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Principles Of Disease Year 1 > Cancer > Flashcards

Cancer Flashcards

1
Q

What is the ectoderm?

A
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2
Q

What is the ectoderm?

A

Outer most layer of cells including the epidermis and nerve tissue

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3
Q

What is the endoderm ?

A

The innermost layer of tissue and cells often form a the lining of gut

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4
Q

What is the middle layer of tissue called?

A

Mesoderm

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5
Q

What are the type of cancer cells?

A

Glandular - breast
Epithelial - squamous
Mesoderm - bone and muscle

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6
Q

What are adenocarcinomas?

A

Glandular cancers

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7
Q

What are sarcomas?

A

Mesoderm cell cancer

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8
Q

What are carcinomas?

A

Epithelial cell cancers

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9
Q

How does invasion and metastasis allow for cancer cell growth?

A

Able to migrate to different areas and metastasis due to lack of cell to cell adhesison

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10
Q

How do cancer cells survive?

A

Evade growth signals
Avoid immune destruction
They have unlimited replication potential
They promote inflammation
Evades cell death
Angiogenesis
Frequent mutation
Reprogrammed metabolism
Increased growth factors
Invade and metastasis

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11
Q

How do cancer cells continually get growth factors?

A

They sustain proliferative signals by bypassing normal growth factor pathways

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12
Q

How do cancer cells avoid growth signals?

A

They use gene silencing to ignore the homeostatic mechanisms

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13
Q

What is gene silencing?

A

Interruptiom of a gene at transcriptional levels

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14
Q

How do cancer cells avoid immune destruction?

A

They hijack the immune checkpoint
They modulate STING

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15
Q

What is STING?

A

It’s an important signalling molecule which is important in controlling the transcription of body defence genes

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16
Q

What is an immune checkpoint?

A

Mechanism that maintains self tolerance during an immune response

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17
Q

What is PDL1 and PDL2?

A

Programme cell death protein
They surpress the adaptive immune system during pregnancy or autoimmune diseases
Give the opportunity for cancer to invade the immune system

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18
Q

What is a telomere?

A

The end of chromosomes

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19
Q

How do cancer cells survive using their replicative potential?

A

Telomeres normally decide when the cell has reached the normal number of divisions and causes the cell to enter senescencebut cancer cells don’t shorten their chromosomes after fission

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20
Q

How does tumour promoting inflammation help the cancer survive?

A

Inflammatory cells release growth factors which stimulate cancer cell growth, This creates new blood vessels for the cancer.

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21
Q

How does necrosis benefit cancer cells?

A

Necrosiss causes inflammation and releases bioactive regulatory factors which stimulates viable cells to proliferate
Radical oxygen speciesrae released by inflammatory cells which increases the risk of mutation

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22
Q

How does angiogenesis help cancer cells?

A

New route for nutrients to reach cancer but also for cancer to metastasis

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23
Q

What does caspases do?

A

Triggers apoptosis
Mutation in the gene allow cancer cells to go unchecked and continue growing

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24
Q

All mutations are somatic.
True or false

A

False
Most are somatic so DNA in cells is damaged due to an acquired muatation
Only egg or sperm mutations are inherited this u a germline mutation

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25
What is haploinsufficiency ?
Only 1 of the mutated alleles can lead to cancer rather than two.
26
What is the basemnte membrane made of?
Extracellular matrix proteins Which are proteoglycans and collagen
27
What is the seed and soil theory?
Cancer spreads via cell surface by providing an ideal microbe environment
28
What is E cadherin?
Type of calcium dependant CAM involved in epithelial cell adhesion Often epithelial cancers down regulate or mutate e cadherin
29
What does sub clonal mean?
They are genetically identical but differed by mutations
30
What are the 2 types of mechanism of metastasis?
Monoclonal or polyclonal
31
What are the 2 patterns of metastasis?
Linear or Branched
32
What are epithelial mesenchymal transition?
When epithelial cells become independent mesenchymal cells with the ability to move and invade their local environment. Loss of cell polarity destroys cell junctions, alongside this there is a down regulation of e chadherin
33
What are the 5 steps of metastais?
Invasion Intravasation Transport Extravasation Colonisation
34
What is invasion?
Entry into ECM Mutations in cadherins which are glycoprotein Integrins enable cells to become mobile by modifying membrane distribution so the cell can leave the ECM Protease can degrade components of the ECM
35
What are mesenchymal cells?
Typically stem cells in the bone marrow
36
Where does EMT happen?
Embryogenesis Cancer
37
All cells in the tumour have the ability to metastasis True or false
False Tumour stroma
38
What are integrins?
-Modify membrane distribution here allow cells to break free
39
How do protease help in metastasis?
Degrade components of ECM
40
What is intravasation?
Entry into blood or lymph
41
What is the stoma side of the basal membrane ?
The side which faces the ECM and blood vessels
42
What is autocrine stimulation?
Cells which release their own growth factors to combine with the cell surface proteins like sarcomas
43
How does intravasation happen?
Protease enzyme breaks down the basement membranes hence enabling tumour cells to pass between endothelial cells And into the bloodstream
44
What is transendothelial migration?
Movement of tumour cells into the bloodstream
45
What is transport?
Circulating tumor cells travelling unidirectionally And infect the first organ they reach
46
What is the first pass organ?
The first organ that CTCs in the bloodstream reach after leaving the primary tumor
47
What is extravasation?
It's how tumor cells leave the blood into new organs E selectin binds the cancer cell to the endothelium Transendothelial migration The basement membrane degrades
48
What is colonisation.
Cells can spread and remain dormant till they reach favourable conditions to colonies taking into account blood vessels and nutrients
49
What is micrometastases?
When cancer cells spread around the body but are dormant because of unfavorable condition or kept at bay by the immune system
50
What is sprouting?
Growth of endothelial cells using a balance of inhibitor and inducer factors (angiogenesis switch)
51
What is chemotherapy?
Chemicals which target DNA RNA and proteins Forces cell to undergo apoptosis Non specific to cancer cells
52
How is chemotherapy delivered?
Orally or using IV Done in cycles (frequency of administration)
53
What 3 settings can chemotherapy be given?
Neoadjuvant Adjuvant Disease Control Palliative
54
What is neoadjuvant?
Before surgery with the aim to reduce cancer aigns
55
What is adjuvant?
Reduce risk of cancer returning
56
What is disease control palliative?
Control the disease for as long as possible
57
What are the 3 types of chemotherapy?
Alkylating agents and pt drugs? Antimetabolites Organic drugs
58
What is an alkylating agent and pt drugs?
Blocks DNA replication Create cross links hence change the structure of the DNA helix All phases of cell cycle
59
What are the 3 organic drugs?
Vince alkaloids Taxanes Anthracyclines
60
What are antimetabolites?
Structurally mimic essential molecules requires so it blocks the enzyme and doesn’t cause cell division Act on S and G phase
61
What do vinca alkaloids do?
Bind to tubulin to prevent formation of mitotic spindle
62
What are taxanes?
Prevent tubulin polymerisation hence prevents mititic spindle formation
63
What do anthracyclines do?
Inhibits an enzyme for mitotic torsion
64
What are personalised systemic therapies?
65
What are hormonal therapies?
Oestrogen plays a key role in increasing cellular replication hence a greater chance of mutation We are targeting these hormones by blocking them or preventing their formation
66
How does tamoxifen work?
Binds to oestrogen receptors
67
What are the types of organic drugs?
Vinca alkaloids Taxanes Anthracyclines
68
What is the most common side effects of chemo?
Nausea
69
What are the personal system therapies?
Hormonal therapies Targeted therapies Immunotherapies

Principles Of Disease Year 1 (16 decks)

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