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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. (103 cards)

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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
what was allowed to pass through the membrane in Rous experiment
the virus but not the bacteria- this was also seen to induce tumour formation in healthy chickens
26
what was allowed to pass through the membrane in Rous' experiment
the virus but not the bacteria- this was also seen to induce tumour formation in healthy chickens
27
what type of virus is Rous sarcoma virus
a retrovirus
28
what was later discovered about the rods sarcoma viral gene
it was a host gene which had been hijacked by a virus
29
what was the host cell protooncogene called
c-src
30
what was the rous sarcoma viral oncogene called
V-SRC
31
what is the c-src gene involved in
the positive regulation of cell growth and cell division
32
what functions can protooncogenes carry out
1. Growth Factors 2. Protein Kinases 3. Membrane Associated G-Proteins 4. Nuclear DNA-Binding/Transcription Factors
33
what are the role on oncogenes in cells
growth factor protein kinases receptors transcription factor
34
what are vascular epithelium growth factors responsible for
formation of new blood vessels
35
what is one way can a growth factor can show mutation
much more overactive than previously
36
what is the difference of v-src and c-src in the body
the difference of their origin and the gene dosage- the gene dosage of v-src is much higher
37
what are protein kinases
they are associated with the receptors recognise the growth factor-
38
what are membrane associated g proteins
also from the family of signal transduction proteins which relay the signal from outside the cell to inside and changes gene expression
39
what is the signal transduction cascade
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
40
what is one way of treating colorectal cancer
blocking the epidermal growth factor signal- block with an antibody and disrupt the signalling pathway
41
how do protein kinases work
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
42
what are protein kinases
protein which can attach a phosphate to another protein-intracellular cell transduction works
43
how can protein kinases become mutated to become oncogenes
by continuing to bind to the receptor and therefore the phosphorylation signal keeps on happening allowing for the change in gene transcription
44
how are cell activities and interactions tightly regulated
by cell signalling
45
what does disruption of cell signalling ultimately lead to
cancer
46
what does the c sis gene encode for
the PDGF beta chain
47
what does PDGF beta chain stand for
the platelet derived growth factor
48
where is the v sis gene found
in the simian sarcoma virus
49
give examples of growth factor oncogenes
c sis gene v sis gene int-2 gene KGF/Hst gene
50
what does the int-2 gene encode for
FGF related growth factor
51
what does the KGF gene encode for
FGF related growth factor ( fibroblasts growth factor)
52
where was the KGF gene identified
in gastric carcinoma and Kaposis sarcoma cells
53
what does KGF Stand for
Keratinocyte growth factor
54
in which population is karposi's sarcoma seen
in people which suffer from AIDS
55
what is important about the signalling pathways
they are all interconnected and we are still learning about them
56
what are RTK
receptor tyrosine kinases
57
how do receptor tyrosine kinases work
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
which type of mutations have been linked to lung and gastric cancer
ERBB2
59
what is erbb2
a specific receptor tyrosine kinase
60
how might cancer be caused
by the mutation in the FGFR( fibroblast growth factor receptor)
61
give example of a GTPase
RAS
62
WHAT IS RAF
a serine/threonine kinase
63
what is CDK4
cyclin dependant kinase
64
what is CDK4 associated with
breast cancer myeloma melanoma
65
what does CDK4 help with
control cell division
66
what happens when CDK4 is mutated
makes an abnormal protein which is too active and this makes cells divide abnormally fast which could lead to tumour formation
67
give examples of transcription factors
Myc gene Fos gene P53 gene
68
describe the Myc transcription factor gene
A disrupted human c- myc gene has been involved in haematopoietic neoplasias
69
where was Myc gene originally found
in avian myelocytomatosis virus
70
what does disruption of the c-myc gene cause
haemotopoietic neoplasms and has been linked to retroviral integration and transduction as well as chromosomal rearrangements
71
Where was the fos gene identified
In the feline osteosarcoma virus
72
What complex is formed with fos
A transcriptional regulatory complex- fos jun complex
73
What joins with fos to form the transcriptional regulatory complex
A second protooncogene called Jun
74
Where was p53 first identified
As a major nuclear antigen I’m transformed cells
75
What is the most identified mutant protein in human tumours
P53
76
what is the gene product of the p53 gene
a tumour supressor gene
77
how were tumour suppressor genes first identified
by making cell hybrids between tumour and normal cells
78
give examples of of tumour suppressor genes
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
what is the function of p53 genes
to check if there is damage in the DNA and then if there is proteins are produced to repair that Damaged DNa
80
what has been associated with tumours of the lung colon and breast
the loss of heterozygosity in the short arm of chromosome 17 which includes p53 gene
81
what has seen to be lost in chromosome 17
the loss of heterozygosity in the short arm- this is where p53 is located
82
when we analysed murine leukemia cell lines what was shown
the p53 locus was lost by insertions or deletion of both alleles
83
what can p53 detect
senses DNA damage: hyperproliferative signals dna damage telemere shortening hypoxia
84
describe p53
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
what can p53 do when it detects a damage
cell cycle arrest senescence- not killed but doesnt do much apoptosis
86
what are cells exposed to
environmental carcinogens
87
what bacteria is linked to stomach cancer
helicobacter pylori
88
which parasite is linked to bladder cancer
SCHISTOSOMA HAEMATOBIUM
89
which parasite is linked to billary cancer pancreatic cancer and gallbadder cancer
Clonorchis sinensis AND | opisthorchis viverrini
90
what are the two distinct types of tumour viruses
DNA genomes papilloma and adenovirus | RNA genomes retrovirus
91
what are rna tumours common in
chickens cats mice
92
what is the known human retrovirus
human t cell leukemia virus and HIV
93
how does the transformation of DNA tumour viruses into cancer occur
by protein protein interaction
94
describe t antigens
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
how can oncogenesis by retrovirus occur
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
what virus is involved in stomach cancer | hodgkin and non hodgkin lymphomas and nasopharyngeal cancer
epstein barr virus
97
what virus is associated with hepatocellular carcinoma
hep b/C- causes liver inflammation
98
what virus is associated with karposi sarcoma and non hodgkin lymphoma
HIV
99
what virus is associated with cervical anogenital head neck and oral cancers
HPV- AKA an std | some strains are high risk strains
100
what cancer is associated with merkel cell polyomavirus
skin cancer
101
what cancer is associated with human t cell lymphotrophic virus type 1
t cell leukemia and lymphoma
102
how do people get oral cancer | HELP- the two pathways
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
how do 7% of people get oral cancer
from no currently identified tissue therefore have some genetic disposition

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