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Transmissible Cancer Flashcards

(64 cards)

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1
Q

Mutations which cause cancer often occur in which genes?

A

Genes encoding:

  • Oncogenes
  • Tumour suppressor proteins
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2
Q

What are examples of oncogenes?

A

Ras, Myc, RTK

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3
Q

Example of a tumour suppressor protein?

A

P53

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4
Q

What is the role of P5S?

A
  • Cell cycle checkpoint
  • DNA repair
  • Induction of apoptosis if DNA cannot be repaired
  • Increased cell adhesion to reduce tumour metastasis
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5
Q

How many copies of P53 are required to prevent formation of cancers?

A

A single copy of P53 is enough to prevent excessive tumour formation

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6
Q

Main characteristics of cancer cella/

A
  • Can rapidly proliferate
  • Can prevent induction of apoptosis
  • Can prevent cell cycle arrest
  • Can develop their own blood supply= angiogenesis
  • Can spread to invade other locations of the body via metastasising
  • Can rapidly develop mutations
  • Can evade immune detection
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7
Q

How do cancers develop?

A
  1. Neoplastic progression: mutations arise e.g. in tumour suppressor genes
  2. There is clonal expansion. Rapid excessive proliferation and selection
  3. The tumour cells move to different parts of the body (metastasis) or can even invade other individuals (transmissible tumours)
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8
Q

Where do many tumours tend to metastasise?

A
  • Liver
  • Bone marrow
  • Lung
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9
Q

Why do many tumour cells metastasise to certain locations?

A

Due to the overexpression of CXCR4 on the surface of tumour cells, causes them to move to locations expressing high levels of CXCL12 ligand

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10
Q

What is required for cancers to be transmissible?

A
  • Require a means of transmission

- Require an ability to evade immune detection

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11
Q

What prevent transmissible cancers in humans?

A
  • MHC variation between individuals. Very good ability of our immune systems to discriminate self from non-self
  • No route of direct transmission
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12
Q

Which species can transmissible cancers be observed in?

A

Tasmanian devils
Syrian hamsters
Canines
Marine bivalves

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13
Q

Tasmanian devils were found in Australia up until?

A

500 years ago

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14
Q

Tasmanian devils now have a restricted distribution where?

A

Mainland tasmania

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15
Q

What is DFTD?

A

Devil Facial Tumour Disease

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16
Q

When was DFTD first recognised?

A

1996

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17
Q

DFTD has spread through?

A

85% of the population

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18
Q

DFTD causes death within?

A

6 months

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19
Q

Death is caused by?

A

Organ failure
Metastasis
Starvation

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20
Q

We expect the natural population to go extinct within the next?

A

20-30 years

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21
Q

How did they recognise this was not caused by a virus but through allograft transmission?

A

Identical karyotypes between the tumours

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22
Q

What was the common karyotype compared to normal cells?

A

Normal cells: 14 chromosomes

Tumour cells: 13 chromosomes and non sex chromosomes

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23
Q

What is the karyotype?

A

The number and appearance of chromosomes in a eukaryotic nucleus

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24
Q

What else showed that the tumours were of the same origin?

A

Microsatellite analysis showed that the tumours from different devils were more closely related to eachother than they are to other devils

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25
What is the original origin of these cells?
From a female devil 20 years ago Schwann cell origin
26
How did they know the tumour cells are of neural cell origin?
Transcriptome of the tumour cells was very similar to the transcriptome of schwann cells
27
Where does DFTD cause tumours?
On the face
28
How is DFTD transmissible?
Biting during feeding and sex
29
How does DFTD evade immune detection?
- Has the same MHC alleles as the devils - Devils show low MHC diversity, probably due to the population bottle neck and due to high levels of inbreeding in fragmented populations
30
Why did they believe DFTD would not spread from Eastern to Northwestern populations?
As they showed varying MHC alleles More MHC diversity Skin allografts were rapidly rejected between the two populations
31
Did the northwestern devils catch DFTD?
Yes
32
How did the northwestern devils catch DFTD if skin allografts were rejected?
The DFTD was mutating to develop immune evasion techniques
33
What methods of immune evasion?
Down regulation of MHC-I to avoid T cell detection (reduced expression of genes associated with antigen processing and expression e.g. TAP1 and TAP2) Reduced recognition by NK cells
34
Why was the DFTD observed in the Northwestern populations less virulent?
It was strain 2 which is less virulent and tetraploid | There are different strains of DFTD, different karyotypic strains
35
Why was strain 2 less virulent?
Tetraploid which means it grows slower as it takes longer to replicate its DNA As the tumours grow slower the devils live for longer and virulence is reduced
36
Why is lower virulence associated with directly transmitted diseases unsurprising?
As for directly transmitted diseases there is a transmission-mortality tradeoff. Lower virulence is selected for and expected as it is more likely to be transmitted
37
What is DFT2?
A second transmissible neoplastic cell line which was discovered
38
DFT2 origin?
Male devil
39
DFT1 origin?
Female devil
40
Discovered of DFT2 showed that?
Multiple transmissible tumours can arise
41
How can we prevent the extinction of devils?
- Creating captive bred insurance populations - Developing a vaccine - Culling of infected devils
42
Why might we think that DFTD will evolve to become non-harmful?
Due to CTVT in canines, this has almost no virulence
43
What transmissible tumours were seen in laboratory syrian hamster populations?
Contagious reticulum cell sarcoma
44
Contagious reticulum cell sarcoma was spread via?
Mosquitos | Social contact
45
CTVT?
Canine Transmissible Venereal Cancer
46
CTVT is what type of cancer?
Histiocytic tumour
47
Where do the tumours grow?
Genitalia
48
Origin?
Wolf | ~11,000 years ago
49
CTVT spreads via?
Sexual transmission
50
How does CTVT overcome host immunity?
Developed immune evasion mechanisms: - Down regulation of MHC - Production of immunosupressive cytokines
51
Is CTVT virulent?
Not very virulent Self-limiting Regressive
52
Does CTVT metastasise?
Only in immunosuppressed canines
53
CTVT is very responsive to?
Chemotherapy
54
Transmissible cancer in bivalves is?
Haemic cancer
55
Haemic cancer?
Haemocytes | Leukaemia like
56
What cancer is CTVT?
Histiocytic tumour
57
What transmissible cancer is present in bivalves?
Haemic neoplasm | Hamocytes, leukaemia like
58
How are haemic neoplasms transmitted?
In the water | Via filter feeding
59
How are they not rejected?
Do not believe they have MHC | Immune systems have yet to be fully characterised
60
In bivalves the tumours can spread from?
One species to another
61
Example of spread from one species to another?
Spread from pallet clam to a golden carpet shell clam
62
The pallet clams are resistant to the?
Haemic neoplasm
63
Transmissible cancers only occur in humans in which cases?
- Immune suppression due to organ transplant | - From mother to child during development: Placental transmission
64
In order for placental transmission?
- Mother must have homozygotic HLA loci - Developing immune system may be tolerized by early exposure - Deletion of different HLA loci

Parasitology (17 decks)

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