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Biology of stem cells, ageing and cancer > Cancer > Flashcards

Cancer Flashcards

1
Q

Oncogene

A

a gene capable of transforming a normal cell into a tumour cell

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2
Q

Tumour suppressors

A

factors that reduce the ability of oncogenes turning normal cells into cancerous ones

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3
Q

Major carcinogenic factors

A

chemical
parasites
radiation
viruses

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4
Q

How are tumours heterogenous?

A

cells within the same tumour often exhibit differences in terms of differentiation, proliferation, migration and invasion, size, therapeutic resistance and tumorigenicity

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5
Q

Stochastic model

A

all tumour cells are equipotent and a proportion of them stochastically proliferate to fuel tumour growth
other tumour cells differentiate targets for anti-cancer treatments

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6
Q

Cancer stem cell model

A

only a small subset of tumour calls have the ability for long term self renewal and these cells give rise to committed progenitors
regulated by same signalling as normal stem cells

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7
Q

Why are cancer stem cells drug resistant?

A

they have a slow cell cycle and are more dominant, so drugs that target fast proliferating cells don’t work as well

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8
Q

Pathway of how CSCs arise

A

specialised cell > reprogramming to a CSC like entity or oncogenic transformation of pre-existing stem cells > CSC

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9
Q

In vitro potential of CSCs

A

establishment of cell lines that can self renew and differentiate

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10
Q

In vivo potential of CSCs

A

ability to give rise to cancer following transplantation into animals

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11
Q

Leukaemia

A

blood cancer affecting the myeloid lineage

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12
Q

Glioblastoma

A

aggressive and invasive form of brain cancer
treatment involves surgical resection, radiation and chemotherapy
recurrant and low survival rate

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13
Q

What are the main approaches to studying cancer?

A

xenograft models
cancer cell lines
genetically modified animals using oncogene or tumour suppressor mutations

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14
Q

What are the limitations of current cancer studies?

A

failure to capture the transition from normal to tumorigenic phenotype in a tractable manner and in a human context
lack of mechanism insight

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15
Q

What could cause neuroblastomas?

A

neural crest cells arise in resopnse to Wnt and BMP
these are marked by Sox10 and overexpressionof this could be the cause

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16
Q

What cells are most commonly connected to cancer? why?

A

tissues that are continuously replaced and have an active cell population- epithelia and blood
cells are already proliferating and each time the genome is copied there is more of a chance for mistakes to occur

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17
Q

Teratoma

A

cancers that grow a variety of tissues
cells similar to embryonic cells as can give rise to tissues from all three germ layers

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18
Q

Tumour suppressor genes

A

Rb
P53
ATP

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19
Q

What are the alternative ways cancer cells are able to proliferate without GFs?

A

production of GFs by themselves
signals that stimualte surrounding cells to produce GFs
deregulation of GF receptor signalling
constitutive activation of signalling downstream of GFs
disruption of negative feedback mechanisms

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20
Q

When is the discrete window where a cell can consult the extracellular environment?

A

from the onset of G1 to an hour or 2 before S

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21
Q

What is the restriction point?

A

the point in the cell cycle when the cell becomes fully committed to the cycle at the G1/S transition
extracellular signals are no longer needed for proliferation

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22
Q

Flow cytometry

A

cells treated with fluroescent dye that labels DNA quantitatively
as DNA content doubles during S phase the intensity of fluorescence increases in proportion
so cells in G1/0 have half of those in S

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23
Q

Immunofluorescence

A

staining for proteins that are specifically expressed in different phases of the cell cycle to measure its progression

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24
Q

BrdU

A

replaces thymidine during DNA synthesis
short pulse identifies cells in S phase

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25
Cyclin B1
marker for G2/M
26
Histone H3
has a role in mitotic chromosome condensation and is phosphorylated during mitosis
27
FUCCI
fluorescence ubiquitin cell cycle indicator allows for in vivo analysis of spatial and temporal patterns of cell cycle dynamics
28
What are the two components of the replication control system in eurkaryotes?
licensing factor Ctd1 Ctd1 inhibitor geminin
29
Licensing factor Ctd1
peaks in G1 before the onset of DNA replication and declines abruptly after initiation of S phase
30
Ctd1 inhibitor geminin
expressed at high levels during S and G2 phase low levels during mitosis
31
Colours of cells when sorted by FACS
early G1- no/low red late G1- high red G1/S- red and green S/G2/M- green
32
What phase of the cell cycle are cells likely to have higher invasive abilities?
G1 cells are able to disrupt the ECM and therefore invade tissues
33
What viruses are known to induce cancer?
human papilloma virus hepatitis C virus
34
Viral genetics
have very simple genomes with very few but potent genes these perturb the complex regulatory circuitry of the cells they infect
35
Peyton-Rous
chicken embryo fibrobalsts injected with rous sarcoma showed traits associated with cancer transformation phenotype was transmitted from an initially infected cell to its descendents
36
What were the 2 possible explanations for the rous sarcoma experiment?
RSV particle transformed progenitor cells and all descendents but virus must be present to maintain phenotype RSV particles only needed to transform progenitors that transmit phenotype to inheritants so acts in a hit and run fashion
37
ts RSV mutant
partially defective proteins but can function at permissive temperatures
38
What was the eventual conclusion of the rous experiment?
transformed state was lost when cells were kept at non-permissive temps so the viral transforming protein was required to both initiate and maintain tumour phenotype
39
What are the 3 genes coding for viral replication?
gag pol env
40
gag
virion nucleoprotein core
41
pol
reverse transcriptase and integrase
42
env
glycoprotein spikes of the virion
43
What additional viral gene is required for transformation?
src
44
Proto-oncogenes
genomes of normal vertebrates can carry a gene that has the potential under certain circumstances to induce cell transformation and thus cancer
45
What were other proposed causes of cancer?
activation of endogenous retrovirus induction by mutagens
46
Mutagens
physical or chemical agents that induce cancer through their ability to mutate growth and controlling genes such as UV light, x-rays, base analogs and DNA intercalating agents
47
Oncogene transfection
if a transforming gene is present in the donor DNA, it may become incorperated in the genome of one of the recipient cells and transform the latter → these will form loci
48
What are proto-oncogenes regulated by?
in normal cells- by their own transcriptional proteins in cells acquired by viruses- retroviral promoter
49
How was the difference between a normal gene and oncogene identified?
cleaved by restriction enzymes recombinant genes made by ligation transforming activity using transfection locus assay mutation responsible for activation localised to 350bp fragement and sequence was determined
50
What are the 3 types of ras genes found to carry point mutations in human tumours?
H-ras K-ras N-ras
51
Which ras gene is the most frequent driver of tumour development in humans?
K-ras KRASG12C most prevalent in lung cancer
52
KRAS inhibitor
AMG 510 forms a covalent bond with GTP-bound KRAS high specificity for mutant protein inhibits downstream signalling + cell proliferation in vitro inhibits tumour growth in mice
53
What improves efficiency of AMG510?
when in combination with standard chemo or a drug that inhibits MEK which acts as a downstream of Ras not effective on immunocompromised
54
What improves efficiency of AMG510 in immunocompromised mice?
when in combination with immunotherapy called anti-PD1 leads to complete tumour regression
55
What effect does AMG510 have on the immune system?
boosts the expression of pro-inflammatory cytokines in tumour bearing animals increases infiltration of tumours by T and dendritic cells
56
What happens when KRAS cancer cells are reintroduced to animals cured by combination therapy?
no tumour formation due to long term T cell response induced by treatment
57
What are the 3 members of the myc oncogene family?
C-myc N-myc L-myc
58
What are the 3 mechanisms that can cause the myc oncogene to arise?
gene amplification chromosomal translocation pro-virus integration
59
What is the function of myc proteins?
growth promoting TFs in the nucleus
60
Gene amplification
driven by its normal promoter but the gene is amplified causing increased gene product levels drives uncontrolled cell proliferation
61
Chromosomal translocation
region of one chromosome is fused with a region from a second unrelated one gene comes under control of foreign transcriptional promoter
62
Pro-virus integration
Avian leukosis virus viral transciptional promoter disrupts the mechanisms normally controlling the expression of myc increases expression causing extremely high levels of myc protein
63
How can deregulation of EGF lead to cancer?
extracellular domain of EGFR is deleted in some lung cancers and glioblastomas consitutive signalling in the absence of EGF- uncontrolled release of GFs
64
Cell fusion technique
comparison of 2 alternative alleles and specified phenotypes when both alleles are forced to co-exist dominant allele wins
65
What is the fusing agent used in cell fusion technique?
sendai virus or PEG
66
How did hybrid cells formed by cell fusion prove the existance of tumour suppressors?
hybrid cells were unable to form tumours genes carried by normal cell were inactivated during development of a tumour
67
Retinoblasts
population of cells in the developing eye, which normally stop growing during embryogenesis and differentiate
68
Retinoblastomas
tumour of the retina which arises in the precursor of photoreceptor cells, retinoblasts, which fail to differentiate and divide
69
What are the 2 forms of retinoblastoma?
sporadic form- children from families with no history of retinoblastoma developing a single tumour in one eye → unilateral retinoblastoma familial form- genetically predisposed children developing multiple tumours in both eyes → bilateral retinoblastoma + elevated susceptibility to developing other tumours
70
Alfred Knudson
used maths to determine whether data followed a 1 or 2 hit model of gene mutation sporadic requires 2 random events familial requires only 1
71
Mutations in what gene cause retinoblastomas?
Rb
72
Mitotic recombination of Rb
chromosomal arm carrying Rb allele might be replaced with one carrying mutant allele far easier than mutational activation
73
What are mechanisms to stop cancer development?
- direct suppression of cell proliferation in response to growth inhibitory and differentiation inducing factors - components of the cellular machinery that inhibits proliferation in response to metabolic imbalance and DNA damage
74
What were the first tumour suppressor genes to be intensively studied?
P53 Rb
75
How do TSGs other than P53 and Rb function?
dispatch of gene products to intracellular sites where they suppress cell proliferation involved in virtually all of the control circuits that govern cell proliferation and survival
76
Neurofibromatosis
caused by loss of heterozygosity of NF1 familial cancer syndrome causing benign tumours in the PNS called neurofibromas some progress to malignant neurofibrosarcomas
77
NF1
neurofibromin Ras GAP, mutations result in a protein with 1000 fold decreased GTPase stimulating activity
78
What happens when NF1 is lost?
Ras remains active for longer cells show overactivation of AKT and mTOR target S6K tumour formation
79
What does rapamyacin do?
completely blocks the mTOR target S6K reverses the ability of NF1 null cells to form colonies in anchorage independent conditions
80
APC
adenomatous polyposis coli, prone to develop into colon carcinomas loss of APC gene is first step in colon cancer followed by oncogene mutations of ras and p53
81
What do mutations in APC lead to?
blocking of the out-migration of cells from gut crypt leads to mutated cells accumulating in the crypt rather than being lost
82
What is the function of APC?
negatively regulates the levels of b-catenin in the cytosol as cells move upwards, APC expression is increased
83
What happens when APC is inactivated?
destruction complex does not form → B-catenin cytosolic accumulation and nuclear translocation → transcription of growth promoting genes including myc
84
pHVL/ von Hippen-lindau syndrome
hereditary disposition to developing a varitey of tumours includes clear cell kidney carcinomas, pheochromocytomas, and hemangioblastomas
85
What causes pVHL tumours?
germ line mutations in the tumour suppressor VHL which codes for the pVHL protein
86
What is the function of pVHL?
modulates the hypoxic response destruction of transcription factor HIF-1a target genes- angiogenesis, erythropoiesis and glycolysis and glucose uptake

Biology of stem cells, ageing and cancer (5 decks)

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