines or spirits).

Exposure to the HPV-16 virus (human papilloma virus –type 16), a recently identified aetiology, and the same one which is responsible for the vast majority of cervical cancers in women.

103
Q

how do 7% of people get oral cancer

A

from no currently identified tissue therefore have some genetic disposition

IBMS SR (38 decks)

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