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Oncogenes Flashcards

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1
Q

what do proto-oncogenes do

A

promote cell division, proliferation and growth

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2
Q

what do tumour suppressor genes do

A

counter proto oncogenes by promoting cell cycle arrest or cell death (prevents excessive growth of cells or tissue

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3
Q

balance of what genes allows maintanence of homeostasis

A

proto onco and tumour suppressor genes

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4
Q

what is burkitts lymphoma

A

highly aggressive B cell non hodgkins lymphoma that is predisposed by EBV and malaria infection

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5
Q

how does EBV immortalise cells causing lymphoma

A

reciprocal translocation in chromosomes 8:4 = deregulation of the c-myc proto oncogene by placing it under the control of the immunoglobulin gene loci

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6
Q

what are onco genes and what do they do

A

derivatives of proto oncogenes that are often mutated, amplified or deregulated in cancers
positive regulators of cell growth and division

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7
Q

do oncogenes act in a dominant or recessive manner- why

A

dominant

often have a mutations which are dominant and because of this only one allele needs to be mutated

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8
Q

what does mutation of proto oncogenes cause

A

either:
-constitutively active (super active) protein
or
-locus of gene amplified making multiple copies of and producing an excess of the stimulus to proliferate

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9
Q

what stages of the proliferation pathway are targets for oncogenic transformation

A 
all:
growth factors 
GFr
signal transducers 
nuclear proteins, transcription factors and coactivators
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10
Q

what are the steps in the proliferation pathway

A 
GF
GFR
(phosphorylation/vdephosphorylation) 
signal transducers (amplification) 
nuclear proteins 
transcription factors and coactivators
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11
Q

what do oncogenes essentially cause

A

stimulate progression through the cell cycle and allow the cell to proliferate in the absence of growth signals

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12
Q

why is the phosphorylation/ dephosphorylation caused by GFrs no longer needed when oncogenes present

A

as there have been point mutations and/or truncations that have made the protein constitutively active

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13
Q

what happens when there is a mutation in a tumour suppressor gene

A

gene behaves RECESSIVELY
the wild type can cover the mutation but if there is a second mutation then both tumour suppressors are inactivated promoting cell transformation

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14
Q

do oncogenes or tumour suppressors behave recessively

A

tumour suppressor genes

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15
Q

what are the ways in which oncogenes can be activated

A

point mutations/ deletions in coding sequence that make protein constitutively active (hyperactive protein made in normal amounts)

regulatory mutation (normal protein made in excessive amounts)

chromosome amplification- multiple copies of the gene, normal protein in excess amounts

chromosomal rearrangement:

  • insertion of enhancer (too much normal protein)
  • chromosomal translocation- gene placed in area of high transcription (too much normal protein)
  • gene fusion (hyperactive protein)

retro viral insertion (mutagenesis)- insertion which can cause mutations or deletions either in gene or upstream (normal protein in excess OR hyperactive protein)

retroviral transduction- retrovirus inserts into genome and carries oncogene onto any cell into infects (protein made in excessive amounts)

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16
Q

give examples of point mutations oncogenes

A

Ras, Raf

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17
Q

give examples of chromosome amplification

A

Abl, Myc

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18
Q

give examples of chromosomal rearrangement

A

insertion of enhancer: Ig enhancer in Myc t[8:14]

happens in EBV-> burkitts lymphoma

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19
Q

give an example of gene fusion

A

philadelphia chromosome is a translocation between BCR and Abl t[9:22]

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20
Q

what is Ras

A

guanine nucleotide binding protein

sits on inside of cell membrane

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21
Q

what are the family member of Ras

A

H-
Ki-
N-

is a member of the GTPase superfamily

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22
Q

what does ras do and how is it activated

A

is a positive regulator of cell growth

activated by viruses and mutations which causes activation of downstream signalling pathways

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23
Q

what are the two forms of Ras and why are they important

A

Ras-GDP = inactive
Ras- GTP = active

balance between these forms acheived by guanine neucleotde exchange factors (GEFs) and GTPase activating proteins (GAPs)

Ras-GTP transduces the signal to multiple effectors Raf-MEK- ERK and PI3K/Rac/Ral

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24
Q

what does Ras activate downstream

Study These Flashcards
A

Raf-Mek-Erk (cell division)

Pi3K/Rac/Ral (proliferation and invasion)

25
how do you activate Ras
vRas mutations (makes Ras constitutively active, bound to GTP) or wildtype - increasing upstream stimulation e.g. activation of EGFR or by removing GAPS by deletion of NF-1 (makes more GTP Ras)
26
what is Raf
serine/ threonine kinase, found inside cytoplasm
27
what are the family member of Raf
A- B- C-
28
how do you activate Raf
mutations and viruses BRAF mutations especially V600e means BRAF doesnt need signals from Ras and EGFr
29
what does Raf usually do
responds to EGFR signalling and activates BRAF pathway (MEK->ERK-> normal cell growth)
30
what is C-Abl
tyrosine kinase found inside cytoplasm | normally is a positive regulator of cell growth
31
how is C-Abl activate
viruses, mutations chromosomal translocations
32
give an example of a chromo translocation activating c-Abl
philadelphia chromosome
33
what is the philadelphia chromosome
t[9:22] | fusion between BCR gene (22) and Abl gene (9) to make contitutively active fusion protein BCR-Abl
34
why is Abl usually inactive
as N terminal cap covers the catalytic site stopping downstream phosphorylation BCR-Abl fusion protein reconstructs this and exposes active site, meaning it doesnt need up stream signals to activate it= constitutively active
35
what can is Abl activated in
leukaemias e,g, CML [9:22]
36
what is epidermal growth factor receptor
(ErbB1, ErbB2) receptor tyrosine kinase, in cell membrane positive regulator of cell growth
37
what activated EGFR
viruses and mutations if mutated doesnt need upstream signalling or if upstream EGF increased
38
what is EGFR normally like
inactive in cell membrane until EGF binds to it | stimulates downstream cell division
39
what down stream pathways does EGFR stimulate
Ras-Raf-Mek-MAPK PI3k-AKT all ones it activates result in cell survival, invasion, proliferation, metastasis and angiogenesis
40
what does a cancer netwrok mean
oncogenes talk to each other, multiple effectors, depending on the context they are in and can be tumour promoting or cause apoptosis extracellular signals will talk to several oncogenes implications for drug Tx
41
what is Myc
nuclear oncogene transcription factor (that also regulates translation) positive regulator of proliferation (generally) Normally in conjunction with Max, Myc is a transcription factor of cell cycle genes e.g. cyclin D
42
how is myc activated
chromo translocation to a region of high expression (e.g. in burkitts from 8 to 14)
43
what are the two outcomes for overexpression of Myc
in presence of GFs (serum) will cause proliferation and survival without GF will cause apoptosis
44
how do drugs target Ras
vemurafenib and dabrafenib target BRAF- if there is a mutated BRAF with by constitutively active and doesnt need upstream signals resistance problems as just switch to substitute pathway
45
what BRAF mutation is important and in which cancer
V600e | melanoma
46
what drugs target BCR-Abl fusion protein
ST1-571/ gleevac/imantinib. This binds to the active site of the kinase domain, stopping the phosphorylation of downstream targets mutation of active site stopping binding of drug or over expression of other factors creates resistance tho
47
what drugs target EFGR signalling
Active site analogues e.g. iressa/ gefitinib bind to active site to stop the downstream signalling Another can target ErBB2 or Her2 via monoclonal antibody therapy e.g. trastuzumab (Herceptin) which is an antibody against the EGF binding site (not the kinase site so blocks the EGF binding site without activating the receptor- stopping the binding of the egf). Advanced by linking it to DM1 (emantsine) which is a cyotoxic drug that binds tublin and causes depolymersation of microtubules. These linked drugs are internalised by the cell, degraded by lysosomes which releases DM1- this then binds to tubulin in microtubules and inhibits their function, leading to cell cycle arrest and apoptosis. So stop signalling from Her2 and then also causes apoptosis
48
what is a way to prevent resistance
using combos of drugs early on when resistance is likely not yet developed
49
what are oncogenes markers of
diagnostic and prognostic markers for the cancer e,g, Her 2
50
what do enhancers do
vastly stimulate transcription of genes
51
what is c-Abl
normal protein made by Abl
52
how does a retrovirus do viral insertion
``` reverse transcriptase (enzyme coded for by retrovirus) catalyzes the transcription of retrovirus RNA into DNA recombination events happen to small bits of DNA in nucleus into cell genome (most likely due to errors during cell replication) ```
53
what happens if when viral insertion happens upstream or in gene
upstream and in gene can increase transcription in gene can alter gene
54
where is the oncogene in retroviral transduction
in the retroviruses genome (by recombination)
55
what happens when you get rid of NF-1 (a GAP- GTPase activator protein)
will make more Ras-GTP
56
what is NF-1
a negative regulator of Ras
57
what causes neurofibromatosis
loss of NF-1
58
why does substrate conc not limit constitutively active proteins (enzymes)
as kinase activity rate limiting step, usually a lot of substrate so depends on rate of action of enzyme
59
why in the absence of growth factors does c-Myc overexpression cause apoptosis
as GFs act as survival signals, without them c-myc signals cell death C-myc action really depends on what else is being expressed in the cell and what stresses the cells are under Oncogenes generally positive regulator of proliferation, angio and growth, but there are some cases where overexpression can end up causes cell cycle arrest or senescence

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